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Issue. Articles

¹3(50) // 2016




1. Original researches


Diagnostic accuracy of home blood pressure measurement versus ambulatory monitoring for the assessment of antihypertensive therapy effectiveness in real clinical practice

K.M. Amosova, Yu.V. Rudenko

O.O. Bogomolets National Medical University, Kyiv

Objective — to assess the diagnostic accuracy of home and office blood pressure measurement (BP) for the evaluation of algorithmic antihypertensive therapy effectiveness in comparison with the ambulatory monitoring data, as the reference method, in patients with arterial hypertension (AH) after 6 months treatment in real clinical practice.
Materials and methods. The analysis included data of 103 patients with uncontrolled uncomplicated essential AH (age (56.1 ± 10.0) years), treatment algorithm of whom provided the initial administration of fixed combination of perindopril and amlodipine, followed by (if necessary) indapamide­retard, spironolactone, moxonidine or doxazosin to achieve target office BP. The duration of follow up was 6 months. Home BP was determined within 7 days, ambulatory monitoring was performed during the day within 2 weeks before the visit to the doctor. Office and home BP were measured by certified oscillometric automatic device. The target level of the office BP was determined as 140/90 mm Hg, recommended level of home BP — 135/85 mm Hg, 24-­hours BP — 130/80 mm Hg, daily BP — 135/85 mm Hg, night BP — 120/70 mm Hg. Sensitivity, specificity, positive and negative predictive value and the frequency of correctly classified cases for the office and home BP to control the results of treatment were determined in comparison with the ambulatory as the reference method. Agreement of the results of office and home BP measurements with ambulatory monitoring data was determined by the kappa Cohen coefficient (k) for categorical variables and the method of Bland—Altman for quantitative.
Results and discussion. After 6 months of treatment, the proportion of patients, who attained therapeutic goals for office BP was 65.7 %, for home — 41.3 %, for 24­hours BP monitoring — 31.5 %, for BP monitoring during the day —
42.4 %, for BP monitoring the night — 21.7 %. Sensitivity, specificity, positive and negative predictive value,
and k Cohen of home BP to determine the frequency of achieving recommended BP compared with the 24­-hours BP monitoring were 72.4 %, 73 %, 55.3 %, 85.2 %, 72.8 % and 0.42 (95 % CI 0.21—0.63) with daily BP monitoring — 73.2 %, 84.3 %, 78.9 %, 79.6 %, 79.3 % and 0.56 (95 % CI 0.36—0.76) respectively. The absolute value of the office and home BP is not fully agree with the data of the 24­-hours and the daily BP monitoring of the results of the analysis of the Bland—Altman. Controlled, masked uncontrolled, uncontrolled hypertension and the effect of «white coat» was determined according to home BP measurement in 38 %, 27.2 %, 31.5 % and 3.3 %, according to the 24­-hours BP monitoring — in 27.2 %, 38 %, 30.4 % and 4.3 %, according to daily BP monitoring — 37 %, 28.3 % and 29.3 % to 5.4 %. Agreement of the results of home BP measurements for diagnosing of controlled, masked uncontrolled, uncontrolled hypertension and the «white coat» effect in comparison with the 24­-hours BP monitoring (k) Cohen was 0.43 (0.18—0.62). 0.43 (0.21— 0.65). 0.97 (0.91—1.03) and 0.79 (0.40—1.18). with daily BP monitoring — 0.61 (0.42—0.80) 0.57 (0.21—0.65) 0.93 (0.84—1.02) 0.65 (0.21—1.09) respectively.
Conclusions. The results of home BP measurements for achieving recommended BP are agree with 24­-hours BP monitoring results in 72.8 % and daily BP monitoring — in 79.3 % of cases, have a moderate agreement with them with a sensitivity of 72.4 %, specificity 73 %, positive and negative predictive value of 55.3 % and 85.2 %, and with the monitoring during the day — 73.2 %, 84.3 %, 78.9 % and 79.6 % respectively. The results of home BP measurements for diagnostic of controlled, masked uncontrolled, uncontrolled hypertension and the «white coat» effect in hypertensive patients after 6 months of algorithmic antihypertensive therapy are agree with 24-­hours BP monitoring results in
73.9 %. 73.9 %. 95.7 % and 97.8 % in the daily monitoring results — in 82.6 %. 82.6 %. 95.7 % and 96.7 %, respectively, have high agreement with them in determining of uncontrolled hypertension and moderate agreement in determining of masked uncontrolled and controlled hypertension, as well as the effect of «white coat».

Keywords: arterial hypertension, blood pressure measurement, home blood pressure, ambulatory blood pressure monitoring, masked uncontrolled hypertension.

List of references:
1.    Amosova EN, Rudenko YV, Rokita OI, Katzitadze IYu. Efektyvnist' unifikovanoho pokrokovoho alhorytmu likuvannya dlya zabez­pechennya kontrolyu arterial'noho tysku u khvorykh z arterial'noyu hipertenziyeyu v ambulatorniy praktytsi: rezul'taty doslidzhennya PERFEKT [Effectiveness of a unified step treatment algorithm to control blood pressure in patients with hypertension in ambulatory practice: PERFECT findings]. Sertse i sudyny [Heart and vessels]. 2014;1:34-46. (Ukr).
2.    Bland JM, Altman DG. Statistical method for assessing agree­ment between two methods of clinical measurement. Lancet. 1986:307-310.
3.    Cohen J. A coefficient of agreement for nominal scales. Educ. Psychol. Meas. 1960;20:37-46.
4.    Hänninen M-RA, Niiranen TJ, Puukka PJ, Jula AM. Com­parison of home and ambulatory blood pressure measurement in the diagnosis of masked hypertension. J Hypertens. 2010;28:709-714.
5.    Hara A, Tanaka K, Ohkubo T et al. Ambulatory Versus Home Versus Clinic Blood Pressure The Association With Subclinical Cerebrovascular Diseases: The Ohasama Study. Hypertens. 2012;59:22-28.
6.    Hodgkinson J, Mant J, Martin U et al. Relative effectiveness of clinic and home blood pressure monitoring compared with ambulatory blood pressure monitoring in diagnosis of hyper­tension: systematic review. BMJ. 2011;342:3621-3638.
7.    Imai Y, Hosaka M, Elnagar N, Satoh M. Ambulatory & Home Blood Pressure Measurement in the Management of Hyper­tension. Clinical significance of home blood pressure measu­rements for the prevention and management of high blood pressure. Clin Exp Pharmacol Physiol. 2014;41:37-45.
8.    Kang Y-Y, Li Y, Huang Q-F et al. Accuracy of home versus ambulatory blood pressure monitoring in the diagnosis of white-coat and masked hypertension. J Hypertens. 2015;33:1580-1587.
9.    Mancia G, Fagard R, Narkiewicz K et al. 2013 ESH/ESC Guidelines for themanagement of arterial hypertension TheTask Force for the management ofarterial hypertension of the Euro­pean Society of Hypertension and of the European Society of Cardiology. J Hypertens. 2013;31:1281-1357.
10.    Mancia G, Verdecchia P. Clinical Value of Ambulatory Blood Pressure Evidence and Limits. Circ Res. 2015;116:1034-1045.
11.    McHugh ML. Interrater reliability: the kappa statistic. Biochemia Medica. 2012;22:276-282.
12.    Nasothimiou EG, Tzamouranis D, Rarra V et al. Diagnostic ac­­curacy of home vs. ambulatory blood pressure monitoring in un­treated and treated hypertension. Hypertens Res. 2012;35:750-755.
13.    Niiranen TJ, Hanninen MR, Johansson J et al. Home-measu­red blood pressure is a stronger predictor of cardiovascular risk than office blood pressure: the Finn-Home study. Hypertens. 2010;55:1346-1351.
14.    Nunana D, Thompson M, Heneghan CJ et al. Accuracy of self-monitored blood pressure for diagnosing hypertension in primary care. J Hypertens. 2015;33:755-762.
15.    Paratia G, Stergiou GS, Asmar R et al. European Society of Hypertension guidelines for blood pressure monitoring at home: a summary report of the Second International Consensus Conference on Home Blood Pressure Monitoring. J Hyper­tens. 2008;26:1505-1530.
16.    Pickering TG, Miller NH, Ogedegbe G et al. Call to action on use and reimbursement for home blood pressure monitoring: Executive summary: A joint scientific statement from the American Heart Association, American Society Of Hypertension, and Preventive Cardiovascular Nurses Association. Hypertens. 2008;52:1-9.
17.    Powers BJ, Olsen MK, Smith VA et al. Measuring blood pressure for decision making and quality reporting: where and how many measures?. Ann. Intern. Med. 2011;154:781-788.
18.    Reino-González S, Pita S-Fernández,  Cibiriain-Sola M et al. Validity of clinic blood pressure compared to ambulatory moni­toring in hypertensive patients in a primary care setting. Blood Pressure. 2015;24:111-118.
19.    Stergiou GS, Bliziotis IA. Home blood pressure monitoring in the diagnosis and treatment of hypertension: a systematic review. Am J Hypertens. 2011;24:123-134.
20.    Stergiou GS, Kollias A, Zeniodi M et al. Home blood pressure monitoring: primary role in hypertension management. Curr Hypertens Rep. 2014;16:462-468.
21.    Stergiou GS, Asayama K, Thijs L et al. Prognosis of White-Coat and Masked Hypertension International Database of Home Blood Pressure in Relation to Cardiovascular Outcome. Hypertens. 2014;63:675-682.
22.    Zhang L, Li Y, Wei F-F et al. Strategies for Classifying Patients Based on Office, Home, and Ambulatory Blood Pressure Measurement. Hypertens. 2015;65:1258-1265.

