Get Adobe Flash player

AMYLOIDOSIS OF CARDIOVASCULAR SYSTEM

Аuthors:  Hetmanska V. M., Zakorko I.-M. S., Moskalenko Y. V., Moskalenko R. A., Diachenko О. О.

Pages: 1–9

Abstract

         

In most industrialized countries with a high level of urbanization diseases of the cardiovascular system are the leading cause of morbidity and mortality. Every year about 9.4 million people die from cardiovascular diseases. One of the causes of cardiovascular disease is an amyloidosis. Its incidence in the population, according to recent data, is 1 in 50 thousand of people, there is a tendency to more frequent detection of cases.

The aim of the study is to analyze the literature to determine different proteins’ role in the etiopathogenesis of amyloidosis of the cardiovascular system.

Amyloid deposition in the heart may have different anatomical allocation, including atrial, ventricles, perivascular spaces such as heart valve leaflets, and in some cases – in the cardiac conductive system. Amyloidosis of the heart is established or by the help of positive cardiac biopsy with the presence of amyloid infiltration, or by an increase of left ventricular wall > 12 mm, in the case of arterial hypertension (AH) absence or absence of other potential causes of the genuine LV hypertrophy with a positive cardiac biopsy.

Among amyloid proteins, which affect a heart, there are such types: AL-amyloidosis (amyloid of light chains), family amyloidosis (F), senile systemic amyloidosis (SSA), isolated atrial amyloidosis (IAA) and the secondary (AA) amyloidosis.

Recently amyloidosis of heart went out of the category of rare diseases; it has become possible thanks to the different methods of research, including the possibility of studying the heterogeneity of the protein composition of amyloid fibril formation. However, systemic amyloidosis and particularly amyloidosis of the heart continue to belong to diseases, which are diagnosed difficult, considering the non-specific symptoms of disease, a small suspicion among physicians with regard to amyloidosis and multiple organ destruction.

Keywords: amyloidosis, cardiovascular system, amyloid proteins, heart failure, atherosclerosis, biomineralization.

This email address is being protected from spambots. You need JavaScript enabled to view it.

The full text

To view the full text

References

  1. The European health report 2005: public health action for healthier children and populations. Copenhagen: WHO Regional Office for Europe, 2006.
  2. Fikrle M, Paleceka T, Kuchynka P. et al. Cardiac amyloidosis: A comprehensive review. Cor et vasa. 2013; 55:e60–e75.
  3. Gaidev YuO, Cornatsky VM. [Health problems and directions of its improvement in current conditions]. Ukrainian Journal of Cardiology. 2007; 5: 12–16. [In Ukrainian].
  4. Falk RH. Diagnosis and management of the cardiac amyloidosis. Circulation. 2005; 112(13): 2047-60.
  5. Kumar V, Abbas AK, Fausto N. (Eds.) Diseases of immunity: amyloidosis. Pathologic Basis of Disease, Elsevier Saunders Philadelphia, PA. 2005, pp. 258–264.
  6. Sipe JD., Cohen AS. Review: history of the amyloid fibril. J. of Structural Biology. 2000; 130: 88-98. doi:10.1006/ jsbi.2000.4221.
  7. Linke RP. Highly sensitive diagnosis of amyloid and various amyloid syndromes using Congo red fluorescence. Virchows Arch. 2000; 436: 439–48.
  8. Prusiner SB, DeArmond SJ. Prion protein amyloid and neurodegeneration. Amyloid Int. J. Exp.Clin. Invest. 1995; 2:39-65.
  9. Gertz MA., Lacy MQ, Dispenzieri A. Amyloidosis: diagnosis and management. Clin Lymphoma Myeloma. 2005; 6 (3): 208-19.
  10. Goette A, Rocken C. Atrial amyloidosis and atrial fibrillation: a gender-dependent arrhythmogenic substrate? European Heart Journal. 2004; 25: 1185–1186.
  11. Collins A.B, Smith RN., Stone JR. Classification of amyloid deposits in diagnostic cardiac specimens by immunofluorescence. Cardiovasc Pathol. 2008; 18(4):205-16. doi: 10.1016/j.carpath. 2008.05.004. 
  12. Westermark P. Benson MD, Buxbaum JN et al. A primer of amyloid nomenclature. Amyloid. 2007. Vol. 14. P.179-183.
  13. Dubrey SW. Cha K, Anderson J et al. The clinical features of immunoglobulin light-chain (AL) amyloidosis with heart involvement. QJM. 1998; 91: 141-157.
  14. Falk RH. Ethnic disparity in intracranial hemorrhage among anticoagulated patients with atrial fibrillation: an answer in search of a question? J Am Coll Cardiol. 2007; 50(4):316-8. Epub 2007 Jul 6.
  15. Mohtya D, Damyc T, Cosnayd P et al. Cardiac amyloidosis: Updates in diagnosis and management. Archives of Cardiovascular Disease. 2013; 106: 528-540.
  16. Falk RH, Dubrey SW. Amyloid Heart Disease. Progress in Cardiovascular Diseases. 2010; 52: 347–361.
  17. Magy-Bertrand N. Transthyretin amyloidoses. Rev Med Interne. 2007; 28: 306-13.
  18. Gillmore JD, Booth DR, Pepys MB et al. Hereditary cardiac amyloidosis associated with the transthyretin Ile122 mutation in a white man. Heart. 1999; e2:82.
  19. Saraiva MJ. Sporadic cases of hereditary systemic amyloidosis. N Engl J Med. 2002; 346:1818-9.
  20. Ng B, Connors LH, Davidoff R et al. Senile systemic amyloidosis presenting with heart failure: a comparison with light chain-associated amyloidosis. Archives of Internal Medicine. 2005; 165: 1425–1429.
  21. Falk RH. Cardiac amyloidosis: a treatable disease often overlooked. Circulation. 2011; 124 (9): 1079-85. doi: 10.1161/CIRCULATIONAHA. 110.010447.
  22. Glaudemans AW, Slart RH, Zeebregts CJ et al. Nuclear imaging in cardiac amyloidosis. Eur J Nucl Med Mol Imaging. 2009; 36: 702-14.
  23. Andreola A. Bellotti V, Giorgetti S et al. Conformational switching and fibrillogenesisin the amyloidogenic fragment of apolipoprotein A-I. J Biol Chem. 2003; 278: 2444-51.
  24. Tanskanen M, Kiuru-Enari S, Tienari P et al. Senile systemic amyloidosis, cerebral amyloid angiopathy, and dementia in a very old Finnish population. Amyloid. 2006; 13: 164 –9.
  25. Benson MD, Breall J, Cummings OW et al. Biochemical characterisation of amyloid by endomyocardial biopsy. Amyloid. 2009; 16: 9-14.
  26. Esplin BL, Gertz MA. Current trends in diagnosis and management of cardiac amyloidosis. Curr Probl Cardiol. 2013; 38: 53-96.
  27. Cornwell GG, Murdoch WL, Kyle RA et al. Frequency and distribution of senile cardiovascular amyloid. A clinicopathologic correlation. Am J Med. 1983; 75: 618-23.
  28. Takemura G, Takatsu Y, Doyama K et al. Expression of atrial and brain natriuretic peptides and their genes in hearts of patients with cardiac amyloidosis. J Am Coll Cardiol. 1998; 31: 754–65.
  29. Mugnai G, Cicoira M, Rossi A et al. Syncope in cardiac amyloidosis and chronic ischemic heart disease: a case report. Exp Clin Cardiol. 2011; 16:51-3.
  30. Rocken C, Tautenhahn J, Buhling F et al. Prevalence and pathology of amyloid in atherosclerotic arteries. Arterioscler Thromb Vasc Biol. 2006; 26: 676–7.
  31. Kyle RA, Gertz MA. Primary systemic amyloidosis: clinical and laboratory features in 474 cases. Semin Hematol. 1995; 45-59.
  32. Jacobson DR, Pastore RD, Yaghoubian R et al. Variant sequence transthyretin (isoleucine 122) in late-onset cardiac amyloidosis in Black Americans. The New England Journal of Medicine. 1997; 336:466–473.
  33. Kristena AV, Schnabelb PA, Wintera B et al. High prevalence of amyloid in 150 surgically removed heart valves-a comparison of histological and clinical data reveals a correlation to atheroinflammatory conditions. Cardiovascular Pathology. 2010; 19: 228–235.
  34. Rapezzi C, Merlini G, Quarta CC et al. Systemic cardiac amyloidoses: disease profiles and clinical courses of the 3 main types. Circulation. 2009; 120: 1203-12.
  35. Steiner I. The prevalence of isolated atrial amyloid. J Pathol. 1987;153(4): 395-8.
  36. McCormick M, Rahimi F, Bobryshev YV et al. S100A8 and S100A9 in human arterial wall. The journal of biological chemistry. 2005; 280 (50): 41521–41529.
  37. Howlett GJ, Moore KJ. Untangling the role of amyloid in atherosclerosis. Curr Opin Lipidol. 2006; 17: 541–7.
  38. Yanamandra K, Alexeyev O, Zamotin V et al. Amyloid formation by the pro-inflammatory S100A8/A9 proteins in the ageing prostate. Plos One. 2009; 4(5): e5562.
  39. Gharibyan AL. Amyloids here, amyloids there…What’s wrong with them? VMC-KBC, Umeå University. 2012. 67 p.
  40. Moskalenko RA. [Role of calprotectin S100a8/S100a9 in pathological biomineralization]. J Clin Exp Med Res. 2016. Vol. 4. (2). P. 186-194.

INFLUENCE OF KORVITYN ON IMMUNE RESPONSE INDICES IN EXPERIMENTAL PNEUMONIA DEVELOPMENT

Аuthors: O. O. Chuhay

Pages: 10–16

Abstract

         

Introduction. Despite all attempts of doctors, pneumonia remains a common medical and social problem in the 21st century both in developing and developed countries. According to WHO, pneumonia is an acute, usually, infectious disease predominantly of the respiratory part of the lungs / respiratory bronchioles and alveoli / with the presence of exudate with neutrophil content in the alveoli and is seen on X-ray as infiltrative darkening of the lungs. Currently, bioflavonoids are often used as an accompanying therapy to correct disturbances, induced by long-lasting inflammatory process. There are over 150 such biologically active substances with similar properties. Flavonoids possess antioxidant, membrane-protective, angioprotective, anti-inflammatory, immunomodulating properties, etc. Quercetin has the most powerful antioxidant action among flavonoid substances.

Purpose: to investigate the influence of korvitin on indices of cell-mediated and humoral immunity in experimental pneumonia development.

Materials and Methods. Experimental investigation was performed on 30 guinea pigs (males) weighing 180–220 g, distributed into 5 groups, 6 animals in each: I group – intact guinea pigs (control); II group – guinea pigs with experimental pneumonia on the 6th day; III group – guinea pigs with experimental pneumonia on the 10th day; IV group – guinea pigs with experimental pneumonia on the 20th day; V group – guinea pigs with experimental pneumonia under the action of korvityn. This antioxidant was injected in the dose 40 mg/kg intraperitoneally for 7 days (from 13 to 20 day). Experimental pneumonia was induced by intranasal introduction of Staphylococcus aureus culture to animals by the method of V. N. Shlyapnikov and co-authors. The animals were decapitated on the 6th, 10th and 20th day of EP development. Amount of T- and B-lymphocytes (CD3+ and CD19+) in the blood was determined by the method of E. F. Chernushenko, L. S. Kogosova. The level of circulating immune complexes was determined by the method of V. Haskova, J. Kaslik.

Discussion. Both early and late periods of EP were characterized by the disturbance of immune system functioning. Experimental pneumonia in guinea pigs was accompanied by inhibition of cell-mediated immunity, which was marked by the decrease in T-lymphocyte level in the blood. Simultaneously, activation of humoral immunity was observed, marked by increase in B-lymphocytes and CIC in the blood in early and late periods of EP. This condition may be caused by the nature of the agent itself. Since EP in guinea pigs was caused by Staphylococcus aureus, which is a gram-positive bacterium, activation of humoral immunity plays a significant role in combating this infection. Medication «Korvityn» prevented further development of immune system imbalance, limiting inflammatory reaction. This effect may be caused by anti-inflammatory and immunomodulating properties of Korvityn, which may be recommended as an accompanying therapy in pneumonia.

Keywords: pneumonia, Korvityn, humoral immunity, cell-mediated immunity.

This email address is being protected from spambots. You need JavaScript enabled to view it.

The full text

To view the full text

References

  1. Drannik GM. Klinicheskaya immunologiya i alergologiya [Clinical immunology and allergology]. K.: LCC «Poligraf plus» Publ., 2010. 552 p.
  2. Chen K, Kolls K. T cell-mediated host immune defenses in the lung. Annu Rev Immunol. 2013;31:605–633.
  3. Moore BB, Moore TA, Toews GB. Role of T- and B-lymphocytes in pulmonary host defences. Eur Respir J. 2001;18:846–856.
  4. Marshall NB, Swain SL. Cytotoxic CD4 T cells in antiviral immunity. J Biomed Biotechnol. 2011;2011:954602.
  5. Chopyak VV, Potomkina HO, Gavrylyuk AM et al. Posibnyk dlia provedennia praktychnykh zaniat z klinichnoi imunolohii ta alerholohii [A guide for conducting practical classes in clinical immunology and allergology]. Lviv: Tetyuh TV Publ., 201 5. 208 p.
  6. Kuznetsov LV, Babadzan VD, Harchenko NV et al. Imunolohiia: pidruchnyk [Immunology: textbook]. Vinnitsa: TOV «Merkuri Podillya» Publ., 2013. 526 p.
  7. Ataman OV. Patofiziolohiia. T.1. Zahalna patolohiia [Pathophisiology. V1. Common pathology]. Vinnitsa: Nova knyga Publ., 2012. 592 p.
  8. Chekman IS. Klinichna fitoterapiia [Clinical phytotherapy]. K: A.S.K. Publ., 2003. 552 p.
  9. Mohort MA, Danova IV, Myslyvets OV. [Pharmacodynamics of quercetin and its pharmaceutical forms]. Ukr. Pharmacology and drug toxicology. 2009;6(13):3-7.
  10. Levitskiy AP, Skydan MI, Skydan KV. [The use of quercetin in dentistry]. Rus. Herald of dentistry. 2010;1:81–87.
  11. Shlapnykov VI, Solodova TL, Stepanova SA et al. Eksperimentalnyye modeli ostrykh pnevmoniy. vyzvannykh uslovno-patologicheskimi bakteriyami i ikh assotsiatsiyey: metod. ukazaniya [Experimental models of acute pneumonia caused by opportunistic bacteria and their association: methodical guidelines]. Saratov. 1988. 30 p.
  12. Chernushenko EF, Kogosova LS. Immunologiya i immunopatologiya zabolevaniy legkikh [Immunology and immunopathology of lungs diseases]. К.: Zdorovya Publ., 1981. 208 p.
  13. Haskova V, Kaslik J, Matejckava M. Novy zpusob stanoveni circulujicich imunokomplexy w lidskych serech. Cas. Lek. Ces. 1977;116(14):436–437.

ULTRASTRUCTURAL CHANGES IN THE SPINAL CORD OF RATS WITH EXPERIMENTAL ALLERGIC ENCEPHALOMYELITIS IN THE BACKGROUND OF MESENCHYMAL STEM CELLS AND INTERLEUKIN-10

Аuthors: V. V. Vaslovych, L. D. Pichkur, T. A. Malysheva, S. T. Akinola, S. A. Verbovska, O. K. Toporova, N. S. Shuvalova

Pages: 17–30

Abstract

         

Introduction. Human umbilical cord derived mesenchymal stem cells (UCd-MSC) are multipotent. They are able to migrate to the sites of central nervous system damage, contribute to the restoration of the number of endogenous oligodendrocytes, produce immunomodulatory effects and are able to synthesize antiinflammatory cytokines (IL-10).

Purpose. To investigate the effect of UCd-MSC and IL-10 on the processes of de- and remyelination of nerve fibers of the spinal cord of rats with experimental allergic encephalomyelitis at the ultrastructural level.

Materials and methods. The study was performed on 23 white female rats, weighting 210 g. The relapsing course of EAE was obtained by inserting Freund's adjuvant into the rat’s hind limb pads. Six groups of animals were formed. 18 rats from EAE were intravenously or suboccipitaly administered in different combinations of IL-10 (0.1 μg) and MSC no transfected (1 million) and MSC (1 million) transfected with the IL-10 gene. Electron microscopy was used to investigate the ultrastructural changes in the lumbar spinal cord of experimental animals at the 35th and 60th day of the experiment. Also, the ratio of the width of the myelin sheath (MS) to the diameter of the axial cylinder (AC) was determined on the semi-thin sections. Statistical analysis of the results was performed using non-parametric rank discriminant Kruskel–Wallis analysis followed by application of the U-Mann-Whitney criterion using STATISTICA 6.1 statistical software package.

Results. In animals of all experimental groups, the peak of EAE was observed for 19–20 days and developed a chronic remitting flow. In the comparison group (EAE), part of the oligodendrocytes already in the early stages are in a para apoptotic state, the degree of which increases over time. Reactive modified swollen forms of oligodendroglia, along with destructive, are more often represented in the study group III EAE + IL-10. Hypertrophic oligodendrocytes are more likely to be detected after the introduction of MSCs. Oligodendrocytes of group V (EAE + MSK transfected with IL-10 gene) for 60 days of study have signs of functional tension (swollen mitochondria with crysts fragmentation). In all experimental animal groups, with the exception of the comparison group, a reduced degree and demyelination area with a simultaneous partial reduction of the intralamilar and almost complete – periaxonal edema. In the study group III (EAE + IL), none of the terms of the study showed normalization of the structure of myelin membranes. Figures of remyelination of nerve fibers in all experimental groups were detected already on the 35th day of the study. The ratio of the thickness of the myelin sheath to the diameter of the axial cylinder is statistically significantly reduced relative to the comparison group in all treated groups except for the III (EAE + IL) for 35 days and III (EAE + IL) and V (EAE + MSC (T) at 60 days of the experiment.

Conclusions. MSCs help reduce interlamilar, periaxonal edema and demyelination in animals with EAE.Suboccipitaly introduced into CSF IL-10 does not produce statistically significant effects, however, to some extent, strengthens the effect of MSC.In all animal groups and in all terms, MSCs promote stimulation of remyelination processes.

Keywords: experimental allergic encephalomyelitis, mesenchymal stem cells, morphological changes, interleukin-10.

This email address is being protected from spambots. You need JavaScript enabled to view it.

The full text

To view the full text

References

  1. Starzl TE. Chimerism and tolerance in transplantation. Proc Natl Acad Sci U S A. 2004 Oct 5;101 Suppl 2:14607-14. doi: 10.1073/pnas.0404829101. PMID: 15319473. PMCID: PMC521985.
  2. Pichkur LD, Verbovskaya SA, Akinola ST, Chitaeva GE. [The main pathogenetic mechanisms of the demyelination process in the central nervous system and the possibility of its correction.] Ukr. neurological journal. 2017;(2):12–19. Ukrainian. http://www.ukrneuroj.com.ua/ svizhij_nomer.php?nid=43.
  3. Constantin G, Marconi S, Rossi B, Angiari S, [et al] Adipose-Derived Mesenchymal Stem Cells Ameliorate Chronic Experimental Autoimmune Encephalomyelitis. Stem Cells. 2009 Oct;27(10):2624-35. doi: 10.1002/stem.194. PubMed PMID: 19676124.
  4. Kovalchuk MV, Deryabina OG, Pichkur LD, Verbovskaya SA et al. Distribution of transplanted human mesenchymal stem cells from Wharton’s Jelly in the central nervous systems of the EAE rats. Biopolymers and Cell. 2015;31(5):371 – 378. doi: 10.7124/bc.0008F9.
  5. Tsymbaliuk VI, Velychko OM, Pichkur OL, Verbovska SA et al. Effects of human Wharton’s jelly-derived mesenchymal stem cells and interleukin-10 on behavioral responses of rats with experimental allergic encephalomyelitis. Cell and organ transplantology. 2015; 3(1): 40-45. http://transplantology.org/2015-3-1-uk/article-4.
  6. Theotokis P, Kleopa KA, Touloumi O, Lagoudaki R et al. Connexin43 and connexin47 alterations after neural precursor cells transplantation in experimental autoimmune encephalomyelitis. Glia. 2015 Oct;63(10):1772-83. doi: 10.1002/ glia.22843. Epub 2015 Apr 27. DOI: 10.1002/glia.22843. PMID: 25914045.
  7. Muja N, Cohen M, Zhang J, Kim H et al. Neural precursors exhibit distinctly different patterns of cell migration upon transplantation during either the acute or chronic phase of EAE: A serial MR imaging study. Magn Reson Med. 2011 Jun;65(6):1738-49. doi: 10.1002/ mrm.22757. Epub 2011 Feb 8. PMID: 21305597 PMCID: PMC3190231.
  8. Bai L, Lennon DP, Eaton V, Maier K et al. Human bone marrow-derived mesenchymal stem cell induce Th2 polarized immune response and promote endogenous repair in animal models of multiple sclerosis. Glia. 2009 Aug 15;57(11):1192-203. doi: 10.1002/glia.20841. PMID: 19191336 PMCID: PMC2706928.
  9. Barhum Y, Gai-Castro S, Bahat-Stromza M, Barzilay R et al. Intracerebroventricular transplantation of human mesenchymal stem cells induced neurotrophic factors attenuates clinical symptoms in a mouse model of multiple sclerosis. J Mol Neurosci. 2010 May;41(1):129-37. doi: 10.1007/s12031-009-9302-8. Epub 2009 Nov 10. PMID: 19902385.
  10. Fedulov AS, Borisov AV, Moskovskikh YV, Zafranskaya MM. et al. [Autologichnaya transplantatsiya mezenkhimal'nykh stvolovykh kletok kak metod modifikatsii klinicheskogo techeniya rasseyannogo skleroza] Nevrologiya i neyrokhirurgiya. Vostochnaya Yevropa. 2016;4:516-22. ISSN 2226-0838.
  11. Zheleznikova GF, Scripchenko NV, Ivanova GP, Surovzeva AV et al. [Faktory immunopatogeneza rasseyannogo skleroza] Ros. Immunolog. zhurn. 2015;9(3):261-82. ISSN: 1028-7221. https://elibrary.ru/contents.asp?issueid=1554991&selid=25474994.
  12. Zafranskaya MM, Nizheharodava DB, Ivanchyk HI, Borisov AV et al. [Dinamika tsitokinov u patsiyentov s rasseyannym sklerozom do i posle kletochnoy terapii.] Immunopatologiya, allergologiya, infektologiya. 2014; 3:82-91. ISSN: 2412-320X. DOI: 10.14427/jipai.2014.3.82. https://elibrary.ru/item.asp?id=22860604.
  13. Shchоkina EG, Shtrygol SY, Drogovoz SM. Achievements аnd Prospects оf Cytokine аnd Anti-Cytokine Therapy. Scientific Journal of the Ministry of Health of Ukraine. 2013;1(2): 121-29. http: //irbis-nbuv.gov.ua/.../cgiirbis_64.exe?..
  14. Bathina S, Das UN. Brain-derived neurotrophic factor and its clinical implications. Arch Med Sci. 2015 Dec 10;11(6):1164-78. doi: 10.5114/ aoms.2015.56342. Epub 2015 Dec 11. PMID: 26788077 PMCID: PMC4697050.
  15. Tsymbaliuk V, Deriabina E, Shuvalova N, Maslova O. et al. [Phenotypical changes and proliferative potential of mesenchymal stem cells from humans Wharton’s jelly in the cultivation conditions.] Ukranian Neurosurgical Journal. 2015;(2):17-24. Ukrainian. doi: 10.25305/unj.45290.
  16. Palade GE. A study of fixation for electron microscopy. J Exp Med. 1952 Mar;95(3):285-98. PMID: 14927794 PMCID: PMC2212069.
  17. Gayyer G. Elektronnaya gistokhimiya. Per. s nem. M.: Mir, 1974. 488 p. http://www.studmed.ru/gayer-g-elektronnaya-gistohimiya _362a532de03. html.
  18. Reynolds ES. The use of lead citrate at high pH as an electronopague stain in electron microscopy. J Cell Biol. 1963 Apr;17:208-12. PMID: 13986422 PMCID: PMC2106263.
  19. Tsymbalyuk VI, Markova OV, Pichkur LD, Vaslovych VV et al., vynakhidnyky; Natsionalnyy medychnyy universytet, patentovlasnyk. [Sposib otsinky stupenya demiyelinizatsiyi aksoniv pry eksperymentalnomu alerhichnomu entsefalomiyeliti] Patent Ukrayiny 17499. 2006. Ver 15.
  20. Rebrova OYu. [Statistical analysis of medical data. Application of the application package STATISTICA.] M .: Media Sphere; 2002. http://www. studmed.ru/rebrova-oyu-statisticheskiy-analiz-medicinskih-dannyh_0149fe87d1d. html. Russian.
  21. Shabanov DA. [Onlayn-konspekt kursa "Biometricheskaya obrabotka dannykh v zoologii i ekologii"]. 2011. adres dostupa: https://batrachos.com/ biometria.
  22. Mastitskiy SE, Shitikov VK. [Statisticheskiy analiz i vizualizatsiya dannykh s pomoshch'yu R.] 2014. Elektronnaya kniga, adres dostupa: http://r-analytics.blogspot.com. http://www.soc.univ.kiev.ua/sites/default/files/library/elopen/mastitsky_and_shitikov_2014_r_tutorials.pdf.
  23. Polenov AL, Onishchenko IL, Krasnovskaya IA. [Morfofunktsional'nyy analiz yadernogo apparata nonapeptidergicheskikh neyrosekretornykh kletok gipotalamusa pozvonochnykh] Tsitologiya. 1996;38(1):28-38.
  24. Schröder JM, Sommer C. Mitochondrial abnormalities in human sural nerves: fine structural evaluation of cases with mitochondrial myopathy, hereditary and non-hereditary neuropathies and review of the literature. Acta Neuropathol. 1991;82(6):471-82. PMID: 1785260.

EXPRESSION OF TAU-PROTEIN IN THE SENSORIMOTOR CORTEX OF THE CEREBRAL HEMISPHERES IN THE MODELING OF TRANSIENT ISCHEMIA AGAINST THE BACKGROUND OF PREVIOUS SENSITIZATION BY THE BRAIN ANTIGEN AND IMMUNOCORRECTION OF THE CHANGES

Аuthors: L. M. Yaremenko, S. E. Shepelev, L. P. Вidna, A. N. Grabovoi

Pages: 31–37

Abstract

         

Introduction. Ischemic brain damage may was caused by a violation of synaptic transmission after primary thromboembolism. One of the proteins, synaptic pulse transfer and axonal transport is tau-protein. The scientific literature has extensively studied the detection of tau protein in Alzheimer's disease, and is practically was not described in cases of ischemic brain damage in conditions influencing the body of immunomodulator of the new generation. Therefore, the purpose of the work was to study the peculiarity of the expression of tau protein in the sensomotor cortex in the modeling of transient ischemia against the background of the prior sensitization of the brain antigen and immunocorrection of their effects.

Materials and Methods. Studies performed were on 135 male Wistar rats. Histological, immunohistochemical, densiometric and statistical methods of investigation were used. Immunohistochemical reaction performed was according to the manufacturer's protocol with a polyclonal rabbit antibody against tau protein 1: 200 (Thermo, USA). EnVisionTM FLEX Detection System (Dako, Denmark) used was to visualize reaction products. Sections contrasted with Gyll Hematoxylin.

Discussion. It has been established that sensitization with the brain antigen leads to diffuse degenerative changes in the cerebral cortex accompanied by an increase in the expression of the tau protein. Previous sensitization by the brain antigen leads to an increase in the severity of brain damage and the potentiation of the expression of the tau protein in acute circulatory disturbance. The use of immunophan provides a reduction in the expression of tau protein in the sensorimotor cortex caused by both sensitization of the brain antigen and its combination with transient disturbance of cerebral blood flow.

Keywords: brain, sensitization by brain antigen, brain ischemia, tau-protein, imunophan.

This email address is being protected from spambots. You need JavaScript enabled to view it.

The full text

To view the full text

References

  1. Mishchenko TS, Darius VI, Baranova KV. [Interconnection of inflammatory and anti-inflammatory markers in patients with acute period of cerebral stroke]. Ukr. Journal of Psychoneurology. 2014;22(79):16-18.
  2. Scholz T, Mandelkow E. Transport and diffusion of Tau protein in neurons. Cellular and molecular life sciences. 2014;71(16):3139-3150.
  3. Kadavath H, Jaremko M, Jaremko Ł, Biernat J, Mandelkow E, Zweckstetter M. Folding of the tau protein on microtubules. Angewandte Chemie International Edition. 2015;54(35), 10347-10351.
  4. Ren X, Hu H, Lewis SE, Hunsberger H, Reed M, Simpkins JW. Human Tau Protects Ischemic Brain Injury. Stroke. 2016;47(Suppl 1):A128-A128.
  5. Bielewicz J, Kurzepa J, Czekajska-Chehab E, Stelmasiak Z, Bartosik-Psujek H. Does serum tau protein predict the outcome of patients with ischemic stroke? Journal of Molecular Neuroscience, 2011;43(3): 241-245.
  6. Lebedev VV, Pokrovskii VI. Vestn. Ros. Akad. Med. Nauk, 1999;4:56–61.
  7. Fujii H, Takahashi T, Mukai T, Tanaka S, Hosomi N, Maruyama H, Sakai N, Matsumoto M: Modifications of tau protein after cerebral ischemia and reperfusion in rats are similar to those occurring in Alzheimerʼs disease hyperphosphorylation and cleavage of 4- and 3-repeat tau. J Cereb Blood Flow Metab. 2017;37: 2441–2457.
  8. Hurn PD, Macrae IM. Estrogen as a neuroprotectant in stroke. J. Cereb. Dlood. Flow. Metab. 2000;20:631-652.
  9. Grabovoy OM, Yaremenko LM. Sposib modeliuvannia kombinovanoho sudinno-imunnoho poshkodzhennia mozku [Method of modeling of combined vascular-immune brain damage]. Ukrainian patent, no 36843, 2008.
  10. Zapadnyuk IP, Zapadnyuk VI, Zakhariya EA, Zapadnyuk BV. Laboratornii zhivotnii. Razvedenie, soderzhanse I ispolzovaniia v eksperemente [Laboratory animals. Breeding, content and use in the experiment]. Kiev: Vishcha school,, 1983. 383 p.
  11. Grabovoy AN, Jaremenko LM. [The condition of brain hemisphere cortex at circulation problems modulation and at the correction of accompanying changes in immune system in rats]. Naukoviy visnik of Bohomolets National medical university. 2009;4(26):28–33.
  12. Yaremenko LM, Garboviy OM. Influence of sensitization with brain antigen sensitization on the condition of cerebral cortex sensomotor neuroglial elements of their immunohistochemical detection. Deutscher Wissenschaftsherold. 2016;2:6-9.
  13. Yaremenko LM, Graboviy OM, Slichna GM, Chukhrai SN, Slichniy IV. [Expression of tau protein in the sensorimotor cortex of large hemispheres of the brain during modeling and transient ischemia under conditions of immunocorrection]. Prikladni asperti morfolodiy: materialy naukovo-praktychnoi konferencii [Applied Aspects of Morphology (Collection of Materials of the Scientific and Practical Conference, October 20 – 21]. Ternopil: TDMU, 2016, pp. 210-212 (In Ukrainian)
  14. Wen Yi, Shaohua Ya, Liu R, James W. Simpkins Transient cerebral ischemia induces site-specific hyperphosphorylation of tau protein. Brain Research. 2004;1022:30–38.
  15. Lopes S, Vaz-Silva J, Pinto V, Dalla Chr, Kokras N, Bedenk B, Mack N, Czisch M, Osborne F, Almeida X, Sousa N, Sotiropoulos I. Tau protein is essential for stress-induced brain pathology. Proc Natl Acad Sci USA. 2016 Jun 28; 113(26): 3755–3763.
  16. Karaulov AV. [Molecular-biological substantiation of the use of imunofan in clinical practice]. The attending physician. 2000;4:46-47.
  17. Yaremenko LM, Grabovoy OM. [State of titers of autoantibodies to tissue antigens of the brain and circulating immune complexes in the modeling of disorders of blood supply to the brain of varying degrees of severity and its correction] Immunology and Allergology. 2009;2-3:55-59.
  18. Mukaetova-Ladinska EB, Li M, Kalaria RN. Tau protein, ischemic injury and vascular dementia. Future Neurology. 2015;10(6):559-575.

ALBUMIN LEVEL IN CEREBROSPINAL FLUID IN PATIENTS WITH ACUTE BACTERIAL AND VIRUS MENINGITIS

Аuthors: A. V. Sokhan

Pages: 38–44

Abstract

         

Introduction. Due to neuroinfections there is a violation of the barrier function of blood-brain barrier (BBB), accompanied by the penetration of various substances into the tissues of the central nervous system that change the metabolism and may have a toxic effect on the central nervous system. Determination of the level of permeability of the BBB in patients with meningitis is not sufficiently studied and promising direction of diagnosis.

Purpose. Determine the diagnostic value and predictive significance of albumin levels in CSF of patients with acute neuroinfections.

Materials and Methods. For the purpose of the study, 164 patients with a confirmed etiology of neuroinfection were examined. We observed patients with meningococcal, pneumococcal, HSV 1, 2, EBV, VZV, HHV-6, and enteroviral meningitis. As a control group, we used data from 15 ARI patients with meningism. In addition to analyzing the clinical course of the disease, cerebrospinal fluid (CSF) level of albumin upon admission to the hospital and on the 10th–12th day of treatment was determined.

Results. The level of albumin in the CSF depend both on the severity of the patient's condition and on the etiology of neuroinfection. In patients with severe course on the first day of treatment, the content of albumin in the CSF was higher compared with patients of moderate severity in both viral and bacterial neuroinfections (P < 0,001). Among the viral meningitis, high rates of albumin were found in patients with VZV of meningitis (P < 0.0001). There was no significant difference in CSF albumin levels of survivors and non-survived patients. On the 10th –12th day of treatment, the albumin level decreased in patients of all groups (P < 0.05), but remained high in bacterial neuroinfections compared with viral meningitis (P < 0.001).

Conclusions. The level of albumin in the CSF of patients with acute neuroinfections depends both on the severity and etiology of the disease. The highest levels of albumin are observed in patients with bacterial meningitis on the first day of hospitalization. The level of albumin in the CSF of meningitis patients does not matter in the prognosis of the lethal outcome of the disease.

Keywords: meningitis, cerebrospinal fluid, albumin, blood-brain barrier.

This email address is being protected from spambots. You need JavaScript enabled to view it.

The full text

To view the full text

References

  1. Hillary R. Mount, Sean D. Boyle, DO. Aseptic and Bacterial Meningitis: Evaluation, Treatment, and Prevention. Am Fam Physician. 2017;96(5):314–322.
  2. Hladky SB, Barrand MA. Fluid and ion transfer across the blood–brain and blood–cerebrospinal fluid barriers; a comparative account of mechanisms and roles. Fluids and Barriers of the CNS. 2016;13:19. doi:10.1186/s12987-016-0040-3.
  3. Saunders NR, Dziegielewska KM, Møllgård K, Habgood MD. Markers for blood-brain barrier integrity: how appropriate is Evans blue in the twenty-first century and what are the alternatives? Frontiers in Neuroscience. 2015;9:385. doi:10.3389/fnins.2015.00385.
  4. Fanali G, di Masi A, Trezza V, Marino M, Fasano M, Ascenzi P. Human serum albumin: from bench to bedside. Mol Aspects Med. 2012;33:209–90. doi: 10.1016/j.mam.2011.12.002.
  5. Hladky SB, Barrand MA. Fluid and ion transfer across the blood–brain and blood–cerebrospinal fluid barriers; a comparative account of mechanisms and roles. Fluids and Barriers of the CNS. 2016;13:19. doi:10.1186/s12987-016-0040-3.
  6. Colombo G, Clerici M, Giustarini D, Rossi R, Milzani A, Dalle-Donne I. Redox albuminomics: oxidized albumin in human diseases. Antioxid Redox Signal. 2012;17:1515–27. doi: 10.1089/ars.2012.4702.
  7. Taverna M, Marie AL, Mira JP, Guidet B. Specific antioxidant properties of human serum albumin. Ann Intensive Care. 2013;3:4. doi: 10.1186/2110-5820-3-4.
  8. Jiao K, Mandapati S, Skipper PL, Tannenbaum SR, Wishnok JS. Site-selective nitration of tyrosine in human serum albumin by peroxynitrite. Anal Biochem. 2001;293:43–52. doi: 10.1006/abio.2001.5118.
  9. Carballal S, Radi R, Kirk MC, Barnes S, Freeman BA, Alvarez B. Sulfenic acid formation in human serum albumin by hydrogen peroxide and peroxynitrite. Biochemistry. 2003;42:9906–14. doi: 10.1021/bi027434m. 
  10. Ghasemi M, Fatemi A. Pathologic role of glial nitric oxide in adult and pediatric neuroinflammatory diseases. Neurosci Biobehav Rev. 2014;45:168–82. doi: 10.1016/j.neubiorev.2014.06.002. 
  11.  Hassel B, Iversen EG, Fonnum F. Neurotoxicity of albumin in vivo. Neurosci Lett. 1994;167:29–32. doi: 10.1016/0304-3940(94)91020-0.
  12. Byun K, Bayarsaikhan E, Kim D, et al. Induction of Neuronal Death by Microglial AGE-Albumin: Implications for Alzheimer’s Disease. Iijima KM, ed. PLoS ONE. 2012;7(5):e37917. doi:10.1371/journal.pone.0037917.
  13. Takeshima S, Shiga Y, Himeno T. et al. Clinical, epidemiological and etiological studies of adult aseptic meningitis: Report of 11 cases with varicella zoster virus meningitis. Clinical Neurology. 2017;57(9):492-498. doi: 10.5692/clinicalneurol.cn-001054.
  14. Arruti, M., Piñeiro, L., Salicio, Y. et al. Incidence of varicella zoster virus infections of the central nervous system in the elderly: a large tertiary hospital-based series (2007-2014). J. Neurovirol. 2017;23:451-459. doi: 10.1007/s13365-017-0519-y.