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Original language: Ukrainian

2. Original researches


Disorders of oxidative metabolism and activity of enzymatic antioxidants in patients with non-alcoholic steatohepatitis combined with obesity and biliary tract pathology

A.Yu. Filippova

SE «Dnipropetrovsk Medical Academy of Health Ministry of Ukraine»

Objective — to investigate the state of lipid peroxidation (LPO) based on the levels of intermediate and final LPO products, and to assess the diagnostic characteristics and activity of enzymatic antioxidants in the blood serum of patients with  non-alcoholic steatohepatitis (NASH) combined with obesity and biliary tract (BT) pathology depending on the body mass index (BMI) parameters.
Materials and methods. The study involved 100 patients with NASH in combination with obesity (OB) and BT pathology, who at the time of sonographic and morphological study of liver biopsy revealed signs of hepatic steatosis. The group consisted of 40 men and 60 women with the mean age (53.67 ± 1.11) years. The control group consisted of
20 healthy persons (HP). BMI was defined with Ketle formula Depending on the degree of increase in body mass index (BMI), all patients with NASH were divided into three groups: Group 1 included subjects with BMI of 25—29.9 kg/m2 (overweight); Group 2 consisted of patients with a BMI 30—34.9 kg/m2 (OB I degree); Group 3  with a BMI 35— 39.9 kg/m2 (OB II degree). The LPO state was assessed based on the malondialdehyde (MDA) levels in blood plasma and red blood cells (RBC), and levels of the LPO intermediate products in two phases of lipid extracts — isolated double bounds (IDB), diene conjugates (DC), oxydiene conjugates (ODC), and final LPO products — Schiff bases (SO). The antioxidative defense (AOD) factors were evaluated by the activity of ceruleoplasminà (CP), superoxide dismutase (SOD) and catalase in the RBC hemolysate.
Results and discussion. All LPO indices were activated in two phases of lipid extracts (from p < 0.05 to p < 0.001 in comparison with healthy controls) and depended on the BMI increase (from p < 0.05 to p < 0.001). Analysis of AOD indices in NASH patients showed activation of all parameters of the system in the investigated groups. Thus, there was defined the significantly marked intensification of LPO processes in the two phases of the lipid extract against the background of changes in the activity of enzymes of AOD—SOD system, catalase, and compensated CP changes, that directly correlated with presence of obesity.
Conclusions. In patients with NASH combined with obesity and BT pathology, the comorbid course of disease was associated with the considerable disorders of the oxidant-antioxidant balance based on the levels of LPO indices, related to the increase of BMI parameters.

Keywords: non­alcoholic steatohepatitis, obesity, body mass index, lipid peroxidation, antioxidative defense.

List of references:
1.    Kamyishnikov VS. Clinical and laboratory diagnosis of liver diseases] Moscow: MEDpress-inform 2-e izd; 2014:92 (Rus).
2.    Leschine OA, Skvortsov VV. Clinical-diagnostic value of serum ceruloplasmin in patients with chronic hepatitis B and C. Poliklinika. Special Laboratory LPU.2012:29-30 (Rus).
3.    Order of HM from Ukraine 13.06.2005 N 271. On approval of the protocols of medical care to patients with a degree in Gastroenterology (Ukr).
4.    Order of HM from Ukraine 06.08.2014 N 826. Unified clinical protocols of primary, secondary (specialized) medical care "Nonalcoholic steatohepatitis" (Ukr).
5.    Lelukhina OV, Domashneva NA, Averyanova LP. Comparative characteristics of penetration of erythrocyte membranes, status of lipid peroxidation and antioxidant protection in patients with hepatic steatosis combined with diseases of the biliary tract. Gastroenterology. Dnepropetrovsk. 2007;39:73-80 (Ukr).
6.    Volchegorskiy IA, Nalimov FG, Yavoryanskiy BG. Comparison of various approaches to the definition of peroxidation products in heptane-isopropanol extracts of blood. Questions of medical chemistry.1989:127-130 (Rus).
7.    Filippova AYu. Condition of lipid peroxidation and antioxidant system in patients with non-alcoholic fatty liver disease Vrachebnoe delo. 2013;7:36-43 (Ukr).
8.    Novakovic T, Mekic M, Smilic L. Anthropometric and biochemical characteristics of patients with nonalcoholic fatty liver diagnosed by non-invasive diagnostic methods. Med Arch. 2014;68(1):22-26.
9.    Hernaez R, Lazo M, Bonekamp S. Diagnostic accuracy and reliability of ultrasonography for the detection of fatty liver: a meta-analysis. Hepatology. 2011;54(3):1082-90.
10.    Dietrich P, Hellerbrand C. Non-alcoholic fatty liver disease, obesity and the metabolic syndrome. Best Pract Res Clin Gastroenterol. 2014;28(4):637-653.
11.    Toouli J, Fried M, Ghafoor KA. Obesity World Gastroenterology Organisation Global Guideline. 2009:1-30. Available from: http://www.worldgastroenterology.org/assets/downloads/en/pdf/guidelines/22_obesity.pdf
12.    Filippova A. Non-alcoholic and alcoholic fatty liver disease in patients suffering from biliary tract pathology and obesity: clinical and functional aspects. Modern Science Moderni Vĕda. 2015;4:134-149.

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Original language: Ukrainian

3. Original researches


Peculiarities of the macroscopic state of the upper digestive tract in patients with chronic gastritis combined with osteoarthrosis

M. Yu. Zak, L.M. Pasiyeshvili

Kharkiv National Medical University

Objective — to determine the macroscopic state of the upper digestive tract in patients with chronic gastritis (ChG) who received selective non­steroidal anti­inflammatory drugs (NSAIDs) for osteoarthrosis (OA).
Materials and methods. The investigation involved 507 patients (310 women and 197 men), mean age (52.5 ± 4.32) years, who were divided into 2 clinical groups: I group consisted of 357 patients with OA in combination with ChG, and group II — 150 patients with ChG without comorbidity. Among the surveyed subjects, the non­atrophic gastritis (NAG) was present in 117 patients and 51 patients in the I and the II groups, respectively, and atrophic gastritis (AG) in 240 and 99 patients in I and II groups, respectively. To treat OA, all patients of I group received selective NSAIDs meloxicam in a dose of 15 mg/day or nimesulide in a dose of 200 mg/day. The NSAIDs therapy duration ranged from 1 week to several years. All patients were undergone the esophagogastroduodenoscopy based on the signs of abdominal pain, dyspepsia and cancer screening.
Results and discussion. Administration of selective NSAIDs in standard regimen to treat OA in patients with ChG caused a number of functional and structural changes in the upper digestive tract, the character and severity of which depended on the morphological type of gastritis. Erosive esophagitis of grade A and B in patients with NAG in combination with OA were fixed in 1,6 times more often (p < 0.05) and in patients with hypertension in combination with OA — 1.5 times (p < 0.05) more frequently than in NAG and hypertension without comorbidities, respectively. It is established that in group I erosion in the cardial part of stomach was observed only in AG, but in the body of the stomach in hypertension was recorded in 2.0 times more frequently (c2 = 2.12, p = 0.002) than in NAG in combination with OA. Patients with OA development of individual erosions are not dependent on the morphological type of gastritis, however, multiple erosions 1.9 times (c2 = 2.01, p = 0.001) was more common in hypertension than in NAG. The NSAIDs caused the development of a number of functional disorders: when a NAG in combination with OA gastro­esophageal reflux occurred in 1.5 times c2 = 4.11, p = 0.021) most of the time, and duodenogastric reflux in 2.1 times more frequently (c2 = 2.02, p = 0.011) than in NAG without comorbidities.
Conclusions. Administration of selective NSAIDs in standard regimen to treat OA in patients with AG caused more severe structural and functional disorders in the upper digestive tract, than in patients with NAG. The development of individual erosions did not depend from the morphological ChG form, however, multiple erosions were observed in
2 times oftener at AG than in NAG (c2 = 2.01, p = 0.001). At ChG in combination with OA, the gastro­esophageal reflux was observed in 1.9 times more often (c2 = 15.67, ð = 0.017), and duodenogastric reflux in 1.7 times more frequently (c2 = 18.1, ð = 0.011), than in ChG without comorbidity.