ANALYSIS OF THE ASSOCIATION OF THE C677T POLYMORPHISM IN THE METHYLENETETRAHYDROFOLATE REDUCTASE (MTHFR) GENE IN PATIENTS WITH TYPE 2 DIABETES MELLITUS COMPLICATED BY DIABETIC FOOT SYNDROME

Аuthors: O. V. Rusanov,Y. D. Chumachenko

Pages: 45–51

Abstract

         

Introduction. Diabetic foot syndrome complicates the course of diabetes mellitus in 4–25 % of patients. The identification of the genetic components of type 2 diabetes is the most important part of research in diabetes, since the identification of candidate genes for diabetes will influence all efforts to understand the pathogenesis of the disease, its complications, diagnosis, treatment and prevention.

Purpose. The purpose of the study was to investigate the possible connection of the C677T polymorphism of the methylenetetrahydrofolate reductase gene with the development of diabetic foot syndrome.

Materials and Methods. The subject of the study was 154 patients with type 2 diabetes, complicated by diabetic foot syndrome, and 124 practically healthy individuals. To determine the polymorphism of the C677T gene, a polymerase chain reaction method was used, followed by an analysis of the length of the restriction fragments. The static analysis was performed using the SPSS 17.0 software package.

Results. The distribution of homozygotes by the main allele (C/C), heterozygote (C/T) and homozygote in the minor allele (T/T) amron patients with DFS was 39.0 %, 46.8 % and 14.3 %, respectively, in practically healthy people – 46 %, 48.4 %, 5.6 % respectively (P = 0.056 for χ 2-Pearson criteria). In homozygote T / T, the risk of developing DFS is greater than that of carriers of the main allele (C/C and C/T) (OR = 2.79; P = 0.02).

Conclusion. The M7FR gene of the C677T-polymorphism is associated with the development of diabetic foot syndrome in the Ukrainian population. In the homozygote for the minor allele T / T, the risk of developing VDS is greater than that of the carriers of the minor allele.

Keywords: diabetic foot syndrome, diabetes mellitus, endothelial dysfunction, gene polymorphism, methylene tetrafolate reductase.

This email address is being protected from spambots. You need JavaScript enabled to view it.

The full text

To view the full text

References

  1. Shlapak IP, Galyshko OA. [Diabetes. A view from the position of an anesthetist] Kiev: Kniga plus, 2010.160p.
  2. Yehuda H, Zachary T. Bloomgarden, et al. Updated Clinical Recommendations on diagnostics and treatment of diabetes mellitus American Association of Clinical Endocrinology (AACE) and American College of Endocrinology (ACE), 2015. Diabetes. Adiposity. Metabolic syndrome 2015, 4: 17–21.
  3. Liapis MO, Herasimchuk PO. [The syndrome of diabetics foot] Ternopil: Ukrmedkniha, 2001. 276 p.
  4. Das SK: Genetic epidemiology of adult onset type 2 diabetes in asian indian population: past, present and future. Int J Hum Genet 2006, 6(1):1–13.
  5. Rebecca LP, Mary M et al Methylenetetrahydrofolate reductase polymorphism 677C>T is associated with peripheral arterial disease in type 2 diabetes. Cardiovascular Diabetology 2005, 4–17
  6. Pollex RL, Mamakeesick M, et al. Methylenetetrahydrofolate reductase polymorphism 677C>T is associated with peripheral arterial disease in type 2 diabetes. Cardiovasc Diabetol 2005;4–17. [PubMed: 16274479]
  7. Russo GT, Di Benedetto A, et al. Mild hyperhomocysteinemia, C677T polymorphism on methylenetetrahydro-folate reductase gene and the risk of macroangiopathy in type 2 diabetes: a prospective study. Acta Diabetol. Nov 25;2009
  8. Ciccarone E, Di Castelnuovo A, et al. Homocysteine levels are associated with the severity of peripheral arterial disease in Type 2 diabetic patients.; GENDIABET Investigators. Volume 48, Issue 4, Pages 897–904.e1
  9. Surovi H, Brian H. Annex. Biomarkers and Genetics in Peripheral Artery Disease. Clin Chem. 2017 Jan; 63(1): 236–244.
  10. Goyette P, Pai A, et al. Gene structure of human and mouse methylenetetrahydrofolate reductase (MTHFR). Mamm Genome. 1998 Aug;9(8):652–6.
  11. Sibani S, Christensen B. Characterization of six novel mutations in the methylenetetrahydrofolate reductase (MTHFR) gene in patients with homocystinuria. Hum Mutat. 2000;15(3):280–7.
  12. Frosst P, Blom HJ, et al. A candidate genetic risk factor for vascular disease: a common mutation in methylenetetrahydrofolate reductase. Nat Genet. 1995 May;10(1):111–3.
  13. Fetisova IN, Dobrolubov AS, et al. Polymorphism of genes of folate metabolism and human disease. Vestnik novykh meditsinskikh tekhnologiy 2007; 1: 23–28.
  14. Isordia-Salas I, Trejo-Aguilar A, , et al. C677T polymorphism of the 5,10 MTHFR gene in young Mexican subjects with ST-elevation myocardial infarction. Arch Med Res. 2010 May;41(4):246–50.
  15. Abdullah A, Ahmad AS, et al. Association of MTHFR C677T and A1298C gene polymorphisms with hypertension. International Journal of Health Sciences, Qassim University. 2012. – Vol. 6(1).– P. 1433.
  16. Poduri A, Mukherjee D, et al. MTHFR A1298C polymorphism is associated with cardiovascular risk in end stage renal disease in North Indians. Molecular and Cellular Biochemistry 2007, 308(1–2):43–50.
  17. Almawi WY, Khan A, et al. Case-control Study of methylenetetrahydrofolate reductase mutations and hyperhomocysteinemia and risk of stroke. J Stroke Cerebrovasc Dis. 2009 Sep-Oct;18(5):407–8.
  18. Fernández-Peralta AM, Daimiel L, et al. Association of polymorphisms MTHFR C677T and A1298C with risk of colorectal cancer, genetic and epigenetic characteristic of tumors, and response to chemotherapy. Int J Colorectal Dis. 2010 Feb;25(2):141-51.
  19. Fedota OM, Roshcheniuk LV, et al. Analysis of association of a gene of epidermal differentiation complex with dermatologic ang gynecologist diseases. Health Of Woman.2015.1(97):192–194.
  20. Lissowska J, Gaudet MM, et al. Genetic polymorphisms in the one-carbon metabolism pathway and breast cancer risk: a population-based case-control study and meta-analyses. Int J Cancer. 2007 Jun 15;120(12):2696–703.
  21. Zan T, Lei W, et al. The 677C>T (rs1801133) Polymorphism in the MTHFR Gene Contributes to Colorectal Cancer Risk: A Meta-Analysis Based on 71 Research Studies. PLoS One. 2013; 8(2): e55332. Published online 2013 Feb 20. doi: 10.1371/journal.pone.0055332.
  22. Strain JJ, Dowey L, et al. B-vitamins, homocysteine metabolism and CVD. Proc Nutr Soc. 2004 Nov;63(4):597–603.
  23. Alghashama A, Ahmad A Settina et al. Association of MTHFR C677T and A1298C gene polymorphisms with hypertension. International Journal of Health Sciences, Qassim University. 2012. – Vol. 6(1).– P. 1433.
  24. Serbulent Y, Nevin K, et al. Association of MTHFR gene C677T mutation with diabetic peripheral neuropathy and diabetic retinopathy. Mol Vis. 2013; 19: 1626–1630.
  25. Vasilieva YI, Bushueva OY, et al. Smoking as a precipitating factor in the development of diabetic angiopathy of lower extremities in men with methylenetetrahydrofolatereductase 677TT genotype. Klin. med. 2015;93(7) p 45–49.

ANALYSIS OF THE RESULTS OF BLOOD PLASMA DERIVATES USE DURING DENTAL IMPLANTATION PROCEDURE AMONG ELDERLY PATIENTS

Аuthors: O. L. Beley, M. Y. Goncharuk-Khomyn

Pages: 52–62

Abstract

         

Introduction. Given the inconsistency of existing data about the prospects and effectiveness of using blood plasma derivatives and the problem of optimizing dental rehabilitation approaches among older patients, the question of analyzing the success rate of implants inserted during the modification of iatrogenic intervention algorithms with the use of L-PRF and PRGF products remains relevant.

Purpose. To analyze the influence of blood plasma products enriched with thrombocyte-leukocyte elements and growth factors on the short-term results of dental implantation among elderly patients.

Materials and Methods. 46 patients among patients of University Dental Clinic (Uzhhorod) (24 females and 22 males) aged from 60 to 75 years with distal unrestricted defects of dental rows at the area of mandible were selected to take part in the study by their own agreement. In all patients implantation at the one side of the jaw was carried out according to the classic protocol (preparation of the area of ​​osteotomy according to the classical pattern, implant placement with further suturing), but on the other side it was provided with the additional use of plasma derivatives in the form of L-PRF (21 patients – study group 1) and PRGF (25 patients – study group 2). All patients were diagnosed using cone-beam computer tomography (Planmeca ProMax 3D Classic). The assessment of the stability of dental implants was carried out by frequency resonance analysis using the Ostell device (Sweden). The assessment of bone tissue quality was performed by the Lekholm-Zarb scale, while the bone density estimation was performed in Hounsfield units in accordance with the Misch’s recommendations using Planmeca Romexis® Viewer software.

Results. Over the course of three months peri-implant lesions were registered among 9 implants (6.97 % of the total). From the standpoint of evaluating the implants success in each group, we can distinguish the following: in the group with the implementation of the classical protocol of implantation (control), the number of unsuccessful implants was 5 out of 53 (9.43 %); in the group where the implantation was performed using L-PRF the number of unsuccessful implants was 2 implants out of 40 (5.0 %) (study group 1); in the group where the implantation was performed using PRGF the number of unsuccessful implants was 2 out of 36 (5.56 %) (study group 2). The level of peri-implant complications in all study groups, given the size of the samples being studied, and the short observation period did not exceed 10 %, which can be considered an acceptable indicator of the effectiveness of the iatrogenic interventions. Potential factors that negatively impacted on the success rate of implants include the female gender among elderly patients and low density of bone tissue. Resorption rates of peri-implant bone level in the areas of L-PRF and PRGF use were lower compare to the control group, which confirms the fact that plasma derivatives contribute to retention of baseline parameters of bone tissue at least in the approximate time after implantation.

Conclusion. During the implementation of differentiated approach of dental implantation with the use of blood plasma products in the form of L-PRF or PRGF, it was determined that the use of platelet-leukocyte fibrin substrate contributes to better stabilization of dental implants 3 months after implantation procedure, and the use of both types of plasma blood derivatives reduces the dynamics of bone tissue reduction at the peri-implant region in a similar period of observation.

Keywords: L-PRF, PRGF, dental implant, success rate.

This email address is being protected from spambots. You need JavaScript enabled to view it.

The full text

To view the full text

References

  1. Potapchuk AM, Kryvanych VM, Rusin VV, Honcharuk-Khomyn MY. Analysis of success results of immediat-implantation with the use of zircon prior fortis dental implant system. Clinical Dentistry. 2015;10(2):93-99.
  2. Rusin VV. The risk factors of dental implantation (the analytical review). Vestnik Stomatologii. 2015;3:83–88.
  3. M Dohan Ehrenfest D, Bielecki T, Jimbo R, Barbe G, Del Corso M, Inchingolo F, Sammartino G. Do the fibrin architecture and leukocyte content influence the growth factor release of platelet concentrates? An evidence-based answer comparing a pure platelet-rich plasma (P-PRP) gel and a leukocyte-and platelet-rich fibrin (L-PRF). Current pharmaceutical biotechnology. 2012;13(7):1145–52.
  4. M Dohan Ehrenfest D, Bielecki T, Mishra A, Borzini P, Inchingolo F, Sammartino G, Rasmusson L, A Evert P. In search of a consensus terminology in the field of platelet concentrates for surgical use: platelet-rich plasma (PRP), platelet-rich fibrin (PRF), fibrin gel polymerization and leukocytes. Current pharmaceutical biotechnology. 2012;13(7):1131–7.
  5. Öncü E, Alaaddinoglu EE. The effect of platelet-rich fibrin on implant stability. International Journal of Oral & Maxillofacial Implants. 2015;30(3):578–582.
  6. Naik B, Karunakar P, Jayadev M, Marshal VR. Role of Platelet rich fibrin in wound healing: A critical review. Journal of conservative dentistry: JCD. 2013;16(4):284.
  7. Ergun G, Egilmez F, Cekic-Nagas I, Karaca İR, Bozkaya S. Effect of Platelet-Rich Plasma on the Outcome of Early Loaded Dental Implants: A 3-Year Follow-up Study. Journal of Oral Implantology. 2013;39(s1):256–63.
  8. Monov G, Fuerst G, Tepper G, Watzak G, Zechner W, Watzek G. The effect of plateletrich plasma upon implant stability measured by resonance frequency analysis in the lower anterior mandibles. Clinical oral implants research. 2005;16(4):461-5.
  9. Ketabi M, Fahami N, Amini S. Effect of Platelet-rich Plasma on Implant Stability in the Mandible. J Periodontol. 2015;7(2):50–4.
  10. Makeev VF, Uhryn MM, Zablotska OY. Analysis of the Integration of Implants Inserted in the Mandible in the Elderly, Immediately Loaded with Fixed Dentures in Short Time. Noviny Stomatologii. 2012;4:86–90.
  11. Kryachko A, Lihota A, Kovalenko V, Shmatenko A. Experience primereniya dental implant in the elderly. Problemy viyskovoyi ohorony zdorovya. 2012;31:350–356.
  12. Pirpir C, Yilmaz O, Candirli C, Balaban E. Evaluation of effectiveness of concentrated growth factor on osseointegration. International Journal of Implant Dentistry. 2017;3(1):7.
  13. Öncü E, Bayram B, Kantarcı A, Gülsever S, Alaaddinoğlu EE. Posıtıve effect of platelet rich fibrin on osseointegration. Medicina oral, patologia oral y cirugia bucal. 2016;21(5):e601.
  14. Georgakopoulos I, Tsantis S, Georgakopoulos P, Korfiatis P, Fanti E, Martelli M, Costaridou L, Petsas T, Panayiotakis G, Martelli FS. The impact of Platelet Rich Plasma (PRP) in osseointegration of oral implants in dental panoramic radiography: texture based evaluation. Clinical Cases in Mineral and Bone Metabolism. 2014;11(1):59.

EPIDEMIOLOGY OF LEPTOSPIROSIS IN UKRAINE, EVOLUTION OF PATHOGENS, AND CLINICAL COURSE

Аuthors: M. D. Chemych, V. V. Il’yina, N. I. Il’yina, N. G. Malysh, T. I. Fotina

Pages: 63–72

Abstract

         

Leptospirosis remains an issue of common zoonosis in many regions of the world. The level of morbidity depends on climatic conditions, sanitary and hygienic and economic conditions, and remains high every year in many countries, including Ukraine.

The aim of the work: to analyze the epidemiological situation and morbidity of leptospirosis in certain regions of Ukraine; to identify the dominant pathogens of the disease; to study the features of the clinical course of the disease and modern approaches to diagnosis.

Materials and methods. Official statistics was used, and patients with leptospirosis who were treated at the Sumy Regional Infectious Hospital named after Z. Krasovitsky were examined. A retrospective epidemiological analysis of leptospirosis in the Sumy oblast during 1994–2016 was carried out.

Results. In Ukraine, from 1993 to 1999, there was an increase in the incidence of leptospirosis, and since 2000 it has been gradually decreasing. Enzootic territories with leptospirosis are located around 373 settlements (practically in all regions of Ukraine). The most affected are Kyiv, Cherkasy, Kirovograd, Ivano-Frankivsk, Ternopil, Chernihiv oblasts and Kyiv, which account for 35–40 % of the total incidence of this infection in Ukraine. Among patients with leptospirosis, persons of working age (59.4 %), males (69.8 %), and rural residents (69.8 %) dominate. From the late 90's – early 2000's, a tendency towards an increase in the number of diseases caused by leptospirals of serotypes Icterohaemorrhagiae (> 60.0 %) is observed in Ukraine. In the Sumy region, 52.3 % of the patients were infected with tuberculosis, 31.0 % were in the natural, and 16.7 % had no source of infection. Currently, in the territory of the region in natural cells predominate leptospiri serogroups Grippotyphosa, in the smaller number – Pomona, Hebdomadis. In anthropogenesis centers, the leptospirosis of the serogroups Pomona, Grippotyphosa, Tarasovi, and Icterohaemorrhagiae prevail. Leading clinical symptoms: intoxication, fever, kidney and liver damage. To date, modern laboratory diagnostic methods – PCR and ELISA – are used to confirm the diagnosis.

Conclusions. Leptospirosis is an important common zoonosis, the level of which depends on climatic conditions, sanitary and hygienic and economic conditions. Among the pathogens, the leptospiri serotypes are dominated by Icterohaemorrhagiae. The leading clinical symptoms are intoxication, fever, kidney and liver damage. Modern diagnostic methods – PCR and ELISA – should be used to confirm the diagnosis.

The clinical course of leptospirosis in the Sumy region and other regions of Ukraine is not significantly different from the classical one. The leading syndromes are intoxication, hemorrhagic, kidney and liver damage.

Keywords: leptospirosis, epidemiology, morbidity, clinic.

This email address is being protected from spambots. You need JavaScript enabled to view it.

The full text

To view the full text

References

  1. Vasylʹyeva NA, Andreychyn MA. [Leptospirosis: monograph]. TDMU. 2016:276.
  2. Vasylʹyeva NA, Lutsuk OV, Pavliv OS. [Evolution of the epidemic process of leptospirosis]. Profilaktychna medytsyna. 2011;2(14).
  3. Savchenko ST, Fylyppov NV, Vysotskyy AA. [The etiological structure of leptospirosis in the Volgograd Oblast] Épydemyolohyya y ynfektsyonnye bolezny. 2004;6.
  4. Pappas G, Papadimitriou P, Siozopoulov V, Christou L, Akritidis N. The globalization of Leptospirosis: worldwide incidence trends. Inf. J. Infect. Dis. 2008;12(4):351–357.
  5. Lomar AV, Diament D, Torres JR. Leptospirosis in Latin America. Infect. Dis. Clin. North Am. 2000;14:23–39.
  6. Zubach YeA, Telegina TV, Zinchuk AN. [Modern ideas about the specific diagnosis of leptospirosis]. Klinicheskaya infektologiya i parazitologiya. 2016;4(5):411–418.
  7. Ariyapruchya B, Sungkanuparph S, Dumrongkitchaiporn S. Clinical presentation and medical complication in 59 cases of laboratory-confirmed leptospirosis in Bangkok. Southeast Asian J. Trop. Med. Public. Health, V. 2003;34(1):159–164.
  8. Tangkanakul W, Smits HL, Jatanasen S, Ashford DA. Leptospirosis: an emerging health problem in Thailand. Southeast Asian J. Trop. Med. Public Health. 2005;36(2):281–288.
  9. Bernasovskaya YeP, Ugryumov BL, Vovk AD, Mogireva LA. [Leptospirosis]. Zdorov’ya. 1989:152.
  10. Berezhnov SP, Padchenko AP. [Analytical review of infectious morbidity in Ukraine for 11 months of 1998]. Suchasni infektsiyi. 1999;(1):5–15.
  11. Bernasovsʹka YEP, Kondratenko VM, Melʹnytsʹka OV. [The problem of leptospirosis in Ukraine]. Infektsiyni khvoroby. 1996;2:37–39.
  12. Kirin SP. [Leptospirosis: general characteristics, prevalence, urgency, anti-epidemic measures]. Suchasni aspekty viysʹkovoyi medytsyny: sb. nauk. pr. 1998:233–235.
  13. Vasylʹyeva NA, Kravchuk YUA, Dementʹyev YUH. [Extension of the etiological spectrum of pathogens of leptospirosis in Ternopilly]. Materialy naukovo-praktychnoyi konferentsiyi z mizhnarodnoyu uchastyu, prysvyachenoyi 60-richchyu stvorennya kafedry epidemiolohiyi Lʹvivsʹkoho natsionalʹnoho medychnoho universytetu imeni Danyla Halytsʹkoho «Aktualʹni problemy epidemiolohiyi infektsiynykh, parazytarnykh i neinfektsiynykh zakhvoryuvanʹ» ( Lʹviv, 12-13 travnya 2016 roku). 2016:63–65.
  14. Dementʹyev YUH, Kravchuk YUA. [Some aspects of the epidemiology of leptospirosis in the territory of the Ternopil region in 2011-2015]. Materialy naukovo-praktychnoyi konferentsiyi z mizhnarodnoyu uchastyu, prysvyachenoyi 60-richchyu stvorennya kafedry epidemiolohiy Lʹvivsʹkoho natsionalʹnoho medychnoho universytetu imeni Danyla Halytsʹkoho «Aktualʹni problem epidemiolohiyi infektsiynykh, parazytarnykh i neinfektsiynykh zakhvoryuvanʹ» ( Lʹviv, 12–13 travnya 2016 roku). 2016:96–97.
  15. Zinchuk OM, Zubach OO, Orfin AYA. [Epidemiological patterns of leptospirosis in Lviv region: current state of the problem]. Materialy naukovo-praktychnoyi konferentsiyi z mizhnarodnoyu uchastyu, prysvyachenoyi 60-richchyu stvorennya kafedry epidemiolohiyi Lʹvivsʹkoho natsionalʹnoho medychnoho universytetu imeni Danyla Halytsʹkoho «Aktualʹni problem epidemiolohiyi infektsiynykh, parazytarnykh i neinfektsiynykh zakhvoryuvanʹ» (Lʹviv, 12-13 travnya 2016 roku). 2016:113–114.
  16. Shulyarenko SV, Vynohrad NO, Zozulya AV. [Epidemiological features of leptospirosis in Rivne oblast for 2011-2015]. Materialy naukovo-praktychnoyi konferentsiyi z mizhnarodnoyu uchastyu, prysvyachenoyi 60-richchyu stvorennya kafedry epidemiolohiyi Lʹvivsʹkoho natsionalʹnoho medychnoho universytetu imeni Danyla Halytsʹkoho «Aktualʹni problem epidemiolohiyi infektsiynykh, parazytarnykh i neinfektsiynykh zakhvoryuvanʹ» ( Lʹviv, 12-13 travnya 2016 roku). 2016:243–244.
  17. Yanko NV, Vynohrad NO, Dudkovsʹka LV, Hnatyuk OYA, Havryshchuk VY, Bondarsʹka OA. [Epidemiological features of cells of leptospirosis in the Volyn region] Materialy naukovo-praktychnoyi konferentsiyi z mizhnarodnoyu uchastyu, prysvyachenoyi 60-richchyu stvorennya kafedry epidemiolohiyi Lʹvivsʹkoho natsionalʹnoho medychnoho universytetu imeni Danyla Halytsʹkoho «Aktualʹni problem epidemiolohiyi infektsiynykh, parazytarnykh i neinfektsiynykh zakhvoryuvanʹ» ( Lʹviv, 12-13 travnya 2016 roku). 2016:248–249.
  18. Pantyukhova TN, Karan' LS, Chulanov VP, Vazhnenkova IS, Pantyukhova RA, Ivanova IV, Pak SG. [Clinical features and modern laboratory diagnostics of the leptospirosis of the serigroup Grippotyphosa]. Terapevticheskiy arkhiv. 2006;11:44–48.
  19. Sofia Andalib, Ahmed Abu Saleh, Shaila Munvar Bangladesh. Laboratory methods for diagnosing leptospirosis: A review. J. Med. Microbiol. 2009;3(01):39–43.
  20. Mohit Bhatia, Umapathy Bl. Deciphering leptospirosis a diagnostic mystery: an insight. Inf. Med. Res. Health. Sci. 2015;4(3):693–701.

MEDICAL EVALUATION OF HAZARD ANALYSIS AND CRITICAL CONTROL POINT SYSTEMS EFFECTIVENESS IN THE PRODUCTION OF HIGH-RISK FOODS

Аuthors: Tsv. Vitkova, R. Enikova, M. Stoynovska

Pages: 73–80

Abstract

         

The current European legislation assigned the responsibility for food safety to the food producers and traders. The introduction and functioning of HACCP systems strives to achieve serious medical goals – consumer’s health protection, minimizing the risk for foodborne toxicoinfections, infections and intoxications, for chemical contamination and additives, as well as for other specific hazards. The approach is entirely preventive. The current experience has revealed numerous omissions and discrepancies in HACCP elaboration and functioning referring to the real extent of the hazard. This paper presents results from a critical analysis of the performance of HACCP systems in the production of confectionary, ready-to-serve foods, pasteurized egg products, sterilized canned foods, etc., highlighting the major defects in hazard analysis, adequacy of the critical points, correction activities, and verification procedures. Suggestions are provided concerning the optimization of the relationships between the producers and the control authorities aiming to eliminate the established system discrepancies.

Keywords: HACCP, microorganisms in foods, microbiological criteria, pasteurized egg products, confectionery products, vegetable canned foods, ready-to-serve dishes.

This email address is being protected from spambots. You need JavaScript enabled to view it.

The full text

To view the full text

References

  1. Enikova R, Baklova I, Kozareva M, Ribarova F, Petrova S, Peshevska M, Zahariev I, Shishkov S, Kvinto A, Varbanova G, Petrov M, Yankov Y. Meicobiological characteristics of dry egg mélange produced in the People’s Republic of Bulgaria. Hranitelno-promishlena nauka. 1986; 2(6):25-33.
  2. Hersum AS, Holland ED. Canned foods. Thermal sterilization and microbiology. M., Publishing House Legkaya I pishtevaya promishlenost. 1983. 319 p.
  3. Encyclopedia Of Food Safety. Editors Yasmine Motarjemi, Gerald G Moy, Ewen CD Tod. Academic Press is an imprint of Elsevier, USA. 2014. 2356 р.
  4. Food Quality and Safety Systems – A  Training  Manual  on  Food  Hygiene  and  the Hazard  Analysis   and   Critical   Control   Point (HACCP) System. FAO, Rome, 1998, FAO Information Division, ISBN 92-5-104115-6. 148 р.
  5. Guide to good manufacturing practice for  "Liquid, concentrated, frozen and dried egg products" used as food ingredients (non-ready to eat egg products). European Egg Processors Association. January 2006. 24 р.
  6. Guidelines for Assessing the Microbiological Safety of Ready-to-Eat Foods Placed on the Market. London: Health Protection Agency, November 2009, 34 р.
  7. Microbial Food Safety. LLC. Editors Omar A. Oyarzabal, Steffen Backert. Springer Science+Business Media. 2012. 259 р.
  8. Regulation (EC) No 853/2004 of the European Parliament and of the Council of 29 April 2004 laying down specific hygiene rules for food of animal origin (OJ L139, 30.4.2004).
  9. Requirements For A HACCP Based Food Safety System. Option A: Management System Certification Compiled by the National Board of Experts – HACCP The Netherlands. Gorinchem, the Netherlands: 4th Version. June 2006. 48 p.

DYNAMICS OF THE VASCULAR- PLATELET HEMOSTASIS INDICATORS IN PATIENTS WITH POSTINFARCTION CARDIOSCLEROSIS DEPENDING ON THE PRESENCE OF LIVER STEATOSIS AND LIFE STYLE MODIFICATION

Аuthors: I. I. Vakalyuk, N. G. Virstyuk

Pages: 81–88

Abstract

         

Introduction. Coronary heart disease remains the main cause of mortality in middle and elderly ages in most countries of the world and leads to a high level of disability of the able-bodied population. In turn, nonalcoholic fatty liver disease often occurs on the background of cardiovascular diseases and is closely associated with the prothrombotic state. Moreover, the liver plays an immediate role in hemostasis, since most coagulation factors, anticoagulant proteins and components of the fibrinolytic system are synthesized by its parenchymal cells.

Aim. The aim of this study is to evaluate the effectiveness of antiplatelet therapy in patients with postinfarction cardiosclerosis on the background of nonalcoholic fatty liver disease in the stage of steatosis.

Materials and Methods. We examined 249 patients (aged 54.2 ± 5.3 years) with stable coronary heart disease. Among them 160 patients without nonalcoholic fatty liver disease (Group I) and 89 patients with nonalcoholic fatty liver disease in the stage of steatosis (Group II) were identified. Patients of Group II were divided according to the compliance with lifestyle recommendations. General-clinical examination, electrocardiography, echocardiography, coronary angiography, liver ultrasound, evaluation of liver functional state and platelet haemostasis, determination of the blood vascular soluble adhesion molecules levels were revealed to all patients. All patients received standard therapy, which included acetylsalicylic acid at a dose of 75 mg per day.

Discussion. It was established that the effectiveness of antiplatelet therapy by platelets aggregation activity parameters depended on the presence of nonalcoholic fatty liver disease and, accordingly, applied approaches to lifestyle modification. In particular, adequate effectiveness of antiplatelet therapy in patients without nonalcoholic fatty liver disease was proved. In addition, such effectiveness took place in patients with liver steatosis in the case of following by the recommendations of lifestyle modification. Nevertheless, a sufficient control of platelet haemostasis in such patients was not achieved under the influence of a three-month treatment. This necessitates the use of prolonged antiplatelet therapy in this category of patients. Consequently, the inclusion of recommendations of lifestyle modification to the complex treatment of the patients with stable coronary heart disease combined with nonalcoholic fatty liver disease in the stage of steatosis contributes to more effective control of platelet haemostasis and endothelial function compared with those who do not follow by the appropriate recommendations.

Keywords: stable coronary heart disease, nonalcoholic fatty liver disease, antiplatelet therapy.

This email address is being protected from spambots. You need JavaScript enabled to view it.

The full text

To view the full text

References

  1. Kovalenko VM, Kornats'kyy VM, Moroz DM. Problemy zdorov"ya i medychnoyi dopomohy ta model' pokrashchennya v suchasnykh umovakh [Problems of health and medical care and a model of improvement in modern conditions]. Kyiv, 2016, 261 p.
  2. Bilovol OM, Fadyeyenko HD. Profilaktyka neinfektsiynykh zakhvoryuvan' [Prevention of non-communicable diseases]. Kyiv: LLC Health Ukraine, 2016, 352 p.
  3. Kushnir SM. [Therapeutic Effectiveness of Acetylsalicylic Acid in Cardiovascular Diseases]. Arterial hypertention. 2012;2(22). Retrieved from: http://www.mif-ua.com/archive/article/28853.
  4. Tripodi A, Fracanzani AL, Primignani M, et al. [Procoagulant imbalance in patients with nonalcoholic fatty liver disease]. J. Hepatol. 2014;61(1): 148–154.
  5. Barrera F, George J. [Prothrombotic Factors and Nonalcoholic Fatty Liver Disease: An Additional Link to Cardiovascular Risk?]. J. Hepatol. 2014;59(1):16–18. doi: 10.1002/hep.26588.
  6. Verrijken FS, Mertens I, Prawitt J, et al. [Prothrombotic factors in histologically proven NAFLD and NASH]. J. Hepatol. 2014;59:121–129.
  7. Potze W, Siddiqui MS, Boyett SL, et al. [Preserved hemostatic status in patients with nonalcoholic fatty liver disease]. J. Hepatol. 2016;65(5): 980–987.
  8. Solomenchuk TM. [Modern problems of antithrombotic therapy in patients with a high cardiovascular risk]. Health of Ukraine. 2013;4:38–39.
  9. Levyih AE, Mamchur VI. [Acetylsalicylic acid as an effective and safe basis for antiplatelet therapy]. Arterial hypertention. 2015;6(44). Retrieved from: http://www.mif-ua.com/archive/article/41818.
  10. Shen H, Shahzad G, Jawairia M, et al. [Association between aspirin use and the prevalence of nonalcoholic fatty liver disease: a cross-sectional study from the Third National Health and Nutrition Examination Survey]. Aliment Pharmacol Ther. 2014; 40(9):1066–1073. doi: 10.1111/apt.12944.
  11. Kravchenko VV, Sokolov MYu, Talayeva TV, ta in. Unifikovanyy klinichnyy protokol "Stabil'na ishemichna khvoroba sertsya". Nakaz MOZ Ukrayiny # 152 vid 02.03.2016 roku [Unified clinical protocol "Stable coronary heart disease". Order of the Ministry of Health of Ukraine #152 from 02.03.2016]. Retrieved from: http://www.moz.gov.ua/docfiles/dn_20150716_1dod.pdf.
  12. Khobzey MK, Kharchenko NV, Lishchyshyna OM, ta in. Unifikovanyy klinichnyy protokol "Nealkohol'nyy steatohepatyt". Nakaz MOZ Ukrayiny # 826 vid 06.11.2014 roku [Unified clinical protocol "Non-alcoholic steatohepatitis". Order of the Ministry of Health of Ukraine #826 from 06.11.2014]. Retrieved from: http://moz.gov.ua/docfiles/dn_20141106_0826_dod_ukp_nsg.pdf.
  13. Kharchenko NV, Lishchyshyna OM, Anokhina HA, ta in. Adaptovana klinichna nastanova, zasnovana na dokazakh "Nealkohol'na zhyrova khvoroba pechinky" [Adapted clinical guidance, based on the evidence "Non-alcoholic fatty liver disease"]. 2014. [Електронне джерело]. Retrieved from: http://www.moz.gov.ua/docfiles/dod_akn_dn_20140616_2.pdf.
  14. EASL–EASD–EASO Clinical Practice Guidelines for the management of non-alcoholic fatty liver disease. J Hepatol. 2016; 64(6):1388–1402.
  15. Detektorskaya LN, Zolotnitskaya RP. Laboratornyie issledovaniya v klinike [Laboratory research in the clinic]. Moskov: Medicine, 1987, 368 p.

CLINICAL PREDICTORS OF SUICIDAL BEHAVIOR IN PATIENTS WITH DEMENTIA OF DIFFERENT TYPES

Аuthors: I. H. Mudrenko

Pages: 89–96

Abstract

         

Actuality. A wide range of psychopathological comorbid disorders, including suicidal manifestations is observed in patients with dementia. Most often are met ideational types in the form of antivital mood, thoughts. The involvement of the neurodegenerative process in autoaggression is proved.

Purpose: to study the clinical features of patients with various types of dementia with high risk of suicide.

Materials and methods. There were examined 213 people with different clinical forms of dementia (vascular, caused by Alzheimer's disease of mixed type). The clinical-anamnestic method (clinical interview, observation, collection of complaints, anamnesis), psychometric (MMSE scale, Hamilton scale, method for determining suicide risk), Method of Statistical Processing of the Results were used.

Results of the research. The article highlights the relationship between the clinical features of patients with various types of dementia and the risk of suicide. The predictors of suicide in patients with dementia of Alzheimer and non-Alzheimer types are formulated on the basis of obtained data. The most important predictors in dementia caused by Alzheimer's disease are: early onset of the disease, atypical dementia or dementia of mixed type, mild cognitive impairment, comorbid depression; in case of vascular dementia, the predictor of suicide risk (SR) is a subcortical impression of white matter of the brain (leukoencephalopathy); in the mixed type of dementia process the SR was high in combination of dementia in Alzheimer's disease with early onset and subcortical vascular dementia, signs of dementia in Alzheimer's disease with late onset and unspecified vascular dementia, atypical dementia in Alzheimer's disease and multiple myocardial vascular dementia with additional depressive and hallucinatory symptoms.

To the factors of anti-risk of suicidal behaviour in dementia as a result of Alzheimer's disease are referred: early onset of the disease, severity of dementia, additional mixed psychopathological symptoms; in case of vascular dementia –presence of delusion in the clinical picture; in mixed dementia – combination of clinical signs of dementia in Alzheimer's disease with early onset and mixed or unspecified vascular dementia, the absence of comorbid psychopathological symptoms.

The obtained data are the symptoms-targets for the prevention of suicide in patients with dementia.

Keywords: vascular dementia, mixed dementia, dementia in Alzheimer's disease, suicidal behaviour, clinical predictors.

This email address is being protected from spambots. You need JavaScript enabled to view it.

The full text

To view the full text

References

  1. Solomenchuk TM. [The problem of vascular dementia in general medical practice: rational antihypertensive therapy as a priority direction of treatment]. Arterial hypertension, 2012;1(21): 9–15.
  2.  Rizzi L. Global Epidemiology of Dementia: Alzheimer’s and Vascular Types . BioMed Research International, 2014;3:2. Retrieved from: https://www.hindawi.com/journals/bmri/2014/908915/
  3. World Health Organization, Alzheimer’s Disease International. Dementia: a public health priority. Retrieved from: :http://www.who.int/mental_health/publications/dementia_report_2012/en/].
  4. Mudrenko IH. [Modern views on socio-psychological, clinical and psychopathological patterns of suicidogenesis in dementia and methods of medical and social assistance]. Psykhiatriya, nevrolohiya ta medychna psykholohiya,2017;2(8): 33–42.
  5. Lyubov EB, Enaliev IR, Kryuchenkova TP. [Clinical-epidemiological, pharmacoepidemiological and economic aspects of senile dementia]. Sotsial'naya i klinicheskaya psikhiatriya.2010;3: 33-38.
  6. Levin OS. Diagnostika i lecheniye dementsii v klinicheskoy praktike[Diagnosis and treatment of dementia in clinical practice]. М .: Medpress Publ.,2010. p. 256.
  7. Mishchenko TS, Zdesenko IV. [ Clinical and pathogenetic features of development of various forms of dementia]. Ukrayinsʹkyy visnyk psykhonevrolohiyi,2014; (81): 15–19.
  8. Saiko DYu.[ Features of the clinic and regularities of the formation of mental disorders in Parkinson's disease]. Ukrayinsʹkyy visnyk psykhonevrolohiyi, 2012; 3 (72): 54–58.
  9.  Mudrenko IH. [Pharmacological correction of depressive symptoms in patients with different clinical variants of dementia]. Ukrayinsʹkyy visnyk psykhonevrolohiyi .2017; 3 (92): 49–54.
  10.  Mudrenko IH. [Factors of suicidal behavior in patients with dementia]. Medychna psykholohiya.2017; 3 (47): 53–57.
  11.  Mudrenko IH. [The efficacy of cognifen in the treatment of dementia. Psikhiatriya, psikhoterapiya i klinicheskaya psikhologiya. 2017;81(12): 409–421.