Keywords: chronic gastritis, osteoarthrosis, NSAIDs therapy, macroscopic changes.

List of references:
1.    Mos³ychuk LM, Zak MY. Hvorobi stravohodu ta shlunku: practichniy pos³bnik (Ukr). Dnipropetrovs'k; 2012: 59.
2.    Kovalenko VM, Bortkiewicz OP. Osteoartroz: practichna nastanova, 3 vid., dop. ³z zmin. (Ukr). Kyiv: Mor³on; 2010:607.
3.    Kuryata AV, Grechanik MM. Problema lecheniya sustavnoy boli: focus na bezopasnost’ (Rus). Zdorov’e Ukrainy [Health of Ukraine] (Ukr). 2014:6:43-44.  
4.    Karateev AE, Yahno NN, Lazebnyk LB. Primenemie nesteroidnyh protyvovospalitel’nyh preparatov: klinicheskie rekomendacii (Rus). Moskva: Ima press; 2009:167.
5.    Chernehovskaya NE, Cherepyantsev DP,  Povalyaev AV. Endoscopicheskaya diagnostica zabolevaniy pischevoda, geludka i tonkoy kischki small intestine (Rus). Moskva: MEDpress-inform; 2010:208.
6.    Dixon MF, Genta RM, Yardley JH. Classification and grading of gastritis. The updated Sydney system. International Workshop on the histopathology of gastritis, Houston (Eng). Am J Surg Pathol. 1996;20:1161-1181.
7.    Lanza FL, Chan F, Quigley E. Guidelines for prevention of NSAID-related ulcer complications (England). Am J Gastroenterol. 2009;104:728-738.
8.    Rugge M, de Boni G, Pennelli M. Gastritis OLGA - staging & gastric cancer risk: a twelve year clinico-pathological follow-up study (Eng). Minerva Gastroenterol Dietol. 2010;56:1:13-17.

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4. Original researches


The peculiarities of metabolic profile of Helicobacter pylori infected patients with the combined course of coronary heart disease and type 2 diabetes mellitus

O.V. Kolesnikova, T.Ye. Kozyreva

SI «National Institute of Therapy named after L.T. Mala of NAMS of Ukraine», Kharkiv

Objective — to study the effects of Helicobacter pylori (HÐ) infection on the peculiarities of the  metabolic profile of patients with the combined course of coronary heart disease (CHD) and type 2 diabetes mellitus (DM 2).
Materials and methods. The study involved 60 subjects (29 men and 31 women) with the verified diagnosis of CHD combined with DM2 and with or without  signs of ÍÐ infection, the mean age in the group was (56.6 ± 6.2) years. The patients were divided into two groups: the I group consisted of HP serum-positive patients, who had CHD in combi­nation with 2DM (n = 28), the II group included HP serum-negative patients with the signs of CHD in combination with 2DM (n = 32). The exclusion criteria were: the presence of acute inflammatory processes, oncology diseases, heart failure III. The ELISA measurements of titers of IgG antibodies to ÍÐ were performed to all patients. The levels of total cholesterol (TCh), HDL cholesterol, and triglycerides (TG) were measured to assess the lipid metabolism. To evaluate degree of the carbohydrate metabolism compensation, levels of glycosylated hemoglobin (HbA1ñ) were defined. The levels of C-reactive protein (C-RP) and adiponectin were assessed.
Results and discussion. The obtained results showed that formation of the metabolic changes in HP serum-positive patients, who had CHD in combination with 2DM, took place in the conditions of dyslipidemia, disglycemia and hyperinsulinemia in comparison with HP serum-negative patients. The significant decrease of the adipocytic hormone with the increased C-RP as a marker of the immune inflammation were revealed in patients of I group vs subjects of the II group (ð = 0.001). It can be assumed, that ÍÐ infection stipulates the formation of hormone-metabolic changes in a form of hypo-adiponectinemia, which in turn creates conditions for the aggravation of compensation of the carbohydrate and lipid profiles.
Conclusions. HP serum-positive patients with CHD in combination with 2DM have showed pro-atherogenic lipid profile and more evident changes in the parameters of fasting glucose against the background of hyperinsulinemia  when compared to HP serum-negative patients. The hypo-adiponectinemia and increased C-RP levels can be considered as the factors of cardio-metabolic risks in HP serum-positive patients with CHD in combination with 2DM.

Keywords: infection of Helicobacter pylori, coronary heart disease, lipid metabolism, carbohydrate metabolism, diabetes mellitus type 2.

List of references:
1.    Figura N, Franceschi F, Santucci A et al. Extragastric mani­festations of Helicobacter pylori infection. Helicobacter. 2010;15(1):60-68.
2.    Halvatsiotis I, Tsiotra PC, Ikonomidis I et al. Genetic variation in the adiponectin receptor 2 (ADIPOR2) gene is associated with coronary artery disease and increased ADIPOR2 expression in peripheral monocytes. Cardiovasc Diabetology. 2010;9:10-21.
3.    He C, Yang Z, Lu N. Helicobacter pylori infection and diabetes: is it a myth or fact?. World J. Gastroenterol. 2014;20(16):4607-4617.
4.    Jackson L, Britton J, Lewis SA et al. A population-based epidemiologic study of Helicobacter pylori infection and its association with systemic inflammation. Helicobacter. 2009;14:108-113.
5.    Jafarzadeh A, Rezayati MT, Nemati M. Helicobacter pylori seropositivity in patients with type 2 diabetes mellitus in South-East of Iran. Acta Med Iran. 2013;51:892-896.
6.    Polyzos SA, Kountouras J, Papatheodorou A et al. Helicobac­ter pylori infection in patients with nonalcoholic fatty liver disease. Metabolism. 2013;62:121-126.
7.    Vafaeimanesh J, Hejazi SF, Damanpak V et al. Association of Helicobacter pylori infection with coronary artery disease: Is Helicobacter pylori a risk factor? Sci. World J. 2014. http://doi.org/10.1155/2014/516354.
8.    Vizzardi E, Bonadei I, Piovanelli B et al. Helicobacter pylori and ischemic heart disease. Panminerva Medica. 2011;53(3):193-202.

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5. Original researches


The value of lipid metabolism parameters in predicting the atherosclerotic lesions of the coronary vessels

L.V. Zhuravlyova, N.A. Lopina

Kharkiv National Medical University

Objective — to assess levels and the role of lipid metabolic parameters in predicting the atherosclerotic lesions of the coronary vessels.
Materials and methods. There were examined 131 patients with coronary artery disease (CAD). Depending on the presence of type 2 diabetes mellitus (T2DM) patients with coronary artery disease (CAD) were divided into 2 groups: the first group (n = 70) patients with concomitant diabetes type 2, the second group (n = 61) — patients with CAD without concomitant T2DM. To verify the CAD diagnosis, angiography was performed to all patients. The evaluation of lipid exchange was performed based on the levels of total cholesterol (ÒÑ), HDL cholesterol (HDL-C), low (LDL) and very low density (VLDL), triglycerides (TG), atherogenic factor.
Results and discussion. The results of the study showed that patients with CAD as the 1st and 2nd groups compared with the control group individuals had significantly higher values of ÒÑ, TG, VLDL, the coefficient of atherogenesis, as well as significantly reduced levels HDL cholesterol. In addition, patients of the 1st group recorded significantly higher mean values of TG levels in comparison with the 2nd group, while in the 2nd group of TG levels were not significantly different from the control group. Among patients of the 1st group of the number of patients with a combination of dyslipidemia was significantly higher than in the 2nd group. The majority of patients receiving lipid-lowering therapy in the history did not reach the target levels LDL cholesterol for people with documented coronary angiography vessels belonging to the high cardiovascular risk. The analysis of correlations between the severity of coronary lesions and lipid metabolism in patients with CAD showed the presence of correlation between the level of TC, VLDL, triglycerides, LDL and the severity of the atherosclerotic lesions of the coronary vessels. In relation to predict the presence of atherosclerotic lesions of the coronary arteries, the presence of hemodynamically significant stenosis of the coronary vessels has the greatest value estimate VLDL, HDL-C, in relation to predict the presence of diffuse coronary artery lesions were statistically significant differences were found between the indices of lipid metabolism.
Conclusions. The study results demonstrated non-lipid mechanisms of the development and the progression of atherosclerosis in patients with type 2 diabetes mellitus, and without it, requiring further study for the development of effective strategies for primary and secondary prevention cardiovascular events.