FEATURES OF COMMUNITY-ACQUIRED PNEUMONIA COURSE IN PATIENTS WITH CARDIOVASCULAR EVENTS

Аuthors: V. F. Orlovsky, L. B. Vynnychenko, N. V. Demikhova, O. G. Gayvoronska, R. V. Bezsmertna

Pages: 97–105

Abstract

         

An increased risk of developing cardiovascular complications was found in patients with community-acquired pneumonia (CAP). The literature review suggests that pneumococcal pneumonia, elder age, renal insufficiency, chronic obstructive pulmonary disease (COPD) and insulin-dependent diabetes mellitus are risk factors for cardiovascular events (CVE) in patients with pneumonia. The purpose of this study was to identify the peculiarities of the course of pneumonia in patients with CAP, to establish additional factors that lead to CVE.

A prospective study was conducted in 420 patients who were treated in the pulmonary and therapeutic departments of the Sumy Clinical Hospital No 1. Among them, men were 241 (57 %), women were 179 (43 %). The average age of patients was 56.1 ± 18.5. We evaluated the incidence of CVE, such as acute pulmonary edema, new cases and worsening of cardiac arrhythmias and worsening of chronic heart failure in patients with CAP. Patients with CVE were compared with those who did not have such events to identify additional factors that increase or reduce the risk of such complications.

The results of our research showed that CVE occurred in 51 (13 %) hospitalized patients with CAP. CVE in patients with CAP were more likely to occur in persons older than 65 years of age with atrial fibrillation (AF), hyperlipidemia and late admission. The most commonly in patients with CAP in combination with hyperlipidemia worsened the course of chronic heart failure (CHF). With a high pneumonia severity index (PSI), there is a high risk of pulmonary edema. Both risk factors, hyperlipidemia and high ITP, contribute almost equally to the onset of arrhythmia. The duration of treatment for patients with CVE was statistically higher, however, the early outcomes of patients with and without CVE did not differ statistically. Statins are drugs that improve the prognosis of patients with NF in combination with CVD.

Keywords: community-acquired pneumonia, cardiovascular events, atrial fibrillation, hyperlipidemia.

This email address is being protected from spambots. You need JavaScript enabled to view it.

The full text

To view the full text

References

  1. Ramirez J, Aliberti S, Mirsaeidi M. et all. [Acute myocardial infarction in hospitalized patients with community-acquired pneumonia] Clin Infect Dis. 2008; 47:182–187.
  2. Viasus D, Garcia-Vidal C, Manresa F et all. [Stratification and prognosis of acute cardiac events in hospitalized adults with community-acquired pneumonia] J Infect. 2013; 66: 27-33.
  3. Lichtman JH, Fathi A, Radford MJ, et all. [Acute, severe, noncardiac conditions in patients with acute myocardial infarction]. Am J Med. 2006; 119: 843–850.
  4. Musher DM, Rueda AM, Kaka AS et all. [The association between pneumococcal pneumonia and acute cardiac events]. Clin Infect Dis. 2007; 45:158–65
  5. Demchuk AV. [Features of community-acquired pneumonia in patients with cardiovascular diseases]. Ukrainian pulmonology journal. 2015; 4: 22–26.
  6. Lin SH, Perng DW, Chen CP et all. [Increased risk of community-acquired pneumonia in COPD patients with comorbid cardiovascular disease]. Int J Chron Obstruct Pulmon Dis. 2016; 11:3051–3058.
  7. Torres A, Blasi F, Dartois N, et al. Which individuals are at increased risk of pneumococcal disease and why? Impact of COPD, asthma, smoking, diabetes, and/or chronic heart disease conommunity-acquired pneumonia and invasive pneumococcal disease. Thorax. 2015;70:984–9.
  8. Bobilev АА, Rachina SА, Koslov RS et all [Community-acquired pneumonia in the patients with chronic heart failure: features of diagnosis and treatment Bronchopulmonologia]. 2014; 45:23–27
  9. Svanström H, Pasternak B, Hviid A et all. [Use of azithromycin and death from cardiovascular causes]. N Engl J Med. 2013; 368:1704–1712.
  10. Schembri S, Williamson PA, Short PM. et all. [Cardiovascular events after clarithromycin use in lower respiratory tract infections: analysis of two prospective cohort studies]. BMJ. 2013; 346: 1235.

CLINICAL CASE: FITZ-HUGH-CURTIS SYNDROME AS A CAUSE OF POSTCHOLECYSTECTOMY SYNDROME

Аuthors: N. A. Maiura, M. G. Kononenko

Pages: 106–112

Abstract

         

Fitz-Hugh Curtis syndrome is an important and understudied factor that significantly affects the quality of life of patients. To date, there are no diagnostic standards that would enable to verify the Fitz-Hugh-Curtis syndrome. In the article on the example of a clinical case we considered the contemporary ideas about etiology and pathogenesis of Fitz-Hugh-Curtis syndrome as the causes of pain in the right upper quadrant of abdominal cavity. A 52-year woman presented with right-upper quadrant pain and digestive disorders during long time after laparoscopic cholecystectomy with no organic reason. Clinical and anamnestic features allow us to find the real reason of complaints and to use target antibacterial therapy. Widening of the ideas about the Fitz-Hugh-Curtis syndrome and orientation of general physicians and surgeons to the search for signs of generalized chlamydia is a direction of improvement of individual therapeutic and diagnostic tactics which helps to optimize the therapeutic process and avoid unnecessary surgical interventions.

Keywords: Fitz-Hugh-Curtis syndrome, perihepatitis, chlamydiosis, postcholecystectomy syndrome.

This email address is being protected from spambots. You need JavaScript enabled to view it.

The full text

To view the full text

References

  1. Vasyljuk SM. Syndrom Fitz-Hji-Kurtisa v hirergichnij praktyci [Fitz–Hugh–Cutris syndrome in surgical practice]. Khirurgija Ukrajiny. 2013; 1: 100–106.
  2. Palij IG, Zajika SV. Biliarnyj sladzh: mozhlyvosti diagnostyky ta likuvannja [Biliary sludge: possibilities of diagnostic and treatment]. Suchasna gastroenterologija. 2009; 6: 90–95.
  3. Bolaji II, Shirley KY. [An odyssey through Fitz-Hugh Curtis syndrome]. J Reprod & Contr. 2015; 26(3): 173–186.
  4. van Dongen PWJ. [Diagnosis of Fitz-Hugh-Curtis syndrome by ultrasound]. Eur J Obstetrics & Gynecology Reprod Biol. 1993; 50: 159–162.
  5. Takeuchi H, Kitade M, Sakurai A at al. [Ethiology of Fitz-Hugh and Curtis syndrome?]. Fertil Steril. 2006; 85(2): 533-534.
  6. Pijura B, Sarov B, Sarov I. [Persistence of antichlamydial antibodies after treatment of acute salpingitis with doxycycline]. Eur J Obst Gynecol Reprod Biology. 1993; 48: 117-121.
  7. Reichert JA, Valle R.F. [Fitz-Hugh-Curtis Syndrome. A laparoscopic approach]. JAMA. 1976; 236(3): 266-268.
  8. Ris HW. [Perihepatitis (Fitz-Hugh-Curtis Syndrome)]. J Adol Healthcare. 1984; 5: 272-275.
  9. Risser WL, Risser JM, Benjamins LJ, Feldmann JM. [Incidence of Fitz-Hugh-Curtis syndrome in adolescents who have pelvic inflammatory disease]. J Pediatr and Adolesct Gynecol. 2007; 20: 179-180.
  10. Schofer JM. [Biliary causes of postcholecystectomy syndrome]. J Emerg Med. 2010; 39(4): 406-410.

DIFFERENTIAL APPROACH TO THE USE OF STANDARD THERAPY OF CHRONIC HEART FAILURE IN PATIENTS WITH CORONARY ARTERY DISEASE AND OBESITY

Аuthors: О. Kadykova

Pages: 113–120

Abstract

         

Introduction. Coronary artery disease and obesity have many common pathogenic mechanisms that lead to the development and growth of heart failure severity. Previous studies have indicated that the attention of scientists was focused on the study of the role of polymorphisms of genes at the pathogenesis of cardiovascular diseases and associated conditions. In particular, a number of studies have found that certain genotypes of polymorphisms of genes associated with neurohumoral activation, endothelial dysfunction, immune inflammation and adipocytokine and lipid metabolism disorders are associated with the pathogenesis of heart failure. There is evidence that the efficacy of treatment in patients with cardiovascular pathology depends, in particular, on genomic polymorphisms. At the same time, work in this direction is quite contradictory and the association of genetic polymorphisms with therapeutic efficacy in them is significantly different in different populations, which leads to the continuation of research in this direction.

The aim of the study. To evaluate the influence of different schemes of standard therapy of heart failure in patients with coronary artery disease and obesity with unfavorable genotypes of polymorphisms of genes and, in case of obtaining the likely differences, to develop differentiated treatment of this cohort of patients.

Materials and methods. As a result of randomization, two subgroups of observation were formed: 1 subgroup – 22 patients with coronary artery disease and obesity with unfavorable combinations of genotypes receiving enalapril in a daily dose of 20 mg, carvedilol in a daily dose of 50 mg and spironolactone in a dose of 50 mg per day; 2 subgroups – 20 patients with adverse combination of genotypes, patients with coronary artery disease and obesity who received lisinopril in a daily dose of 20 mg, nebivolol in a daily dose of 10 mg and eplerenone in a dose of 50 mg per day. The effect of therapy on the state of carbohydrate, lipid metabolism, anthropometric and cardiohaemodynamic indices was investigated.

Results and discussion. The study showed positive influence of standard therapy on indexes. There was a significant decrease in the levels of systolic blood pressure, diastolic blood pressure and heart rate in both subgroups. In the analysis of the effect of selected therapy on carbohydrate metabolism rates, no significant deviations were detected. A study of lipid profile in both subgroups after treatment an increase antiatherogenic fraction of high-density lipoproteins and decreasing levels proaterogenic triglycerides, low-density lipoproteins, very low-density lipoproteins and atherogenic factor. The study of changes in the parameters of cardiohaemodynamics demonstrated that the normalization of morpho-functional parameters of the heart was observed on the background of treatment, which was manifested by the decrease of end-systolic volume, end-diastolic volume, end-systolic size, end-diastolic size, mass of myocardium of left ventricular, and an increase of ejection fraction in both subgroups.

Conclusions. In short, analysis of the dynamics of indicators in patients with coronary artery disease and obesity with adverse combinations of genotypes showed that as a result of complex therapy there was an improvement in clinical picture, lipid profiles and cardiohaemodynamic indexes. At the same time, there was no significant difference in the shifts in the indices when different treatment schemes were used.

Keywords: heart failure, coronary heart disease, obesity, standard therapy, adverse combination of genotypes.

This email address is being protected from spambots. You need JavaScript enabled to view it.

The full text

To view the full text

References

  1. Rudyk YuS. KhSN i geneticheskie polimorfizmy: rol β-adrenoretseptorov [CHF and genetic polymorphism: the role of β-adrenergic receptors]. Sertseva nedostatnist. 2009; 2: 20–27.
  2. Chen S, Zhang L, Wang HW, Wang XY, Li XQ, Zhang LL. The M235T polymorphism in the angiotensinogen gene and heart failure: a meta-analysis. J. of the Renin-Angiotensin-Aldosterone Syst. 2014; 15(2): 190–195. doi: 10.1177 / 1470320312465455.
  3. Bai Y, Wang L, Hu S, Wei Y. Association of angiotensin-converting enzyme I/D polymorphism with heart failure: a meta-analysis. Mol Cell. Biochem. 2012; 361(1–2): 297–304.
  4. Zhang H, Wu J, Yu L. Association of Gln27Glu and Arg16Gly Polymorphisms in Beta2-Adrenergic Receptor Gene with Obesity Susceptibility: A Meta-Analysis. PLoS ONE. 2014; 9(6): e100489. doi: 10.1371/journal.pone.0100489.
  5. Tardin OMA, Pereira SB, Velloso MWM, Balieiro HM, Costa B, Alves ThO, Giro C, Pessoa LP, Ribeiro GS, Mesquita ET. Genetic Polymorphism G894T and the Prognosis of Heart Failure Outpatients. Arq Bras Cardiol. 2013 Oct; 101(4): 352–358. doi: 10.5935/abc.20130167.
  6. Li S, Jiао Х, Tао L. Tumоr nесrоsis fасtоr-аlрhа in mесhаniс trаumа рlаsmа mеdiаtеs саrdiоmyосytе арорtоsis. Аm. J. Рhysiоl. Hеаrt Сirс. Рhysiоl. 2007; 293(3): H1847–H1852.
  7. Yang Y, Zhang F, Skrip L, Lei H, Wang Y, Hu D, Ding R. IL-6 gene polymorphisms and CAD risk: a meta-analysis. Mol. Biol. Rep. 2013; 40: 2589–2598. DOI: 10.1007/s11033-012-2345-x.
  8. Leonarduzzi G, Gamba P, Gargiulo S, Biasi F, Poli G. Inflammation-related gene expression by lipid oxidation-derived products in the progression of atherosclerosis. Free Radic. Biol. Med. 2012; 52: 19–34. doi: 10.1016/j.freeradbiomed.2011.09.031.
  9. Shalimova AS. Dyferentsiyovane likuvannya patsiyentiv z komorbidnoyu patolohiyeyu – hipertonichnoyu khvoroboyu i tsukrovym diabetom 2 typu v zalezhnosti vid polimorfizmu hena AGTR1 [Differentiated treatment of patients with comorbid pathology – hypertension and type 2 diabetes depending on the polymorphism of the AGTR1 gene]. Visnyk problem biolohiyi i medytsyny. 2015; 2(121): 198–201.
  10. Shevchenko OV. Vliyaniye geneticheskikh polimorfizmov na effektivnost' lozartana u bol'nykh essentsial'noy arterial'noy gipertenziyey [Influence of genetic polymorphisms on the efficacy of losartan in patients with essential arterial hypertension]. Byulleten' meditsinskikh Internet-konferentsiy. 2012; 2(8): 598–600.
  11. Martínez-Gómez LE, Cruz M, Martínez-Nava GA, Madrid-Marina V, Parra E, García-Mena J, Espinoza-Rojo M, Estrada-Velasco BI, Piza-Roman LF, Aguilera P, Burguete-García AI. A replication study of the IRS1, CAPN10, TCF7L2, and PPARG gene polymorphisms associated with type 2 diabetes in two different populations of Mexico. Ann Hum Genet. 2011 Sep; 75(5): 612–620. doi: 10.1111/j.1469-1809.2011.00668.x..
  12. Nakaz MOZ Ukrayiny vid 02.03.2016 № 152. Unifikovanyy klinichnyy protokol pervynnoyi, vtorynnoyi (spetsializovanoyi) ta tretynnoyi (vysokospetsializovanoyi) medychnoyi dopomohy «Stabilʹna ishemichna khvoroba sertsya» [Order of the Ministry of Health of Ukraine dated 02.03.2016 № 152 "Unified clinical protocol of primary, secondary (specialized) and tertiary (highly specialized) medical care" Stable ischemic heart disease"].
  13. Rekomendatsiyi Asotsiatsiyi kardiolohiv Ukrayiny z diahnostyky ta likuvannya khronichnoyi sertsevoyi nedostatnosti (2017) [Recommendations of the Association of Cardiologists of Ukraine for the Diagnosis and Treatment of Chronic Heart Failure (2017)]. Sertseva nedostatnistʹ ta komorbidni stany. 2017; 1(1): 6–66.

CLINICAL, ECHOCARDIOGRAPHIC, LABORATORY AND PROGNOSTIC ASPECTS OF CHRONIC HEART FAILURE WITH OVERWEIGHT AND OBESITY DEPENDING ON SERUM ADIPONECTIN CONTENT

Аuthors: V. Z. Netyazhenko, P. P. Bidzilya, V. G. Kadjaryan

Pages: 121–131

Abstract

         

Today, chronic heart failure (CHF) is one of the main causes of death and disability among patients with cardiovascular disease. Despite the fact that significant progress has been made in the treatment and diagnosis of CHF, mortality rates remain high. The possible explanation for this is the increase in the age of the human population and the involvement of other mechanisms that have not yet been investigated to the pathogenesis of the disease. Recently, more and more attention of researchers is devoted to the study of the components of the exchange of adipocytokines, biologically active substances, which produced by visceral fatty tissue. One of the most interesting representatives of adipocytokines is adiponectin, which has a number of metabolic and pleiotropic effects. Scientists have proven a significant role in the pathogenesis of diabetes mellitus, lipid metabolism disorders, obesity and cardiovascular pathology. There are a number of studies that examined the effects of adiponectin on the development, course, and results of CHF. Disseminating thoughts of researchers regarding changes in the level of adiponectin in CHF conditions, some of them have shown hypoadiponectinemia, but more and more works have recently shown an increase in adiponectin content and its negative prognostic effect. The World Health Organization has reported obesity as a non-infection epidemic. The abdominal type of obesity and overweight remain one of the main predictors of the onset and progression of many diseases, and CHF in particular. However, recently, more and more works show the better course and results of disease in patients with moderate obesity. This was called as "obesity paradox". Taking into account the foregoing, the study of the effect of adiponectin content in serum on various pathogenetic components of CHF in patients with overweight and obesity is relevant and timely, in order to further develop prognostic criteria and therapeutic effects.

Purpose: to investigate clinical course of CHF, structural and functional changes in the heart, lipid, carbohydrate, adipocytokines metabolism and markers of systemic inflammation in patients with overweight and obesity depending on the serum content of adiponectin, to assess its prognostic effects on the five-year course of the disease.

Materials and methods. Totally 84 patients with CHF II–III functional class (FC) with overweight and obesity I–III degree were examined. Patients were divided into 2 groups depending on adiponectin content in blood serum. To the І group entered 21 investigated, with adiponectin content higher than 31,5 (40,4 [37,3; 47,2]) mcg/ml, the ІІ group was presented by 63 patients with the level of adiponectin lower than 31,5 (12,3 [8,50; 18,7]) mcg/ml. All patients were subject standard clinical, biochemical and to echocardiographic research, in obedience to the existent generally accepted guidelines. Content of adiponectin in serum of blood were measured by ELISA method. Statistical analysis were conducted by means of the licensed package of statistical software’s (Statistica 6.0).

Results. The high content of adiponectin in blood serum of patients with CHF with overweight and obesity was accompanied by higher heart rate, FC of disease, left atrium size, left ventricle posterior wall diameter, left ventricle myocardial mass index1, degree of calcinosis mitral and aortal valve, degree of regurgitation of mitral and tricuspid valve, increasing prevalence of subjective, objective symptoms of the disease, frequency CHF III FC, the content of IL-6, IL-10, TNF-α, the ratios of adiponectin/resistin, TNF-α / IL-10, the incidence of five-year mortality and total cumulative endpoint. At the same time, there were lower systolic blood pressure, left ventricle ejection fraction, very low-density cholesterol and triglycerides contents and resistin/adiponectin ratio. The obtained data indicate that the high content of adiponectin results in a heavier course of CHF in the conditions of overweight and obesity, which is manifested by the deepening of violations of clinical, echocardiographic, laboratory and humoral links pathogenesis of the disease.

Conclusion. The high content of adiponectin in serum of blood in patients with overweight and obesity characterized by a severe course of CHF and has a negative prognostic influence on the results of the disease for five years.

Keywords: heart failure, overweight, obesity, adiponectin.

This email address is being protected from spambots. You need JavaScript enabled to view it.