Keywords: coronary atherosclerosis, coronary artery disease, type 2 diabetes mellitus, lipid metabolism.

List of references:
1.    Biduchak AS, Shkrobanets ID, Leonets SI. Epidemiolohichni osoblyvosti khvorob systemy krovoobihu v Ukraini i Chernivetskii oblasti. Epidemiological features of cardiovascular diseases in Ukraine in Chernivetskii region. Bukovynskyi medychnyi visnyk (Ukr). 2013;17(3):100-103.
2.    Dislipidemiyi: diagnostika, profilaktika ta likuvannya: Metodichni rekomendatsiyi Asotsiatsiyi kardiologiv Ukrayini / Pod red. OI Mitchenko, MI Lutay. K. (Ukr). 2011:25.
3.    Moskalenko VF, Hulchii OP, Holubchykov MV et al. / Pod red. VF Moskalenko. Biostatystyka. [Biostatistics]. Ê.: Knyha plius (Ukr); 2009:184.
4.    Recommendations for management of diabetes, prediabetes and cardiovascular diseases. Rossyiskyi kardyolohycheskyi zhur­nal (Rus). 2014;107 (3):6-70.
5.    Stabilna ishemichna khvoroba sertsia: adaptovana klinichna nastanova, zasnovana na dokazakh. [Stable ischemic heart disease: adapted, evidence based, clinical guidelines] (Ukr). Kyiv: 2016:177.
6.    Unifikovanyi klinichnyi protokol pervynnoi ta vtorynnoi (spet­sializovanoi) medychnoi dopomohy: Stabilna ishemichna khvo­roba sertsia. [Unified clinical protocols of primary and secondary (specialized) care: Stable ischemic heart disease]. Nakaz MOZ Ukrainy vid 02.03.2016 N 152. [Order of MOH Ukraine from 02.03.2016 N 152.] (Ukr):61.
7.    Unifikovanyi klinichnyi protokol pervynnoi ta vtorynnoi (spetsializovanoi) medychnoi dopomohy: tsukrovyi diabet 2 typu. [Unified clinical protocols of primary and secondary (specialized) care: type 2 diabetes]. Nakaz MOZ Ukrainy vid 21.12.2012 N1118. [Order of MOH Ukraine from 21.12.2012 N1118. (Ukr):115.
8.    Huang Y, Cai X, Chen P, Mai W. Associations of prediabetes with all-cause and cardiovascular mortality: A meta-analysis. Annals of Medicine (Eng). 2014;46:684-692.
9.    Naito R, Kasai T. Coronary artery disease in type 2 diabetes mellitus: Recent treatment strategies and future perspectives. World J Cardiol (Eng). 2015;7 (3):119-124.
10.    American Diabetes Association. Standards of medical care in diabetes - 2016. Diabetes Care (Eng). 2016;39 (1):1-109.

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6. Original researches


The relation of polymorphism Gln27Glu gene of b2-adrenal-receptors and heart failure

S.M. Pyvovar

SI «National Institute of Therapy named after L.T. Mala of NAMS of Ukraine», Kharkiv

Objective — to determine the prevalence and relation of polymorphism Gln27Glu gene of b2-adrenal-receptors with the course of h eart failure.
Materials and methods. The study involved 200 patients with heart failure. In whom the clinical course of the disease was assessed. Molecular and genetic study of polymorphism Gln27Glu gene of b2-adrenal-receptors was performed in the laboratory of biochemical and imunoassay research methods of clinical morphology. The peripheral blood leukocytes of patients was sampled for molecular genetic studies. Extraction of the genomic DNA from white blood cells for molecular genetic studies was carried out using a commercial kit «DNA Sorbo-In» («Amplias Sense», Russia) according to the instruction set. For primers sequences were used for polymerase chain reaction.
Results and discussion. It has been established that among 200 patients with heart failure, 33 % were homozygous for the mutated allele Gln27Gln.  From them, 13 % patients had two wild allele (Glu27Glu), and 54 % were heterosigotes. Ur was revealed that 88.4 % of patients with «mutation» allele had a sinus rhythm;  51.1 % carriers of «wild» alleles had atrial fibrillation. At the same time, the analyses of the incidence of ventricular ectopic activity identified the opposite patterns. Thus, the lowest incidence of extrasystole was established in patients with heart failure who were homozygous «wild» C allele, compared with heterozygous and homozygous carriers of that «muti-lated» alleles.
Conclusions. The results of the study showed prevalence of polymorphic variations Gln27Glu gene of b2-adrenal-receptors among patients with heart failure. Among them, 33 % were homozygous for the mutated allele Gln27Gln; 13 % patients had two wild allele (Glu27Glu), 54 % were heterosigotes; 88.4 % of the patients with «mutation» allele had a sinus rhythm, and 51.1 % carriers of «wild» alleles had atrial fibrillation. The lowest incidence of extrasystole jas been revealed in patients with heart failure who are homozygous «wild» C allele, compared with heterozygous and homozygous carriers of that «muti-lated» alleles.

Keywords: heart failure, clinical course, gene polymorphism, b2-adrenal-receptors.

List of references:
1.    Voronkov LG, ²l’nits’ka MR, Babich PM. Prognoz pats³ºnt³v ³z khron³chnoyu sertsevoyu nedostatn³styu ta sistol³chnoyu disfunkts³ºyu l³vogo shlunochka zalezhno v³d danikh ne³nvazivnikh metod³v obstezhennya. Ukra¿ns’kii terapevtichnii zhurnal. 2015;1:24-31 (Ukr).
2.    Moibenko A.A. Problema preduprezhdeniya razvitiya i progressirovaniya serdechnoi ne-dostatochnosti. Sert­se­va nedostatn³st’. 2011;1:8-9. (Rus).
3.    Rudyk YuS, Pivovar SN. Vliyanie polimorfizma β2-adre­noretseptorov na patologiyu serdechno-sosu­distoi sis­temy. Ukrainskii terapevticheskii zhurnal. 2011;4:55-58. (Russ)
4.    Bruck H, Leineweber K, Buscher R. The Gln27Glu β2 adrenoceptor polymorphism slows the onset of desensitization of cardiac functional responses in vivo. Pharmacogenetics. 2003;13: 59-66.
5.    Cinzia Forleo, Nicoletta Resta, Sandro Sorrentino, Pietro Guida, Andrea Manghisi, Viviana De Luca et al. Asso­ciation of β-adrenergic receptor polymorphisms and progression of heart failure in patients with idiopathic dilated cardiomyopathy. Am J Med. 2004;117:451-458. Doi: 10.1016/j.amjmed. 2004.04.012
6.    Covolo L, Gelatti U, Metra M, Nodari S, Picciche A, Pezzali N et al. Role of beta1- and beta2-adrenoceptor polymorphisms in heart failure: a case-control study. Eur. Heart. J. 2004;25 (17):1534-41. Doi: 10.1016/j.ehj.2004.06.015
7.    David M Kaye, Belinda Smirk, Carolyn Williams, Garry Jennings, Murray Esler, Dianne Holst. β-Adrenoceptor genotype influences the response to carvedilol in patients with congestive heart failure. Pharmacogenetics. 2003;13: 379-382. Doi: 10.1097/00008571-200307000-00002
8.    Heckbert SR. β2-Adrenergic receptor polymorphism and risk of incident cardiovascular events in the elderly. Circulation. 2003;107 (15):2021-2024. Doi: 10.1161/ 01.cir. 0000065231. 07729.92
9.    John JV McMurray, Stamatis Adamopoulos, Stefan D Anker et al. ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure 2012. The Task Force for the Diagnosis and Treatment of Acute and Chronic Heart Failure 2012 of the European Society of Cardiology. Developed in collaboration with the Heart Failure Association (HFA) of the ESC European Heart Journal. 2012;33:1787–1847. Doi: 10.1093/ eurheartj/ehs104
10.    Kanki H, Yang P, Xie HG, Kim RB, George AL Jr, Roden DM. Polymorphisms in beta-adrenergic reeceptor genes in the acquired long QT syndrome. J Cardiovasc Electrophysiol. 2002;13(3):252-256.
11.    Lanfear DE, Jones PG, Marsh S et al. Beta2-adrenergic receptor genotype and survival among patients receiving beta-blocker therapy after an acute coronary syndrome. Jama. 2005;294(12):1526–1533.
12.    Nguyen MN, Kiriazis H, Ruggiero D, Gao XM, Su Y, Jian A, Han LP et al. Spontaneous ventricular tachyar­rhythmias in β2-adrenoceptor transgenic mice in relation to cardiac interstitial fibrosis. Am J Physiol Heart Circ Physiol. 2015;309(5):H946-957. Doi: 10.1152/ajpheart.00405.2015. Epub 2015 Jun 26.
13.    Pascal de Groote, Nicolas Lamblin, Nicole Helbecque, Frédéric Mouquet, Eugène Mc Fadden, Xavier Hermant,  et al. The impact of beta-adrenoreceptor gene polymorphisms on survival in patients with congestive heart failure. Eur J Heart Fail. 2005;7:966-973. Doi: 10.1016/j.ejheart.2004.10.006
14.    Piotr Ponikowski, Adriaan A Voors, Stefan D Anker, He´ctor Bueno, John GF Cleland, Andrew JS Coats et al. ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure 2016. The Task Force for the diagnosis and treatment of acute and chronic heart failure of the European Society of Cardiology (ESC) Developed with the special contribution of the Heart Failure Association (HFA) of the ESC. European Heart Journal. 2016:123. Doi:10.1093/eurheartj/ehw128.
15.    Sotoodehnia N, Siscovick DS, Vatta M, Psaty BM, Tracy RP, Towbin JA et al. Beta2-adrenergic receptor genetic variants and risk of sudden cardiac death. Circulation. 2006;113(15):1842-1848. Doi.org/10.1161/circulationaha. 105.582833.
16.    Stuart A. Green, Jamal Turki, Michael Innis, Stephen B. Liggett. Amino-terminal polymorphisms of the human beta 2-adrenergic receptor impart distinct agonist promoted regulatory properties. Biochemistry. 1994;33: 9414-9419. Doi: 10.1021/bi00198a006.
17.    Ulucan C, Cetintas V, Tetik A, Eroglu Z, Kayikcioglu M, Can LH et al. Beta1 and beta2-adrenergic receptor polymorphisms and idiopathic ventricular arrhythmias. J Cardiovasc Electrophysiol. 2008;19(10):1053-1058. Doi: 10.1111/j.1540-8167.2008.01202.x. Epub 2008 May 9.
18.    Wagoner LE, Craft LL, Singh B, Suresh DP, Zengel PW,  McGuire N. et al. Polymorphisms of the β2-adrenergic receptor determine exercise capacity in patients with heart failure. Circ. Res. 2000;86: 834-840. Doi: 10.1161/01.res.86.8.834
19.    Zian H Tseng, Bradley E. Aouizerat, Ludmila Pawlikowska, Eric Vittinghoff, Feng Lin, Dean Whiteman et al. Common β Adrenergic Receptor Polymorphisms Are Not Associated with Risk of Sudden Cardiac Death in Patients with Coronary Artery Disease. Heart Rhythm. 2008;5(6):814–821. 10.1016/j.hrthm. 2008.03.016.

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7. Original researches


New pathogenetic approach in treating patients with a combination of gastroesophageal reflux disease and coronary heart disease

O.V. Izmailova

SI «National Institute of Therapy named after L.T. Mala of NAMS of Ukraine», Kharkiv

Îbjective — to study the effectiveness of various treatment regimens in patients with a combination of gastroesophageal reflux disease (GERD) and coronary artery disease, taking into account the impact of a number of co­morbid conditions and risk factors.
Materials and methods. The study involved 65 patients with a combination of GERD and coronary artery disease,
54 men and 11 women whose age ranged from 32 to 89 years (median — 63 years). Diagnostic algorithm consisted of a survey to identify the severity of GERD, insomnia, depression. The patients received a screening diagnosis of obstructive sleep apnea/hypopnea (SOAGS) and ultrasound of the blood flow in the abdominal aorta branches that feed the lower third of the esophagus. As a treatment different variations regimens were used, focused at correcting the anti­ischemic drug β-­blockers (B), the drug was administered melatonin for 4 weeks (M), conducted diet therapy (D) and the complex of therapeutic exercises (D). The patient was able to choose a convenient schema therapy. The total duration of follow­up was 24 weeks.
Results and discussion. After 24 weeks of treatment, there was a significant improvement in the ultrasonic velocity of blood flow characteristics in arteries that feed the «zone of interest» in GERD — the lower third of the esophagus. The most effective was the treatment regimen involving all components of the lifestyle interventions and treatment — B1M1D1G1. Exactly in this scheme there was also a decrease in the severity of clinical symptoms of GERD and SOAGS after 24 weeks of treatment. The effect of receiving the melatonin has been set for the parameters of blood flow in the abdominal aorta branches, indicators severity of insomnia and depression as a result of the survey.
Conclusions. Complex approach to the treatment of patients with GERD and coronary artery disease with the inclusion in the scheme of treatment of a β-­­blocker bisoprolol, 4­week course of treatment with melatonin, regular «cardio» load, a complex of exercises for the neck muscles, tongue, jaw and dietetics (B1M1D1G1 scheme) can be recommended as the best treatment with positive impact on a number of pathogenetic links of comorbid diseases.

Keywords: gastroesophageal reflux disease, coronary heart disease, sleep apnea, insomnia, melatonin treatment.

List of references:

1.    Algoritm ranniogo viyavlennya gastroezofagealnoy refluksnoy hvorobi [The algorithm for early detection of gastroesophageal reflux disease] (Ukr) Certificate number 26148 / Fadeenko GD, Kushnir IE, Chernova VM etc. Àpplication number 26255; stated 03.07.2008, registered 17.10.2008 (Ukr).
2.    Buzunov RV, Legeyda IV. Snoring and obstructive sleep apnea syndrome. A manual for physicians (Rus). Ì., 2012. http://www.sleep-apnea-guide.com.
3.    Gastroezofagealna refluksna hvoroba 2013 (Unifikovaniy klinichniy protocol pervinnoi vtorinnoi (specializovavanoi) medichnoi dopomogi [Gastroesophageal reflux disease 2013 (unified clinical protocols of primary, secondary (specialized) medical care)] (Ukr). News of Medicine and Pharmacy (gastroenterology) (Rus). 2014;489:49-60.
4.    Ivleva AY. The differences of the pharmacological properties of the beta-blockers and their clinical significance (Rus). Ñonsilium Medicum; 5(11). http://medi.ru/doc/091015.htm.
5.    Koshel VI, Pasechnikov VD, Kucheraviy VS. Differential diagnosis and treatment of obstructive sleep apnea during sleep, associated with gactrooesophageal reflux disease. Modern problems of science and education (Rus). 2012;6. http://science-education.ru.
6.    Krakhmalova EO, Fadeenko GD, Izmailova EV. Communication of endoscopic manifestations of gastroesophageal reflux disease with melatonin levels and the severity of obstructive sleep apnea (Rus). Ukrainskiy pulmonologichniy jurnal [Ukrainian pulmonology journal] (Ukr). 2016;2:19-24.
7.    Maiev IV, Samsonov AA, Godilo-Godlewski VA et al. Drug interaction of proton pump inhibitors and clopidogrel at their joint admission. (Rus). Clin medicine (Rus). 2013;5:15-21.
8.    Osadchuk MA, Kalinin AV, Lipatova TE. et al. The role of the diffuse neuroendocrine system in the pathogenesis and outcome of gastroesophageal reflux disease. Rus J Gastroenterol, Hepatol, Coloproctol (Rus). 2007;17(3):35-40.
9.    Pikulev DV, Alekseeva OP, Dolbin IV. Coronary heart disease and gastroesophageal reflux disease: characteristics of combined flow (review). Medical almanac (Rus). 2012;1:43-47.
10.    Starostin BD. Melatonin in the treatment of patients with gastroesophageal reflux disease. Gastroenterology of St. Petersburg (Rus). 2011;2-3:85.
11.    Syresina OV Zhukova EA, Vidmanova TA et al. Melatonin in complex treatment of gastroesophageal reflux disease in children. Pediatric Pharmacology (Rus). 2012;9(1):77-80.
12.    Fadeenko GD, Izmailova EV, Krakhmalova EO. Features of sleep disorders and depressive disorders in patients with isolated GERD and in conjunction with coronary heart disease. Ñientific Journal «ScienceRise». 2015;15(10/3):145-153.
13.    Helsinki Declaration of the World Medical Association: Guidelines for doctors to conduct biomedical research involving human subjects (Rus). Int J Med Practice (Rus). 2005;6:18-20.
14.    Ai Fujimoto A, Hoteya S, Iizuka T et al. Obesity and Gastro­intestinal Diseases. Gastroenterol. Res Pract. 2013;2013:760574.
15.    Demeter P, Pap A. The relationship between gastroesophageal reflux disease  and obstructive sleep apnea. J Gastroenterol. 2004;39:815-820.
16.    Dent J. Pathogenesis of gastro-oesophageal reflux disease and novel options for its therapy. Neurogastroenterol. Motil. 2008;20;1:91-102.
17.    ESC guidelines on the management of stable coronary artery disease. European Heart Journal. 2013;34:2949-3003.
18.    Laine L, Hennekens C. Proton pump inhibitor and clopidogrel interaction: fact or fi ction?. Am J Gastroenterol. 2010;105:34-41.
19.    Madanick RD. Proton pump inhibitor side effects and drug interactions: much ado about nothing?. Cleveland Clin J Med. 2011;78:39-49.
20.    Vaughan TL, Farrow DC, Hansten PD et al. Risk of esopha­geal and gastric adenocarcinomas in relation to use calcium channel blockers, asthma drugs, and other medications that promote gastroesophageal reflux. Cancer Epidemiol Biomar­kers Prev. 1998;7(9):749-756.

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8. Original researches


The dynamics of the indicators primary disability indices due to cardiovascular diseases system in Ukraine (2011—2015)

A.V. Ipatov, O.M. Lysunets, I.Ya. Khanyukova, Ju.V. Tkachenko, I.M. Zubko

SI «Ukrainian State Institute of Medical and Social Problems of Disability Ministry of Public Health of Ukraine», Dnipro

Objective — to perform analysis of the primary disability due to the cardiovascular disease in Ukraine in the years 2011—2015. The changes of partial weight of cardiovascular pathology in the structure of primary disability of adult and working population have been considered on the basis of the diseases’ forms.
Materials and methods. The work was based on the medical statistical reporting data according to the form N 14 (The report on the causes of disability, the indications for medical, professional and social rehabilitation, the order Ministry of Health of Ukraine dated 10.07.2007, N 378). The data were obtained in 24 regional centers of medical and social expertise, central city medical and social expert commission of Kyiv city.
Results and discussion. Based on the obtained results, cardiovascular diseases take the leading place in the structure of primary disability of population of Ukraine, with this the portion of young people is increasingly registered. The cerebrovascular pathology and ischemic heart disease still prevail among cardiovascular diseases.  
Conclusions. The priority of the activities aimed on the cardiovascular diseases’ prevention and further improvement of the specialized cardiological and medical and social care are determined  by the leading role of population’s disability due to this class of diseases.

Keywords: cardiovascular diseases, primary disability, medical and social examination.

List of references:
1.    Ipatov AV, Moroz OM, Golik VA et al. Osnovni pokaznyky invalidnosti ta dijal’nosti medyko-social’nyh ekspertnyh komisij Ukrai’ny za 2015 r.: analityko-informacijnyj dovidnyk / za red. nachal’nyka viddilu organizacii’ social’noi’ dopomogy okremym kategorijam gromadjan, a takozh pytan’ MSEK MOZ Ukrai’ny SI Chernjaka. Dnipro:«Akcent PP»; 2016:162.
2.    Kovalenko VN, Dolzhenko MN, Nesukaj EG et al. Sravnytel’naja harakterystyka profylaktyky serdechno-sosudystyh zabolevanyj v Ukrayne y Evrope po dannym issledovanyja EUROASPIRE IV: gospytal’naja lynyja. Ukrai’ns’kyj kardiologichnyj zhurnal. 2015;4:17-24.
3.    Manojlenko TS, Dorogoj AP, Gandzjuk VA. Hvoroby systemy krovoobigu jak medyko-social’na i suspil’no-politychna problema (Analitychno-statystychnyj posibnyk) Pid. red. VMKovalenka, VM Kornac’kogo. Kyi’v: «SPD FO «Kolomicyn V.Ju.»; 2014:279.
4.    Pro stanovyshhe osib z invalidnistju v Ukrai’ni. Nacional’na dopovid’ / Ministerstvo social’noi’ polityky Ukrai’ny DU naukovo-doslidnyj instytut social’no-trudovyh vidnosyn. Kyiv; 2013:198.
5.    Regional’ni osoblyvosti rivnja zdorov’ja narodu Ukrai’ny. Analityko-statystychnyj posibnyk - rekomendovanyj dlja kardiologiv, revmatologiv, terapevtiv, organizatoriv ohorony zdorov’ja ta likariv zagal’noi’ praktyky / Pid red. VM Ko­­valenka, VMKornac’kogo. Kyi’; 2011:165.
6.    Rozporjadzhennja Kabinetu Ministriv Ukrai’ny vid 30 bereznja 2011 r. N 245-r «Pro shvalennja Koncepcii’ Derzhavnoi’ cil’ovoi’ programy “Nacional’nyj plan dij z realizacii’ Konvencii’ pro prava invalidiv ta rozvytku systemy reabilitacii’ invalidiv” na period do 2020 roku».
7.    Trybrat TA, Shut’ S, Zodova TM. Analiz invalidnosti vnaslidok hvorob systemy krovoobigu. Visnyk problem biologii’ i medycyny. 2014:3(109):306-309.
8.    Chepelevs’ka LA, Rudnyc’kyj OP, Krapivna AA. Suchasni tendencii’ smertnosti naselennja Ukrai’ny. Ukrai’na. Zdorov’ja nacii’. 2014;1:33-39.
9.    Shhorichna dopovid’ pro stan zdorov’ja naselennja, sanitarno-epidemichnu sytuaciju ta rezul’taty dijal’nosti systemy ohorony zdorov’ja Ukrai’ny. 2014 rik / Za red. O Kvitashvili – K.; 2015:460.
10.    Mont D. Measuring Disability Prevalence. Social Protection discussion paper. March 2007. N 0706. Washington: World Bank, 2007.

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9. MEDICINES in therapy


Intestinal microbiota and functional intestinal disorders, accompanied with bloat. Results of the use «Gastrolact» preparation in the complex treatment of the diseases, accompanied with bloat

O.Yu. Gubs’ka, A.I. Taran, I.O. Rodionova, I.O. Lavrenchuk, A.S. Sitnikov

O.O. Bogomolets National Medical University, Kyiv

The production of intestinal gases in adequate quantities, that do not disturb healthy people and do not cause any discomfort is one of the important signs of a health and normal intestine functioning.  The excessive gases content in the intestinal lumen becomes a serious medical problem. One of the most important causes of the increased gas production in the intestine is the disturbances in quantitative and qualitative microbiota composition in the digestive tract, imbalance between the gas-producing and gas-consuming bacteria. The combined administration of the living probiotic cultures and simethicone is pathogenetically substantiated for bloat correction.

Keywords: bloat, gas-producing microflora, probiotics, simethicone, «Gastrolact».

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10. Reviews


Modern views on the role and place of therapeutic and prophylactic dietetics in the internal organs diseases

 D.K. Miloslavsky

SI «National Institute of Therapy named after L.T. Mala of NAMS of Ukraine», Kharkiv

In a review of the clinical dietetics, given modern views on nutritional therapy in the most common diseases of internal organs, nutrition in endocrinology, cardiovascular disease, diseases of the nervous system, oncology, congenital metabolic disorders, metabolic diseases, food allergies and intolerances, highlights outstanding issues and future directions in nutrition.