The full text

To view the full text

References

  1. Voronkov LG et al. (2016). Kharakteristika imunopatolohichnykh reaktsij u patsientiv iz khronichnoiu sertsevoiu nedostatnistiu zalezhno vid naiavnosti insulinorezistentnosti [Characteristics of immunopathological reactions in patients with chronic heart failure depending on the presence of insulin resistance]. Ukrainiskyi revmatolohichnyi zhurnal, 4 (66): 35-40.
  2. Szabo T, Postrach E, Ma¨hler A, et al. (2013) Increased catabolic activity in adipose tissue of patients with chronic heart failure. Eur J Heart Fail, (15). http://dx.doi.org/10.1093/ eurjhf/hft067 [Epub ahead of рrint]
  3. Hirose H, Yamamoto Y, Seino-Yoshihara Y et al. (2010). Serum high-molecular-weight adiponectin as a marker for the evaluation and care of subjects with metabolic syndrome and related disorders. J. Atheroscler. Thromb, 17: 1201-1211.
  4. Marques MB, & Langouche L. (2013). Endocrine, metabolic, and morphologic alterations of adipose tissue during critical illness. Crit. Care Med., 41 (1): 317–325. doi: 10.1097/CCM.0b013e318265f21c.
  5. Djousse L, Wilk JB, Hanson NQ et al. (2013). Association between adiponectin and heart failure risk in the physicians’ health study. Obesity (Silver Spring), 21, 831–834. doi: 10.1002/oby.20260.
  6. Kistorp C, Faber J, Galatius S et al. (2005). Plasma adiponectin, body mass index, and mortality in patients with chronic heart failure. Circulation, 112: 1756–1762.
  7. Laoutaris ID, Vasiliadis IK, Dritsas A et al. (2010). High plasma adiponectin is related to low functional capacity in patients with chronic heart failure. Int. J. Cardiol, 144: 230.
  8. Szabo T, Scherbakov N, Sandek A et al. (2014). Plasma adiponectin in heart failure with and without cachexia: Catabolic signal linking catabolism, symptomatic status, and prognosis. Nutrition, Metabolism & Cardiovascular Diseases, 24: 50–56. doi: 10.1016/j.numecd.2013.04.015.
  9. Fryar CD, Carrol MD, Ogden CL (2012). Prevalence of overweight, obesity, and extreme obesity among adults: United States, trends 1960–1962 through 2009–2010. NCHS Health E-Stat. http:// www.cdc.gov/nchs/data/hestat/obesity_adult_09_10/ obesity_adult_09_10.pdf.
  10. Wang TJ. (2014). The Obesity Paradox in Heart Failure Weighing the Evidence. Journal of the american colege of cardiology, 64: 2751-2752.
  11. Nagarajan V, Kohan L, Holland E et al (2016). Obesity paradox in heart failure: a heavy matter. ESC Heart Failure, 3: 227–234.
  12. Oga EA, Eseyin OR (2016). The Obesity Paradox and Heart Failure: A Systematic Review of a Decade of Evidence. Journal of Obesity, Article ID 9040248, 9 pages http:// dx.doi.org/10.1155/2016/9040248.
  13. Clark LA, Fonarow GC, Horwich TB. (2014). Obesity and the Obesity Paradox in Heart Failure. Progression cardiovascular diseases, 56: 409 – 414.
  14. Voronkov LG et al. (2013). Rekomendacii po diagnostike i lecheniyu khronicheskoj serdechnoj nedostatochnosti Asotsiatsii kardiolohov Ukraini ta Ukraintskoi asotsiatsii fakhivtsiv iz sertsevoi nedostatnosti (2012) [Guidelines for the diagnosis and treatment of chronic heart failure Association of cardiologists of Ukraine and the Ukrainian Association of specialists in heart failure (2012)]. Ukrainian cardiological journal, 1 (Add), 6–44.

FEATURES OF DISTRIBUTION OF IODINE INTRACELLULAR POOL IN THE BODY OF CHILDREN WITH COMMUNITY-ACQUIRED PNEUMONIA IN PRESENCE OF IODINE DEFICIENCY

Аuthors: О. D. Kibar, V. O. Kosovska, T. M. Kosovska, O. R. Shylo

Pages: 132–138

Abstract

         

Introduction. Community-acquired pneumonia (CAP) is a leading cause of morbidity and mortality globally. The severity of the course of CAP in childhood depends on difficulties with concomitant pathology, the state of the endocrine system and the immunity of the organism, especially among people living in conditions of endemic iodine deficiency.

The aim of the study was to study the features of intracellular distribution of iodine in the blood of children with community-acquired pneumonia (CAP) living in iodine deficiency areas.

Materials and methods. We investigated 74 children with CAP aged 4–14 years (45 children with moderate and 29 with severe pneumonia) and 35 healthy children. The severity of pneumonia in children was assessed according to the classification criteria of the disease. All children were assessed the level of iodine in the urine; inorganic iodine, total and organificated iodine in the blood.

Results. According to iodine median we detected mild iodine deficiency in all study groups (36.2 μg/L, 63.8 μg/L and 61.9 μg/L, respectively (p ˂ 0.05)). When examining the intracellular pool of iodine of patients from group I showed an inverse relationship between the levels of iodine distribution for organic and inorganic iodine (r = -0.737, p < 0.05), which tends to decrease depending on the severity of pneumonia. A close correlation between the levels of total and organic iodine (r = 0.538, p < 0.05) Data of group II patient indicate a slight decrease in the level of total and organificated iodine, as well as a moderate increase in the concentration of inorganic iodine in the blood of patients. These changes are less pronounced when compared with the results of group I, but statistically significant (p < 0.05). It has been established not significant reduction in organic and total iodine and not much increase in the level of inorganic form compared with the control (p ˂ 0.05). When carrying out the correlation analysis among Group I patients, we proved a close соrelation between the changes in the intracellular pool of iodine and the clinical and laboratory data characterizing the severity of the pathological process in pneumonia. In particular, a close relationship was found between the concentration of inorganic iodine and the sum of scores on the Pneumonia Severity Index (r = 0.783; p < 0.05). These data confirm the effect of severe pneumonia on changes in intracellular distribution of iodine in children.

Conclusions. The revealed changes in the indices of the intracellular pool of iodine and its distribution in the child's body are directly proportional to the severity of CAP.

Severe course of СAP in children could be caused by disruption of iodine organification in the body. Reduction in organic and total iodine and an increase in the level of inorganic form during persistent iodine deficiency lead to more severe course of pneumonia in children.

Keywords: pneumonia, iodine deficiency, intracellular iodine distribution.

This email address is being protected from spambots. You need JavaScript enabled to view it.

The full text

To view the full text

References

  1. Leung DT, Chisti MJ, Pavia AT. Prevention and Control of Childhood Pneumonia and Diarrhea. Pediatr Clin North Am. 2016; 63(1):67–79.
  2. Zimmermann M. Iodine deficiency and excess in children: Worldwide status in 2013. Endocrine practice. 2013;19(5):839–846. doi: 10.4158/ep13180.ra
  3. Rodrigues CM. Challenges of empirical antibiotic therapy for community-acquired pneumonia in сhildren. Current Therapeutic Research. 2017;84:e7–e11. Retrieved from: http://dx.doi.org/10.1016/j.curtheres.2017.01.002
  4. Mamenko MYe. [Prevention of iodine deficiency disorders: what should know and can do a pediatrician and general practitioner? (Clinical practice guideline)]. Sovremennaya Pediatriya. 2017;82(2):8‒16.
  5. Taylor PN, Okosieme OE, Dayan CM, et all. Impact of iodine supplementation in mild-to-moderate iodine deficiency: systematic review and meta-analysis. European Journal Endocrinology. 2014;170:R1–R15. Retrieved from: www.eje-online.org doi: 10.1530/EJE-13-0651.
  6. Falfushynska H, Gnatyshyna L, Shulgai A, et.all. Oxidative stress in human thyroid gland under iodine deficiency nodular goiter: from harmless to hazard depending on copper and iodine subcellular distribution. International Journal of Medicine and Medical Research. 2015;1(1):5–11.
  7. Order of МОH of Ukraine from 13.01.05 № 18 [Protocols for the Provision of Medical Aid to Children in the Specialty "Children's Pulmonology"]. (Normative document of the Ministry of Health of Ukraine). Retrieved from: http://www.moz.gov.ua
  8. Majdanny`k VG, Yemchy`ns`ka YeO. [Klinichni nastanovy` z diagnosty`ky` ta likuvannya pozalikarnyanoyi pnevmoniyi u ditej z pozy`ciyi dokazovoyi medy`cy`ny`]. Ky`yiv, 2014. 43 p.
  9. Harris M, Clark J, Coote N, et al. British Thoracic Society guidelines for the management of community acquired pneumonia in children: update 2011. Thorax. 2011; 66:ii1-ii23.
  10. Assessment of iodine deficiency diseases and monitoring their elimination: a guide for program managers. 3rd edition. Kyiv: "K.I.S.", 2008.104 p.
  11. World Health Organization/International Council for the Control of the Iodi' ne Deficiency Disorders/United Nations Children's Fund (WHO/ICCIDD/UNICEF). Assessment of the iodine deficiency disorders and monitoring their elimination. Geneva: World Health Organization, 2007.
  12. Shіdlovs'kij V.O., Stoljar O.B., Osadchuk D.V. ta іn.; [Deklaracіjnij patent na korisnu model'. Method for determining the concentration of iodine in a biosubstrate]. UA patent 45332. 2009 Nov 10. (Ukranian).
  13. Saar VG, Koroleva EM, Nikitina TG. Photomentric determination of iodine in biological samples of complicated compositions. Pharm. Chem. J. 2000;34(8):448–450.
  14. Bowen, S.J. and Thomson, A.H. British Thoracic Society Paediatric Pneumonia Audit: a review of 3 years of data. Thorax. 2013;68:682–683.

DIAGNOSTIC SIGNIFICANCE OF PROSTATE SPECIFIC ANTIGEN IN PROSTATE INTRAEPITHELIAL NEOPLASIA

Аuthors: M. P. Мelnychuk

Pages: 139–147

Abstract

         

Introduction. Prostate specific antigen (PSA) is a biochemical marker that is routinely used in prostate cancer detection, active surveillance and prognosis. In order to improve sensitiveness of PSA, additional parameters were developed such as PSA coefficient, PSA density, PSA velocity. In last decade a lot of investigations have been directed at the study of PSA role in prostate intraepithelial neoplasia diagnostics. Previous investigations had controversial results due to different approaches and patient numbers.

Purpose. To determine PSA role and significance in prostate intraepithelial neoplasia (PIN) diagnostics.

The use of total PSA, PSA coefficient, PSA density and PSA velocity in patients with high grade and low grade PIN was studied.

Materials and methods. The results of examination of 230 patients with PIN were assessed. Patients were divided into three clinical groups: high grade PIN (n = 156), combination of high and low grade PIN (n = 36) and low grade PIN (n = 38). PIN was diagnosed through prostate biopsy or after transurethral prostate resection. Such PSA characteristics as totalPSA, freePSA, PSA coefficient, PSA density and PSA velocity were studied with PIN grade consideration.

Discussion. There was a difference in values of PSA characteristics between high grade PIN and low grade PIN. Compared with normal values low grade PIN had no changes except minimal increase of total PSA (M = 6.1 ± 0.2 ng/ml). PSA coefficient, PSA density and PSA velocity had normal ranges in case of low grade PIN. This is an evidence of low diagnostic value of PSA parameters in low grade PIN detection. Low grade PIN benign prostate hyperplasia has similar properties according to investigation.

PSA parameters in high grade PIN cases differ a lot from those of low grade PIN and normal prostate. It was determined that high grade PIN influences similar way on PSA as prostate cancer. Patients with HGPIN had increased total PSA level (М = 8.4 ± 1.1 ng/ml), PSA coefficient value less than 20 % (М = 18.3 ± 1.3 %), increased PSA density level (M = 15.1 ± 1.8 ng/ml/сm3) and high ranges of PSA velocity.

Further study is required to stratify all PIN patients into groups of high malignisation risk in order to perform detailed examination and treatment.

Keywords: prostate specific antigen, high grade and low grade prostate intraepithelial neoplasia, PSA density, PSA velocity.

This email address is being protected from spambots. You need JavaScript enabled to view it.

The full text

To view the full text

References

  1. Timothy JW, Peter TS, Sigrid VC, Ethan B. Prostate-Specific Antigen Screening in Prostate Cancer: Perspectives on the Evidence. J Natl Cancer Inst. 2014; 106(3):11–16.
  2. Heidenreich A, Abrahamsson P, Artibani W, Catto J. Early detection of prostate cancer: European Association of Urology recommendation. Eur Urol. 2013; 64(3):347–354.
  3. Kostiev FI, Krasyluk LІ. [PIN – peredrak peredmihurovoi zalozy, patogenetychne obgruntuvannya monitoring hvoryh]. Urologiya. 2015; 19(3):230–239.
  4. Maru A, Makwana H, Lakum N, Chokshi T. Study on correlation between PSA and varies prostatic pathology. Int. J. Med. Sci. Public Health. 2014; 3:735–737.
  5. Jung S-H, Shin S, Kim M, Baek I-P. Genetic Progression of High Grade Prostatic Intraepithelial Neoplasia to Prostate Cancer. European Urology. 2016; 69 (5):831–833.
  6. Queisser A, Hagedorn S. Comparison of different prostatic markers in lymph node and distant metastases of prostate cancer. Modern Pathology. 2015; 28:138–145.
  7. Lee W, Lee S, Hong S, Choi W. Clinical utility of prostate-specific antigen mass ratio for prediction of prostate cancer detection on a repeated prostate biopsy. Int. braz. J. urol. 2014; 40(4):484–492.
  8. Donghyun L, Chunwoo L, Taekmin K. Clinical features and prognosis of prostate cancer with high-grade prostatic intraepithelial neoplasia. Korean J Urol. 2015; 56(8):565–571.
  9. Brawer M, Lange P. Prostate-specific antigen and premalignant change: implications for early detection CA. Cancer J Clin. 1989; 39:361–375.
  10. Lee Y, Park J, Jeon B, Lee S. Is prostate specific antigen effective for population screening of prostate cancer?A systematic review. Ann Lab Med. 2013; 33(4):233–241.
  11. Schroder F, Hugosson J Screening and prostate cancer mortality: results of the European Randomised Study of Screening for Prostate Cancer (ERSPC) at 13 years of follow-up. Lancet. 2014; 384:2027–2035.
  12. Akhter R, Reshi R, Dar Z. Histopathological study of prostatic lesions on needle biopsies with serum prostate specific antigen (PSA). Int. Journal of Medicine and Medical Sciences. 2014; 6:87–91.
  13. Kosuke M, Mukul K, Steven S, Brian J, Alberto A, Jae R. Heterogeneous clinicopathological features of intraductal carcinoma of the prostate: a comparison between “precursor-like” and “regular type” lesions. Int J Clin Exp Pathol. 2014; 7(5):2518–2526.
  14. Kang C, Xiangnan L, Yabing D, Xiance T, Seiji A, Yiwei G, Ying X, Han X, Yue Z, Wang M, Tengfei Z. Chemoprevention of prostate cancer in men with high-grade prostatic intraepithelial neoplasia (HGPIN): a systematic review and adjusted indirect treatment comparison. Oncotarget. 2017; 30: 36674–36684. 
  15. Husain I, Shukla S. Role of androgen receptor in prostatic neoplasia versus hyperplasia. Journal of Cancer Research and Theraputies. 2016; 2(1):112–116.
  16. De Luca S, Passera R, Bollito E, Manfredi M. Comparison of Prostate Cancer Gene 3 Score, Prostate Health Index and Percentage Free Prostate-specific Antigen for Differentiating Histological Inflammation from Prostate Cancer and Other Non-neoplastic Alterations of the Prostate at Initial Biopsy. Anticancer Research. 2014; 34(12):7159–7165.
  17. Tarle M, Krajlic I. Free and total serum PSA values in patients with prostatic intraepithelial neoplasia (PIN), prostate cancer and BPH. Is F/T PSA a potential probe for dormant and manifest cancer?. Anticancer Res. 1997; 17(3):1531–1534.
  18. Obralic N, Kulovac B. High grade intraepithelial neoplasia of prostate is associated with values of prostate specific antigen related parameters intermediate between prostate cancer and normal levels. Bosn J Basic Med Sci. 2011; 11(4):223–227.
  19. Cicione A, Nunzio C, Janssen T. Metabolic syndrome diagnosis and widespread high grade prostatic intraepithelial neoplasia significantly increase prostate cancer risk: results from a multicenter biopsy study. BMC Cancer. 2016; 15(77):2103–2108.
  20. Isakay L, Yaman O. Prostate-specific antigen density: The role in benign prostate hyperplasia, prostate intraepithelial neoplasm, organ-confined prostate carcinoma and advanced prostate carcinoma. International urology and nephrology. 2011; 27:757–761.

TULAREMIA: A MODERN VIEW ON THE PROBLEM

Аuthors: М. D. Chemych, N. G. Malysh, N. І. Іlina, V. V. Іlina

Pages: 148–161

Abstract

         

Rationale. Due to the stability of the natural cells of tularemia, the considerable spread of Francisella tularensis in nature, the multiplicity of routes of transmission of the pathogen, the complexity of the diagnosis and the severity of the clinical course of tularemia determine its significance in modern infectious pathology.

Purpose. Evaluate the epidemiological situation with tularemia in Ukraine and the world, to investigate the probable risks of its complication.

Materials and methods. The paper uses PubMed databases, EMBASE, reporting materials of the department of especially dangerous infections, field observations data and laboratory research results of the Sumy Regional Laboratory Center of the Ministry of Health of Ukraine. When processing materials used methods of epidemiological, statistical research, Excel program, Statistica 6.0.

Results. Tularemia is an endemic disease for non-arctic and paleoartic regions, found mostly in the northern hemisphere. In Ukraine and in adjacent to its borders, states of isolated cases of a disease on tularemia are registered. The main reservoirs of Francisellatularensis and sources of infection are rodents. Among the carriers a special place is occupied by ticks. Infection of people occurs more often in natural cells.

Conclusions. It is likely that the current epidemiological situation is "the tip of the iceberg", since this disease, due to its multiplicity, is not aetiologically verified, and the cases of tularemia that appear are hidden under the mask of other diseases. For objective assessment and prediction of the epizootic and epidemiological situation with tularemia in the region it is necessary to conduct a complete epidemiological monitoring.

Keywords: tularemia, Francisella tularensis, epidemiological situation, rodents, ticks.

This email address is being protected from spambots. You need JavaScript enabled to view it.