Keywords: clinical dietetics, clinical nutrition, internal diseases, metabolic disorders, food intolerance, promising directions in nutrition.

List of references:
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2.    Baranovskij AYu, Nazarenko LI, Rajhel’son KL. Nesovmestimost’ pishchevyh produktov i pishchevaya allergiya. Uchebno-metodicheskoe posobie. Sankt-Peterburg: Dialekt, 2006:133 (Rus).
3.    Baranovskij AYu., Nazarenko LI, Rajhel’son KL. Pishchevaya neperenosimost’ (uchebno-metodicheskoe posobie). SPb: «Izd. «Dialekt»: 2006:136 (Rus).
4.    Baranovskij AYu., Nazarenko LI, Haritonov AG. Lechebnoe pitanie pri saharnom diabete: metod. rekomendacii. SPb; 2008:24 (Rus).
5.    Bratus’ VV, Taleva TV, Shumakov VA. Ozhirenie, insulinorezistentnost’, metabolicheskij sindrom: fundamental’nye i klinicheskie aspekty / pod red. Kovalenko VN Kiev Chetverta hvilya,2009:416 (Rus).
6.    Voloshin O², Splavs’kij O². Osnovi ozdorovchogo harchuvannya. Chern³vtc³,2007:535 (Rus).
7.    Getc T., Mal’fertajner P. Nutricionnaya podderzhka pri ostrom pankreatite. Eksperimental’naya i klinicheskaya gastroehnterologiya. 2009;2:170-177  (Rus).
8.    Dietologiya: Rukovodstvo.3-e izd. / Pod red. AYu Baranovskogo. SPb.:Piter;2008:1024 (Rus).
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10.    Docenko VA, Mosijchuk LV. Bolezni izbytochnogo i nedostatochnogo pitaniya. Sankt-Peterburg.: Foliant; 2004:111  (Rus).
11.    ªrmakovich ²², Chernishov VA, Bereznyakov ²G, Bogun LV. Ozhir³nnya: suchasn³ p³dhodi do l³kuvannya: metod. Rekomendacii. Kharkiv; 2006:21 (Ukr).  
12.    Zdorovoe pitanie pri saharnom diabete: rekomendacii dlya pacientov kampanii Vyorvag Farma. http://www.woerwagpharma.kiev.ua/ (Rus).
13.    Kaganov BS, Baturin AK, Pogozheva AV et al. Ocenka ehffektivnosti primeneniya smesi belkovyh kompozitnyh suhih v dietoterapii bol’nyh naibolee rasprostranennymi alimentarno-zavisimymi zabolevaniyami: metodicheskie rekomendacii. Moscow; 2009:60 (Rus).
14.    Karpenko PA Osoblivosti harchuvannya v profilaktici zahvoryuvan’ organiv travlennya: Lekciya dlya likariv. Zhurnal praktichnogo likarya. 2009;2-3:19-23 (Ukr).  
15.    Koval’ SM, Chernishov VA, ªrmakovich ²² et al. Pervinna prof³laktika metabol³chnogo sindromu: metod. rekomendacii. Kharkiv; 2008:20 (Ukr).  
16.    Kravchun NA, Romanova IP, Polozova LG i dr. Ispol’zovanie pishchevyh volokon v kompleksnoj terapii saharnogo diabeta 2-go tipa. Mezhdunarodnyj ehndokrinologicheskij zhurnal. 2014; 6(62):61-65 (Rus).
17.    Kramar’ova VN, Sobol’ VO. Dietichna korekciya metabolichnih porushen’ u hvorih na esencial’nu arterial’nu gipertenziyu z metabolichnim sindromom. Galic’kij likars’kij visnik. 2010;3:52-55. (Ukr).   
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20.    Martinchuk OA, Rotter MM. Eliminacijna dieta u likuvanni ozhirinnya, zumovlenogo harchovoyu neperenosimistyu. Suchasna gastroenterologiya. 2012;4:40-42 (Ukr).  
21.    Marcinik EN, Perceva NO, Malyar E.YU., Mishchenko NV. Effektivnost’ sekvestrantov zhirnyh kislot v gipolipidemicheskoj terapii bol’nyh saharnym diabetom. Mezhdunarodnyj ehndokrinologicheskij zhurnal. 2010;7(31):150-154 (Rus).
22.    Naumova OA. Osobennosti pitaniya bol’nyh celiakiej. Suchasni medichni tekhnologii. 2010;2:124-127 (Rus).
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24.    Pasºchko NV, Loj GYa, Svistun ²². Vpliv preparatu Guarem na masu t³la ta osnovn³ pokazniki l³p³dnogo ³ vuglevodnogo obm³nu u pac³ºnt³v ³z nadm³rnoyu masoyu t³la chi ozhir³nnyam. Mezhdunarodnyj ehndokrinologicheskij zhurnal. 2014;5 (61):31-36 (Ukr).  
25.    P³lec’kij AM, Marchenko NV, Anoh³na GA ta ³n. Suchasna koncepc³ya d³ºtichnogo l³kuvannya hvorih na bronh³al’nu astmu z sindromom hron³chno¿ vtomi. Kiev; 2008:23 (Ukr).  
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27.    Primak AV. Metabolicheskij sindrom: funkcional’nyj podhod k ehtiologii, patogenezu, klinike, diagnostike i lecheniyu. Kiev: «Klinika antistareniya «Medikom»», 2011:120 (Rus).
28.    Rekomendacii po optimizacii pitaniya bol’nyh onkologicheskimi zabolevaniyami: informacionnoe pis’mo / Kaganov BS, Gapparov MG, Sharafetdinov HH, Isakov VA. Moscow; 2009:15 (Rus).
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33.    Shvec NI, Mishchenko SM. Racional’noe pitanie pri zabolevaniyah serdechno-sosudistoj sistemy. Zhurnal praktichnogo likarya. 2009;2-3:44-50  (Rus).
34.    Yalkut SI. Profilaktika opuholej. Kiev: Kniga-plyus; 2006:452 (Rus).
35.    Amiano P, Chamosa S, Etxezarreta N et al. No association between fish consumption and risk of stroke in the Spanish cohort of the European Prospective Investigation into Cancer and Nutrition (EPIC-Spain): a 13 8-year follow-up study. Public Health Nutr. 2016;19(4):674-681. doi: 10.1017/S1368980015001792.  
36.    Carey VJ, Bishop L, Charleston J et al.  Rationale and design of the Optimal Macro-Nutrient Intake Heart Trial to Prevent Heart Disease (OMNI-Heart). Clin Trials. 2005;2(6):529-537.  
37.    Drogan D, Schulze MB, Boeing H, Pischon T. Insulin-Like Growth Factor 1 and Insulin-Like Growth Factor-Binding Protein 3 in Relation to the Risk of Type 2 Diabetes Mellitus: Results From the EPIC-Potsdam Study. Am J Epidemiol. 2016;183(6):553-560. doi: 10.1093/aje/kwv188. Epub 2016 Feb 14.  
38.    Haring B, von Ballmoos MC, Appel LJ, Sacks FM. Healthy dietary interventions and lipoprotein (a) plasma levels: results from the Omni Heart Trial. PLoS One. 2014;9(12):e114859. doi: 10.1371/journal.pone.0114859. eCollection 2014.  
39.    Hauk L.DGAC Makes Food-Based Recommendations in the 2015-2020 Dietary Guidelines for Americans. Am Fam Physician. 2016;93(6):525. No abstract available.  
40.    Human Nutrition / Eds: C. Geissler, H. Powers. Livingstone, Netherlands: Elsevier Churchill, 2005:765.
41.    Koloverou E, Panagiotakos DB, Pitsavos C et al.  ATTICA Study Group Adherence to Mediterranean diet and 10-year incidence (2002-2012) of diabetes: correlations with inflammatory and oxidative stress biomarkers in the ATTICA cohort study. Diabetes Metab Res Rev. 2016;32(1):73-81. doi: 10.1002/dmrr.2672. Epub 2015 Jul 27.  
42.    Kovesdy CP, Kalantar-Zadeh K. Back to the future: restricted protein intake for conservative management of CKD, triple goals of renoprotection, uremia mitigation, and nutritional health. Int Urol Nephrol. 2016;48(5):725-729. doi: 10.1007/s11255-016-1224-0. Epub 2016 Feb 17.  
43.    Lu Y, Vakilzadeh N, Teta D. Chronic renal failure: what is the optimal diet?]. Praxis (Bern 1994). 2015;104(7):361-367. doi: 10.1024/1661-8157/a001959. Review. French.  
44.    Piccoli GB, Vigotti FN, Leone F et al. Low-protein diets in CKD: how can we achieve them? A narrative, pragmatic review. Clin Kidney J. 2015;8(1):61-70. doi: 10.1093/ckj/sfu125. Epub 2014 Dec 2. Review.  
45.    Riccio E, Di Nuzzi A, Pisani A. Nutritional treatment in chronic kidney disease: the concept of nephroprotection. Clin Exp Nephrol. 2015;19(2):161-167. doi: 10.1007/s10157-014-1041-7. Epub 2014 Oct 16. Review.  
46.    Tay J, Thompson CH, Luscombe-Marsh ND et al. Long-Term Effects of a Very Low Carbohydrate Compared With a High Carbohydrate Diet on Renal Function in Individuals With Type 2 Diabetes: A Randomized Trial. Medicine (Baltimore). 2015;94(47):e2181. doi: 10.1097/MD.0000000000002181.  
47.    Teplan V. Effect of keto acids on asymmetric dimethylarginine, muscle, and fat tissue in chronic kidney disease and after kidney transplantation. J Ren Nutr. 2009;19(5):S27-29. doi: 10.1053/j.jrn.2009.06.007. No abstract available.