The full text

To view the full text

References

  1. Otto P, Kohlmann R, Müller W, Julich S, Geis G, Peters M, Johannes Wolf P, Karlsson E, Forsman M, Myrtennäs K, Tomaso H. [Hare-to-Human Transmission of Francisella tularensis subsp. Holarctica]. Germany Emerging Infectious Diseases., 2015; 21(1):153-155. Retrieved from http://www.cdc.gov/eid
  2. Asano S, Mori K, Yamazaki K, Sata T, Kanno T, Sato Y, Kojima M, Fujita H, Akaike Y, Wakasa H . [Temporal differences of onset between primary skin lesion sand regional lymph node lesions for tularemiain Japan: a clinicopathologic and immunohistochemical study of 19 skin cases and 54 lymph node cases]. VirchowsArch. 2012;(460):651–658.
  3. Wang Y, Peng Y, Hai R, Xia L, Li H, Zhang Z, Cai H, Liang Y, Shen X, Yu D, Birdsell D, Wagner DM, Keim P. [Emerging Diversity of Francisella tularensis Subsp. Holarctica Lineages]. China Infectious Diseases. 2014;20(7):1191-1194. Retrieved from http://www.cdc.gov/eid
  4. Aktas D, Celebi B, EmirhanIsik M, Tutus C, Ozturk H, Temel F, Kizilaslan M, Zhu BP. [Oropharyngeal Tularemia Outbreak Associated with Drinking Contaminated Tap Water]. Emerging Infectious Diseases 2013;21(12): 2194-2196. Retrieved from http://www.cdc.gov/eid
  5. Andreychyn M, Kopcha V. Bioteroryzm: Medychnaprotydiya. Ternopil. Ukrmedknyha Publ, 2005. 298 p.
  6. Chumakov M, Shafeyev M, Zorina L. Tulyaremiya. Epidemiologiya i profilaktika. Kazan' . KGMU Publ, 2003. 47 p.
  7. Centers for Disease Control and Prevention (CDC). [Tularemia. United States, 2001-2010.] MMWR Morb. MortalWklyRep 2013;62(47):963-966.
  8. Wayne Conlan J. [Francisella tularensis: A Red-blooded Pathogen.] J InfectDis. 2011;204(1): 6-8.
  9. Timofeev V, Bakhteeva I, Titareva G, Kopylov P, Christiany D, Mokrievich A, Dyatlov I, Vergnaud G. Russian isolates enlarge the known geographic diversity of Francisella tularensis subsp. PLOS ONE. 2017;(09)1-20. Retrieved from https://doi.org/10.1371/journal.pone. 0183714
  10. Zargar A, Maurin M, Mostafavi E. Tularemia, are emerging infectious disease in Iran and neighboring countries. Epidemiology and Health 2015;37:e2015011p. 1-6.
  11. Gürcan Ş. [Epidemiology of tularemia] Balkan medical journal. 2014;31(1):3-10
  12. World Health Organization. [WHO guidelines on tularameia] 2015. Retrieved from: http://www.cdc.gov/tularemia/resourc­es/whotularemiamanual.pdf.
  13. Myrtenna K, Marinov K, Johansson A, Niemcewicz M, Karlsson E, Bystrom M, Forsman M [Introduction and persistence of tularemia in Bulgaria]. Infection Ecology and Epidemiology 2016;6. Retrieved from: http://dx.doi.org/10.3402/iee.v6.32838
  14. Femling JK, Baca JT. [Update on Emerging Infections: News From the Centers for Disease Control and Prevention]. Annals of Emergency Medicine. 2016;68(1):117-118.
  15. Jackson J, McGregor A, Cooley L, Ng J, Brown M, WeiOng C, Darcy C, Sintchenko V [Francisella tularensis Subspecies holarctica Tasmania, Australia, 2011]. Emerg Infect Dis. 2012;18(9): 1484–1486.
  16. Maleyev VV, Martynov VA, Klochkov IN. [Kliniko-endoskopicheskaya kharakteristika ostroy erozivno-yazvennoy patologii verkhnikh otdelov ZHKT u bol'nykh gemorragicheskoy likhoradkoy s pochechnym sindromom, leptospirozom i tulyaremiyey]. Rossiyskiy mediko-biologicheskiy vestnik imeni akademika I.P. Pavlova. 2014;3:48-55.
  17. Polishchuk MV. [Epizooto-epidemiologicheskiye aspekty formirovaniya zabolevayemosti tulyaremiyey v Ryazanskoy oblasti] Nauka molodykh. EruditioJuvenium Publ. 2016;3:16-19.
  18. Aravena-Román M, Merritt A, Inglis TJ. New Microbes and New Infections. 2015;10(8):75-77.
  19. Foley JE, Nieto NC. [Tularemia]. VetMicrobiol. 2010;140:332–8.
  20. Gyuranecz M, Reiczigel J, Krisztalovics K, Monse L, Szabóné GK, Szilágyi A. Factors influencing emergence of tularemia, Hungary, 1984–2010. Emerg Infect Dis. 2012;18:1379– 81. http://dx.doi.org/10.3201/eid1808.111826
  21. Possums R, Eden JS, Rose K, Ng J, Shi M, Wang Q, Sintchenko V, Holmes E. [Francisella tularensis subsp. Holarcticain]. Emerging Infectious Diseases. 2017;23(7):1196-1201 Retrieved from: http://www.cdc.gov/eid
  22. Chayka AN, Savchenko ST, Alekseyev VV. [Epidemiologicheskiy nadzor za tulyaremiyey na territorii Volgogradskoy oblasti v sovremennykh usloviyakh]. Vestnik VolGMu. 2017;№ . 19-21p
  23. Nakaz MOZ Ukrayiny vid 23.07.2003 №342 [Pro zakhody shchodo profilaktyky zakhvoryuvan na tulyaremiyu]
  24. Kılıç S. [A General Overview of Francisella tularensis and the Epidemiology of Tularemia in Turkey]. Flora. 2010;15:37–58.
  25. UPMC Center for Health Security. [Francisella Tularensis (Tularemia)]. 2014;2 Retrieved from: http://www.centerforhealthsecurity.org/our-work/publications/francisella-tularensis-fact-sheet
  26. [USAMRIID's Medical Management of Biological Casualities Handbook]. Six the d. Fort Dietrich, Maryland: U.S. Army Medical Research Institute of Infectious Diseases. 2005:56-57.
  27. Hepburn MJ, Simpson AJH. [Tularemia: current diagnosis and treatment options] Expert Rev. Anti Infect. Ther. 2008;6(2):231–240.
  28. Kravtsov AL, Klyuyeva SN, Shchukovskaya TN, Bugorkova SA. [Effekt immunomodulyatorov i protivotulyaremiynoy vaktsinatsii na apoptoz i lizis splenotsitov, vzaimodeystvuyushchikh in vitro c tulyarinom]. Probl. osobo opasnykh inf. 2017;3:90–94.
  29. Gürcan S. [Francisella tularensis and tularemia in Turkey]. Mikrobiyol Bul. 2007;41(4):621-36.
  30. Dennis DT, Inglesby TV, Henderson DA, Bartlett JG, Ascher MS, Eitzen E. [Tularemia as a Biological Weapon Medical and Public Health Management]. JAMA. 2001;285:2763–73. PMID: 11386933
  31. Gürcan Ş, VarolSaraçoğlu G, Karadenizli A, Özkayın EN, Öztürk ŞZ, Çiçek C. [Tularemia as a result of outdoor activities for children in the countryside]. Turk J Med Sci. 2012;42:1044–9.
  32. Kılıç S. [A General Overview of Francisella tularensis and the Epidemiology of Tularemia in Turkey]. Flora. 2010;15:37–58.
  33. Şahin M. [Francisella tularensis’ in Vektörleri ve Doğal Rezervuarları In: Gürcan Ş., editor. Francisella tularensis ve Tularemi]. İstanbul: Nobel Tıp Kitabevleri. 2009:139–60.
  34. General Directorate of Primary Health Services Zoonotic Diseases Department. [Field Guidance for the Control of the Tularemia Disease]. Ankara: Başak Matavacılık. 2011:1-18.
  35. Petersen JM, Mead PS, Schriefer ME. [Francisella tularensis: an arthropod-borne pathogen]. VetRes. 2009;40:1–9. PMCID: PMC2695023.
  36. Padeshki PI, Ivanov IN, Popov B, Kantardjiev TV. [The role of birds in dissemination of Francisella tularensis: first direct molecular evidence for bird-to-human transmission]. Epidemiol Infect. 2010;138:376–9. PMID: 19664305
  37. Girina AA, Dobrovol'skiy AA, Kurganskaya AY, Koshileva NA, Shcheglinkova NY, Nikolayeva GD. [Vspyshka tulyaremii v Khanty-Mansiyske v 2013 g.: kliniko-epidemiologicheskiye osobennosti v detskoy populyatsii]. Zhurnal infektologii. 2015;7(4):83-88 p.
  38. Dentan FC, Pavese P, Pelloux I, Boisset S, Brion JP, Stahl JP, Maurin M. [Treatment of Tularemia in Pregnant Woman]. Emerging Infectious Diseases. 2013;19(6):996-998. Retrieved from: http://www.cdc.gov/eid
  39. Myrtannas K, Marinov K, Johansson A. [Introduction and persistence of tularemia in Bulgaria]. Infect Ecol Epidemiol. 2016;6:32838. DOI:10.3402/iee. v6.32838
  40. Yevstegneyeva VA, Chestnova TV, Smol'yaninova OL. [O neyrosetevom modelirovanii i prognozirovanii epizootiy tulyaremii na territorii Tul'skoy oblasti]. Vestnik novykh meditsinskikh tekhnologiy. 2014;1.
  41. Trevisanato SI. [The “Hittite plague”, an epidemic of tularemia and the first record of biological warfare]. Med Hypotheses. 2007;69:1371–4. PMID: 17499936
  42. Kukharkina OV, Borisova IA, Borisova OA. [Biologicheskiy terrorizm i yego negativnyye posledstviya (obzor)]. Trudy Federal'nogo tsentra okhrany zdorov'ya zhivotnykh. 2013; 11(1):142-156 p.
  43. Herasymenko TV, Mohilevskyy LY, Khablo ZA. [Imunoprofilaktyka tulyaremiyi v Ukrayini u suchasnykh umovakh]. Infektsiyni khvoroby. 2010; 4:59-62 p.

EXPERIENCE OF COMPLEX TREATMENT OF REPRODUCTIVE-AGE WOMEN WITH CERVICAL ECTOPY ON THE BACKGROUND OF BACTERIAL VAGINOSIS

Аuthors: I. Makagonov, A. Vergun, O. Vergun

Pages: 162–169

Abstract

         

Introduction. The most common background disease of the cervix is ectopia of the cylindrical epithelium (cervical ectopy). Pathological states of the vaginal part of the cervix are one of the leading problems in the structure of gynecological diseases in reproductive age women. The frequency of cervical ectopy is 38.8 %, and in the presence of other gynecological diseases it increases to 49.2 %.

Purpose. The aim of the study was to evaluate the efficacy and safety of the original medicinal product in the pharmacological form of vaginal tablets containing terinidazole 200 mg, neomycin sulfate 100 mg (65,000 IU), nystatin 100,000 IU, prednisolone sodium metasulfobenzoate 4.7 mg.

Materials and Methods. The complex examination of 98 patients of reproductive age with the firstly diagnosed or recurrent cervical ectopy with concomitant bacterial vaginosis was carried out and the results of clinical and laboratory studies of the efficiency and safety of complex treatment were analyzed. The main group included 49 women in whom, in order to normalize the state of the vaginal microbiota, the original complex drug containing ternidazole 200 mg; neomycin sulfate 100 mg (65,000 IU); nystatin 100,000 IU; prednisolone sodium metasulfobenzoate 4.7 mg (Tergynan, Laboratories du Docteur E Bouchara Recordati, France) was administrated intravaginally one tablet per day for ten days. The comparison group included 49 patients, for whom the correction of the vaginal microbiota state was carried out in accordance with the current recommendations.

Discussion. After the end of the treatment, there was a decrease in the total bacterial mass, the frequency of the detection of opportunistic microorganisms with an increase in the dynamics of the Lactobacillus spp. pool in the amount of more than 106 CFU/ml which persisted for the next three menstrual cycles in 46 (93.9 %) of the patients in the main group and in 29 (59.2 %) in the comparison group. As a result of the treatment, in 16 (32,7 %) patients of the main group and 11 (22,4 %) of the comparison group (P < 0,05) absence of cervical ectopy was diagnosed by colposcopy. High efficiency in correction of dysbiotic disorders, changes in the qualitative and quantitative composition of the microflora of the vaginal biotope, long-term positive clinical effect and good tolerability, reduction of the need for the destruction of the focal point of the lesion (elimination of the cervical ectopy in 32.7 % of women) allows to recommend the inclusion of vaginal tablets with an optimized composition into the complex treatment of reproductive age women with cervical ectopy with the concomitant bacterial vaginosis. The obtained results of our research data suggest that a significant frequency of recurrence of cervical ectopy in women of reproductive age is caused by ignoring the assessment of the state of the vaginal microbiota and the corresponding sanation before surgical interventions on the cervix.

Keywords: cervical ectopy, bacterial vaginosis, vaginal microbiota, complex treatment.

This email address is being protected from spambots. You need JavaScript enabled to view it.

The full text

To view the full text

References

  1. Tatarchuk TF, Tutchenko TN. [Patologiya sheyki matki] Reproduktivnaya endokrinologiya. 2013; 1: 39–47.
  2. Bewley S, Cheon Y, Creighton SM. Gynaecology by Ten Teachers Hodder &Stoughton Ltd., 2011. 206p.
  3. Prilepskaya VN. Zabolevaniya sheyki matki, vlagalischa i vulvyi [klinicheskie lektsii]. Moskva: MEDpress-inform, 2005. 356p.
  4. Stoler MH. Advances in cervical screening technology. Mod. Pathol. 2000;13: 275–284.
  5. Hvorostuhina NF, Miheeva YV, Novichkov DA. [Analiz prichin retsidivirovaniya ektopii sheyki matki posle koagulyatsii] Fundamentalnyie issledovaniya. 2014; 10(3):562–566.
  6. Smaga A, Paszkowski T, Walczak R. Analysis of physiologic and abnormal pictures of uterine cervix by means of infrared thermography. Ginekol Pol. 2003; 74(9):847–854.
  7. Gomberg MA, Plahova KI, Aniskova IN. [Standartnaya i nestandartnaya diagnostika i terapiya pri vyideleniyah iz vlagalischa ] Farmateka.2006;2:45–50.
  8. Kremets K. [Sovremennyie predstavleniya o bakterialnom vaginoze i nekotoryie aspektyi terapii] Novosti meditsinyi i farmatsii. 2012; 411:11–12.
  9. Kulavskiy VA, Nasyirova SF. Psevdoeroziya sheyki matki u nerozhavshih zhenschin [klinika, diagnostika, lechenie]. Ufa: 2000. 153p.
  10. Miheeva YV, Hvorostuhina NF, Novichkov DA. [Sovremennyiy podhod k lecheniyu oslozhnennoy ektopii sheyki matki] Akusherstvo, ginekologiya i reproduktsiya. 2016; 2:24–31.
  11. Vaganova S.E. [Kombinirovanoe lechenie dobrokachestvennyih zabolevaniy sheyki matki] Akusherstvo i ginekologiya. 2010; 5:116–120.
  12. [Sravnitelnaya otsenka aktivnosti sostavlyayuschih preparatov Poliginaksi Terginan in vitro] (otchet ob issledovanii, provedennom v laboratorii Nosocotech (Lion, Frantsiya), 15dekabrya 2011.). Meditsinskie aspekty zdorovya zhenschiny. 2012;3(54):44–46. Retrieved from: http://www.nosocotech.fr
  13. Workowski KA, Berman S. Sexually transmitted diseases treatment guidelines MMWR Recomm. Rep. 2010; 59: 101–110.
  14. Dubossarskaya YA, Dubossarskaya ZM. [Terginan – preparat vyibora pri lechenii bakterialnogo vaginoza] Zdorove zhenschiny. 2012; 6 (72): 147–152.
  15. Radzinskiy VE, Ordiyants IM. Dvuhetapnaya terapiya vaginalnyih infektsiy. Moskva: Status Praesens, 2012; 16 p.

ANALYSIS OF ASSOCIATION OF THE ENPP1 RS997509 POLYMORPHISM WITH TYPE 2 DIABETES IN PATIENTS WITH OBESITY

Аuthors: I. V. Marchenko, Ye. A. Harbuzova, Ye. I. Dubovyk, Ya. D. Chumachenko

Pages: 170–175

Abstract

         

Introduction. Type 2 diabetes mellitus (T2DM) is a multifactorial disease with leading genetic determinism. Full-genome association studies identified a large number of polymorphic loci associated with type 2 diabetes. One of the candidate genes is the Ectonucleotide Pyrophosphatase/Phosphodiesterase 1 (ENPP1) gene. Studies in humans have shown a correlation between ENPP1 polymorphisms, including rs997509 and type 2 diabetes mellitus, obesity, insulin resistance and metabolic syndrome in different populations of the world.

Purpose. Study of rs997509 polymorphic variant associations of ENPP1 gene with type 2 diabetes mellitus in patients with obesity in the Ukrainian population.

Materials and Methods. Venous blood of 317 patients with type 2 diabetes mellitus and 302 controls. All learners were genotyped was carried out using method of polymerase chain reaction with further analysis of restriction fragment length.

Discussion. The results of the study show that among the patients without obesity the ratio of genotypes in the experimental and control groups is not significantly different (P = 0.709). Among patients with type 2 diabetes and obesity, the distribution of genotypes C/C, C/T and T/T was 81 %, 19 % and 0 %, and in subjects without diabetes 92, 4 %, 7.6 % and 0 % (P = 0.024). There is a significant difference in the distribution of genotypes by rs997509 polymorphism among obese individuals. The method of binary logistic regression revealed a reliable association of the studied polymorphism with type 2 diabetes in the group as a whole (P = 0.017) and in the subgroup with obesity (P = 0.029).

Conclusion. It was shown that risk of T2DM development in T allele carriers is significantly higher compared to C/C homozygotes in patients with obesity (OR = 3.230; P = 0.023).

Keywords: type two diabetes mellitus, PC-1 gene, Ectonucleotide Pyrophosphatase/Phosphodiesterase 1, allelic polymorphism.

This email address is being protected from spambots. You need JavaScript enabled to view it.

The full text

To view the full text

References

  1. Guja C, Gagniuc P, Ionescu-Tîrgovişte C. Genetic factors involved in the pathogenesis of type 2 diabetes. Proc. Rom. Acad. 2012;1:44–61.
  2. Sanghera DK, Blackett PR. Type 2 diabetes genetics: beyond GWAS. J Diabetes Metab. 2012;3(05):2–17. doi:10.4172/2155-6156.1000198.
  3. Gaulton KJ, Willer CJ, Li Y et al. Comprehensive association study of type 2 diabetes and related quantitative traits with 222 candidate genes. Diabetes. 2008;57(11):3136-3144. doi:10.2337/ db07-1731.
  4. Goldfine ID, Maddux BA, Youngren JF, Reaven G, Accili D, Trischitta V, et al. The Role of Membrane Glycoprotein Plasma Cell Antigen 1/Ectonucleotide Pyrophosphatase Phosphodiesterase 1 in the Pathogenesis of Insulin Resistance and Related Abnormalities. Endocr Rev. 2008;29(1):62-75. doi: 10.1210/er.2007-0004.
  5. Maddux BA, Sbraccia P, Kumakura S, Sasson S, Youngren JF, Fisher A, Spencer S, Grupe A, Henzel W, Stewart TA, Reaven G, Goldfine I 1995 Membrane glycoprotein PC-1 and insulin resistance in non-insulin-dependent diabetes mellitus. Nature 373:448–451.
  6. Maddux BA, Chang YN, Accili D et al. Overexpression of the insulin receptor inhibitor PC-1/ENPP1 induces insulin resistance and hyperglycemia. Am J Physiol Endocrinol Metab. 2006;290:E746–E749.
  7. Heather H. Zhoua, Chen-Ni Chinb, MargaretWuc et al. Suppression of PC-1/ENPP-1 expression improves insulin sensitivity in vitro and in vivo. European Journal of Pharmacology 2009;616(1-3):346-352. https:// doi.org/10.1016/ j.ejphar.2009.06.057.
  8. Bochenski J, Placha G, Wanic K et al. New polymorphism of ENPP1 (PC-1) is associated with increased risk of type 2 diabetes among obese individuals. Diabetes. 2006;55(9):2626-2630. doi: 10.2337/db06-0191.
  9. Yako YY, Madubedube JH, Kengne AP et al. Contribution of ENPP1, TCF7L2, and FTO polymorphisms to type 2 diabetes in mixed ancestry ethnic population of South Africa. Afri Health Sci. 2015;15(4):1149-1160. http://dx.doi.org/10.4314/ahs.v15i4.14.
  10. Matsha T, Fanampe B, Yako Y et al. Association of the ENPP1 rs997509 polymorphism with obesity in South African mixed ancestry learners. East Afr Med J. 2010;87(8):323-329.
  11. Santoro N, Cirillo G, Lepore MG et al. Effect of the rs997509 polymorphism on the association between ENPP1, metabolic syndrome and impaired glucose tolerance in childhood obesity. J Clin Endocrinol Metab. 2009;94(1):300-305. doi: 10.1210/jc.2008-1659.
  12. S Robiou-du-Pont, A Bonnefond, L Yengo et al. Contribution of 24 obesity-associated genetic variants to insulin resistance, pancreatic beta-cell function and type 2 diabetes risk in the French population. International Journal of Obesity 2013;37:980–985. doi:10.1038/ijo.2012.175.

TYPES OF EATING BEHAVIOR AND SEROTONIN LEVELS IN PATIENTS WITH IRRITABLE BOWEL SYNDROME AND CONSTIPATION ON THE BACKGROUND OF OBESITY

Аuthors: V. G. Mishchuk, G. V. Grigoruk

Pages: 176–182

Abstract

         

Introduction. Obesity is the cause of various diseases of the gastrointestinal tract, including dyskinesia of the large intestine with constipation, diverticular disease, polyposis of the large intestine. Among obese individuals, association with functional constipation is observed in 24.9 % of patients. Obesity is accompanied by various types of eating disorders, and violations of eating behavior contribute to constipation, abdominal pain and changes in sensitivity of serotonin receptors in the gut wall.

The purpose of the study is to investigate the nature of changes in eating behavior, its association with serotonin levels in patients with irritable bowel syndrome (SBS) and constipations on the background of obesity.

Materials and methods. The paper analyzes the frequency of various types of behavioral disorders identified by the Dutch Eating Behavior Questionnaire (DEBQ) and the level of serotonin in each of them. In patients with IBS and constipation on the background of obesity and IBS with constipation as an independent disease.

Results. Emotional type of eating behavior was found in patients with IBS and constipation on the background of obesity more than in half of cases, which is 1.86 (p ˂ 0.05) times more often than in patients without excessive body weight. The external type was found in 13.46 % and 16.67 % of patients in both groups. In IBS with constipation as a distinct disease, restrictive type of eating behavior was found 1.9 times more often (57.69 %, p ˂ 0,05) than in IBS with constipation on the background of obesity (29.76 %). The lowest concentration of serotonin in the blood of patients with IBS with constipation was observed in restrictive type of eating behavior (23.3 ± 1.4 ng/ml). In external and emotional variants, serotonin levels were slightly higher and equaled 28.9 ± 1.5 and 32.5 ± 1.3 ng/ml, respectively. In the obese subjects on the background of obesity, serotonin levels in the blood were elevated compared to healthy subjects without disturbances in eating behavior (39.11 ± 2.99 ng /mg) to 103.5 ± 3.4ng/ml with a restrictive and up to 208.3 ± 18.7 and 215.6 ± 14.4ng/ml, p1,2 ˂ 0.05 in external and emotional types.

Conclusion. In case of eating disorders in patients with IBS with constipation on the background of obesity there are more severe violations of serotonin levels, especially in the external and emotional types, and timely correction of eating behavior will improve the mechanisms of regulation of these comorbid pathologies.

Keywords: irritable bowel syndrome with constipation, obesity, eating behavior, serotonin.

This email address is being protected from spambots. You need JavaScript enabled to view it.

The full text

To view the full text

References

  1. Klimusheva TA. [Irritable bowel syndrome through the eyes of a psychiatrist]. RZhHHK. 2008;(4):82-86.
  2. Panova EI, Martyishina OV, Danilov VA. [Pathology associated with obesity: frequency, nature and some mechanisms of formation] Sovremennyie tehnologii v meditsine. 2013;2(2):108-110.
  3. Vd. Baan–Slotweg OH, Ziem O, Bekkali N [et al.]. Constipation and colonic transit times in children with morbid obesity. J. Pediatr. Gastroenterol. and Nutr. 2012;52:442-5.
  4. Dudar LV, Ovdii MO. [The role of nutritional behavior and diet in the development of excess body weight in young people]. Suchasna hastroenterolohiia. 2015;4(72):31-35.
  5. Parvin D, Asghari-Jafarabadi M, Shabnan S. Validity Reliability and Feasibility of the Eating Behavior Patteth Questionnaire (EBPQ) amond Iranian Female Students. Health Promotion Perspectives. 2015;5(2):128-137. doi: 10/1517/hpp.2015. 015http//Journas thzmed.ac.ir HPP.
  6. Kim J, Chone R, Zim H. Differences of Socio-psychology, Eating Behavior, Diet Quality and Quality of Life in South Korean Woman according to Their Weight Status. Clin.Nutr.Res. 2016;Jul.5(3):161-171. Retrieved from: http://ljiorg/10.7762./cgr/2016.5/3/161.
  7. Isachenkova OA. [Eating behavior as an important factor in the development of obesity and comorbid diseases]. Ozhirenie i metabolizm. 2015;12(4):14-17. Doi: 10.14341/Omet.2015.414.17.
  8. Absalyamova LM. [Disorders and disturbances in the behavior of the individual]. Problemy suchasnoi psykholohii 2-14.-вип.25.-с.19-33.
  9. Samsonov AA, Ploshnikova EYu, Andreev NG [i soavt.]. [Irritable bowel syndrome - a disease with many unknowns, some therapeutic aspects]. Lechaschiy vrach. 2012(2):34-38.
  10. Manskaya EG.[Features of eating behavior in young women with primary obesity]. Problems of endocrinology. 2014;(3):54-60.
  11. Bokic T, Storr M, Schicho R. Potential Causes and Present Pharmacotherapy of Irritable Bowel Syndrome: (An Overwiew). Pharmacology. 2015;96:76-85. doi. 1159/000435816.
  12. Duo-Chen Jin, Hai- Zong Cao, Meng-Qwe Xu, Si-Nan Wang, [et al.] Regulation of the serotonin transporter in the pathogenesis of irritable bowel syndrome. World J.gastroenterol. 2016;22(36):8137-8146. Publiced online 2016 Sep. 28. doi 10.3748/wjg.V22;36.8137.
  13. Stasi C, Bellini M, Cyanbaccini E, Duranti E, [et al.]. Neuroendocrine Dysregulation in Irritable Bowel Syndrome Patients: A. Pilot-Study / J. Neurogastroenterol. Motil. 2017 Jul 30; 23(3):428-434. doi:10.5056/jnm16155.
  14. Ja-Zouli M, Wouters MM, Kapur–Pojskis Z [et al.]. Lessons Learned –resolving the enigma of genetic factors in JBS. Nature Reviews Gastroenterology Hepatology. 2016;13:77‑87.doi.10.1038/nrgastro.2015.206.
  15. Soloveva AV. [Risk factors for the formation of eating disorders in obese individuals]. Medical Almanac. 2013;6(30):178-180.
  16. Kruger R, Beck KJ, De Bray [et al.]. Exploring the Relationship between Body Composition and Eating Behaviour Using the Three Factors Eating Questionaire (TFEQ) inYoung New Zealand Women. (Article) June2016;wth35. Reads: Doi 103390/807 0386.
  17. Lacy BE, Mearin F, Chey WD, Zembo AJ. Bowel disorders. Gastroenterology. 2016;150(1):393-407.
  18. Van Strien T, Frijter J, Bergere Y [et al.]. The Dutch Eating Behavior Quastionnare (DEBQ) for assenssment of restrained, emotional and external eating behaviour. Int. J.Eat. Disord. 1986;5(2):295-315.
  19. Dutton E, Dovey TM. Validation of the Dutch Eating Behaviour Questionnaire (DEBQ) amond Maltese Women. Appetite. 2016;1(107):9-14. doi10.1016. j.appet.2016.07.017. Epub. 2016,Jul 15
  20. Braet C, Malley GO, Weghuber D [et al.]. The Assessment of Eating Behaviour in Children Who Are Obese: A Psychological Approach. A Position Paper from the European Childhood Obesity Group. Obesity Facts. 2014;(7):153-164. https//doi. Org/10.1159/.00036839.
  21. Cebolla A, Barrada JR, Van Strien T [et al.]. Validation of the Dutch Eating Behavior Qwestionnaire (DEBQ) in a Sample of Spanish Women. Appetite. 2014;(73 ):58-64.
  22. Nagi M, Hibert H, de Zwan E, Braetiler M [et al]. The German Version of the Dutch Eating Behavior Questionaire: Psychometric Properties, Mea-Surement Invariance and Population Based Normus. Journal pone 0162510 Research 2016; https://doi.org./ 10.1377/ Article http:// Journals.plos;org./plosone/article.id=10.1377/jornal.pone.0162510.
  23. Wurtman RJ. Wurtman JJ Brain serotonin, carbohydrate-craving, obesity and depression. Obesity research, 1995;3 Suppl 4 doi.
  24. Voznesenskaya TG. [Eating disorders in obesity and their correction]. Farmateka. 2009;(12):91-94.
  25. Braun T, Voland P, Kurz I, Prinz C, Jryratzi M [et al. Enterochromaffin cells of the human gut: sensors for spices and odorants. Gastroenterology. 2007;132(5):1890-90.
  26. Psychometric Properties of the Malay Version of the Dutch eating Behavior Questionnare CDEBQ in a Sample of Melasia, Malay-sian Abuets Attending a Health Care Facility. Subramamiam K., Van Vum Zow, Chinna K, Fah Chin K [et al.]. Malays J. Med. Sci. 2017;24(4):64-73. doi 102/315/ mjms.2017.24.4.8.

ASSESSMENT OF TREATMENT EFFICIENCY OF BIOPHYSICAL METHODS IN PATIENTS WITH CHRONIC HYPERTENSIVE CEREBRAL ISCHAEMIAS

Аuthors: F. O. Volokh, K. A. Arkhypova, A. I. Fisun, V. O. Malakhov

Pages: 183–193

Abstract

         

The present work is a part of the multidisciplinary study on optimizing therapy for chronic neurological disorders. This part of research is dedicated to an assessment of treatment efficiency and monitoring rehabilitation process of patients with hypertensive encephalopathy of early- and middle-stage. The article presents the results of the study of the state of the membrane-cellular complex of erythrocytes in order to reveal functional changes, diagnosis and prognosis of chronic cerebral ischemia of hypertonic genesis of various stages (hypertensive encephalopathy (HE) of the first (I) and the second (II) stages) in the course of the therapy. For this purpose, a comprehensive study of the structural and functional state of the sympathoadrenal system, as a leading link in the pathogenesis of cardiovascular and cardiocerebral diseases, has been performed. The examination of blood cell membrane adrenergic activity, as an important criterion of the nervous and cardiovascular systems, during the course of patients’ treatment has been carried out using a complex of physical and biochemical methods. Thus, we have opted for two techniques of in vitro adrenergic receptors sensing via monitoring drug-induced red blood cells' response to a beta-blocker (propranolol). The first one refers to a change in osmotic fragility of red blood cell membranes under the effect of beta-blocker and exploits a principle of hemolysis inhibition in the presence of beta-blocker which binds to beta-adrenergic receptors (beta-ARs) thus reducing the damage degree. Beta-ARs activity is numerically expressed by beta-ARM index. The second one is about tracing dielectric characteristics of blood cells using extra-high frequency (EHF) dielectromentry. The concept of dielectric blood sensing involves iterative measuring blood samples under in vitro effect of adrenergic-like substances (beta-blockers, adrenalin) using the waveguide-based reflectometry at a fixed frequency of 39.5 GHz. The main strategy of the study is to detect reproducible permittivity changes (Δε*) as a response to the pharmaceutical action of beta-blocker. Both methods were performed as the repeated measurements of the parameters under study during the therapy at the beginning, on 10th day, and 60th day of follow-up.

The analysis has shown a clear correlation between the level of beta-adrenergic activity and the stage of HE. It was revealed that the degree of beta-adrenergic receptors activity of erythrocytes decreases with the progression of HE. Specifically, the quantitative assessment of beta-adrenergic receptor activity of erythrocytes between 26 and 45 units and even above should be considered a sign of hyperadrenergic states caused by pathological process.

The obtained results of the dielectric examination also allow monitoring the functional state of adrenergic activity of patients in the course of treatment at the cellular level. It has been shown that dielectric in vitro reactions of blood cells under the influence of beta-blocker depend on the physiological state of patients. The change in the effect size and its sign of erythrocyte dielectric permittivity specifically reflects the direction of the pathological process. Reduction of dielectric reactivity of blood cells in response to in vitro effects of beta-blockers from -0.3 to +0.3 units should be considered a prognostic indicator, which depends on the severity of HE. Thus, determining the index of permittivity of erythrocytes and comparison between groups in patients with HE is advisable in order to predict the transition of pathology from one stage to another. Relative values of dielectric permittivity correlate with the parameters of beta-ARM, thus indicating the relationship between the dielectric characteristics and the structural/functional properties of blood cells depending on the physiological state of a patient. The data obtained by the methods applied are well-correlated and are of great interest for monitoring efficiency of treatment for chronic neurological conditions.

Keywords: beta-adrenergic activity, hypertensive encephalopathy, ЕHF dielectrometry, osmotic fragility, erythrocytes.

This email address is being protected from spambots. You need JavaScript enabled to view it.

The full text

To view the full text

References

  1. Golovach IYu. [Arterial hypertension and cognitive impairment: the importance of antihypertensive therapy in correction of cognitive impairment in patients of middle and advanced age]. Mystetsvo likuvannya. 2009; 8(64):48–52.
  2. Lokshina AB, Zakharov VV. [Mild and moderate cognitive disorders under discirculatory encephalopathy]. Neurol. Journal. 2006;11(1):57–64.
  3. Malakhov VA. Pochatkovi stadii khronichnyh tserebral'nyh ishemiy [Initial stages of chronic cerebral ischemia]. Kharkiv: Shust Publ., 2006. 125 p.
  4. Malaya LT, Schegoleva TYu, Bakhova LK. [On some molecular mechanisms of cardiovascular pathology development]. Bulletin of Experimental Biology and Medicine. 1992;6:572–574.
  5. Zakharov VV. [Clinic, diagnosis and treatment of discirculatory encephalopathy]. Practikuyuschemu neurologu. 2009;5(27):13–19.
  6. Bonovich DC. Hypertension and Hypertensice Encephalopathy, chapter 9 in: The Interface of Neurology & Internal Medicine/ ed. by José Biller, Lippincott Williams&Wilkins, 2008. pp. 67–71.
  7. Golovach IYu. [Discirculatory encephalopathy: some pathogenetic, clinical and therapeutic aspects]. Liky Ukrainy. 2011;4(150):60–67.
  8. Brodersen J, Schwartz LM, Heneghan C, et al. Overdiagnosis: what it is and what it isn’t. BMJ Evid. Based Med., 2018;23:1–3.
  9. Pantoni L, Lammie A. Cerebral small vessel disease: pathological aspects in relation to vascular cognitive impairment. In: Vascular cognitive impairment. London: Martin Dunitz Ltd., 2002, pp. 115–133.
  10. Mischenko TS. [Dyscirculatory encephalopathy: modern views on pathogenesis and diagnosis]. Zdorovya Ukrainy. 2006;15–16.
  11. Voloshin PV, Malakhov VA, Zavgorodnya AN. Endotelial'na dysfunkstiya pry tserebrovaskulyarniy patologii [Endothelial dysfunction with cerebrovascular pathologyї]. Kharkiv: Tarbut Laam, 2007. 136 p.
  12. Postnov YuV, Orlov SN. Pervichnaya hipertenziya kak patologiya membran [Primary hypertension as a pathology of cell membranes]. Moscow: Medicine Publ., 1987. 192 p.
  13. Terentyev VP, Belova EV, Zonys BYa. [Peculiarities of sympathetic adrenal system functioning in patients with arterial hypertension with various variants of remodeling of the left ventricle with its hypertrophy]. Rus. Cardiol. J. 2001;4:39–42.
  14. Stryuk RI, Dlusskaya IG. [Prognostic role of adrenergic reception of cell membranes in the development of left ventricular hypertrophy in patients with essential hypertension]. Cardiologiya. 2001;41(4):44–48.
  15. Sidorov DYu. [Condition of adrenergic receptors of platelets in patients with essential hypertension according to the method of EHF-dielectrometry]. Ukrainsky terapevtychny zhurnal. 2001;4:51–56.
  16. Kuryata AV, Soya EV. [Level of activity of beta-adrenoreceptors, the state of endothelial function and erythrocyte membranes in patients of older age groups with heart failure and their change under the influence of treatment]. Ukrainian Cardiological Journal. 2004;60–65.
  17. Skoromets АА, Skoromets AP, Skoromets TA. Nervnye bolezni: uchebnoye posobie [Nervous diseases: educational guidance]. 4 th ed. Мoscow: MEDpress-inform Publ., 2010. 560 p.
  18. Beta-ARM AGAT. Retrieved from: http://www.agat.ru/documents/instructions/4994/
  19. Krasov PS, ArkhypovaKA. Instrument for measuring the complex permittivity of biological objects. Telecommunications and Radio Engineering. 2009;68(8):727–733.
  20. Arkhypova KA, Krasov PS, Fisun AI, Nosatov AV, Lychko VS, Malakhov VO. Microwave Dielectrometry as a Tool for the Characterization of Blood Cell Membrane Activity for In Vitro Diagnostics. International Journal of Microwave and Wireless Technologies. 2017;9(8):1569–1574.
  21. Arkhypova K, Krasov P, Fisun A, Millimeter-Wave Blood Cell Analysis: Another Outlook for Cellular Diagnostics. IEEE MTT-S IMBioC'17: Proceedings of the IEEE MTT-S International Microwave BioConference, Gothenburg, Sweden: IEEE Digest, 2017, pp. 97–100.
  22. Fellows I. Deducer: A Data Analysis GUI for R. Journal of Statistical Software. 2012;49(8):1–15. Retrieved from: http://www.jstatsoft.org/v49/i08/.
  23. Penionzhkevich DYu. [A new method of restorative treatment of patients with cerebral metabolic disorders by electrophoresis with mexidol]. Bulletin of Experimental Biology and Medicine. 2006; Retrieved from: http://medi.ru/doc/a070162.htm.