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11. Reviews


Extrahepatic manifestations of chronic hepatitis C: early diagnosis improves prognosis

M.B. Shcherbinina, T.N. Shevchenko

Oles Honchar Dnipropetrovsk National University

Objective — to systematization and analysis of scientific literature dealing with the typical characteristics of extrahepatic manifestations of hepatitis C virus (HCV) infection.
Hepatitis C virus is a world-wide medical and social problem. Modern antiviral agents with direct action are capable to achieve a cure of this disease. That’s why  it is important to identify HCV infected subjects and perform therapy in a timely manner. The chronic HCV hepatitis is characterized with oligosymptomatic course for a long time and frequent (74%) extrahepatic manifestations, which can be the first clinical manifestation, masking the liver damage. The review examines the presumptive risk factors and pathogenesis of HCV­associated diseases as well as the frequency of these diseases and clinical peculiarities in the groups with account of the degree of confirmed etiological HCV role.

Keywords: chronic hepatitis C, extrahepatic manifestation, the HCV genotype.

List of references:
1.    Beloborodovà EV, Chvyrina DV, Beloborodovà EI et al. Structural and functional myocardial damage in patients with chronic viral hepatitis (Rus). Sibirskiy medicinskiy zhurnal [Siberian Journal of Medicine] (Rus). 2010;25:33-38.
2.    Ignatova TM. Treatment of extrahepatic manifestations of chronic HCV-infection (Rus). Clinicheskay gepatologiay [Clinical Hepatology] (Rus). 2005;1 (2):3-11.
3.    Maybogin AM. Morphological changes in the brain in patients with hepatitis C virus (review) (Rus). Problemu medicinu i patologii [Problems in Medicine and Ecology] (Rus). 2009:36-38.
4.    Guidelines for screening, care and treatment of patients with chronic hepatitis C (Rus). Revised edition, April 2016 (Eng). 135ð. / www.who.int
5.    Riabokon YY. Spectrum pozapech³nkovih proyav³v from ailments to hepatitis C hron³chny fallow od ³nf³kuvannya r³znimi genotypes v³rusu that v³rusnogo navantazhennya (Rus). Patologiay. [Pathology] (Rus). 2013;2(28):78-80.
6.    Fazylov VH, Enaleeva DSh, Kiyasov AP et al. Clinical and morphological characteristics of the natural course of chronic hepatitis C. (Rus). Prakticheskaay medicina [Practical Medicine] (Rus). 2006;4 (18):18-19.
7.    Fedorchenko SV. Chronic HCV-infection: Monograph (Rus). K.: TNI Medicine (Ukr); 2010:272
8.    Agnello V, De Rosa FG. Extrahepatic disease manifestations of HCV infection: some current issues. J Hepatol. 2004;40:341-352.
9.    Antonelli A, Ferri C, Fallahi P et al. Hepatitis Ñ virus infection: evidence for an associa­tion with type 2 diabetes. Diabetes Care. 2005;28:2548-2550.
10.    Antonelli A, Ferri C, Pampana A et al. Thyroid disorders in chronic hepatitis C. Am J Med. 2004;117:10-13.
11.    Bonkovsky HL, Snow KK, Malet PF et al. Health-related quality of life in patients with chronic hepatitis C and advanced fibrosis. J Hepatol. 2007;46 (3):420-431.
12.    Cacoub P, Poynard Ò, Ghillani P et al. Extrahepatic manifestations of chronic hepatitis C. Arthritis Rheum. 1999;42:2204-2212.
13.    Cartozzo M, Celle P, Gandolfo S. Increased frequency of HLA-DR6 allele in Italian patients with hepatitis C virus-associated oral lichen planus. Br J Dermatol. 2001;144:803-808.
14.    Ferri C. HCV_related cryoglobulinemic vasculitis: an update on its etiopathogenesis and therapeutic strategies. Clin Exp Rheumatol. 2003;21(31):78-84.
15.    Forton DM, Giuggioli D, Cassato M et al. Evidence for a cerebral effect of the hepatitis C virus. Lancet. 2006;358:38-39.
16.    Forton DM. Identification of Unique Hepatitis C Virus Quasis­pecies in the Central Nervous System and Comparative Analysis of Internal Translational Efficiency of Brain, Liver, and Serum Variants. J of Virology. 2004;78(10):5170-5183.
17.    Foster GR, Goldin RD, Thomas HC. Chronic hepatitis C virus infection causes a significant reduction in quality of life in the absence of cirrhosis. Hepatology. 1998;27(1):209-212.
18.    Gisbert JP, Garcia BL, Pajares JM, Moreno OR. Prevalence of hepatitis Ñ virus infection in porphyria cutanea tarda: systema­tic review and meta-analysis. J Hepatol. 2003;39:620-627.
19.    Irving WL, Day S, Johnson DA. Idiopathic pulmonary fibrosis and hepatitis C virus infection. Am Rev Respir Dis. 1993;148:1683-1684.
20.    Jafferbhoy H, Miller MH, Dunbar JK et al. Intravenous drug use: not a barrier to achieving a sustained virological response in HCV infection. J Viral Hepat. 2012;19 (2):112-119.
21.    Lenzi M, Frisoni M, Mantovani W. Haplotype HLA B8/DR3 confers susceptibility to hepatitis C virus mixed cryoglobulinemia. Blood. 1998;91(6):2062-2066.
22.    Meliconi R, Andreoni P, Fasano L et al. Incidence of hepatitis C virus infection in Italian patients with idiopathic pulmonary fibrosis. Thorax. 1996;51:315-317.
23.    Nagao Y, Sato M. Hepatitis Ñ and lichen planus. J. Gastroen­terol. Hepatol. 2004;19:1101-1113.
24.    Panzer S, Seel E. Is there an increased frequency of autoimmune thrombocytopenia in hepatitis Ñ infection? A review. Wien Med Wochenschr. 2003;153:417-420.
25.    Perico N, Cattaneo D, Bikbov B, Remuzzi G. Hepatitis C infection and chronic renal diseases. Clin J Am Soc Nephrol. 2009;4:207-220.
26.    Pileri P, Uematsu Y, Campagnoli S et al. Binding of hepatitis C virus to CD81. Science. 1998;282(5390):938-941.
27.    Rivanera D, Lilli D. Porphyria cutanea tarda and relationship to HCV genotypes. Microbiologica. 1998;21(4):329-334.
28.    Romero-Gomes M. Hepatitis C and insulin resistance: steatosis, fibrosis. Rev Esp Enferm Dig. 2006;98:605-615.
29.    Sene D, Chilliani-Dalbin P, Thibault V. Long term course of mixed cryoglobulinemia in patients infected with hepatitis C virus. J Reumatol. 2004;31(11):2199-2207.
30.    Sene D, Limal N, Cacoub P. Hepatitis Ñ virus-associated extrahepatic manifestations: a review. Metabolic Brain Disease. 2004;19:357-381.
31.    Shiffman ML, Benhamou Y. Cure of HCV related liver disease. Int. 2015;35(1):71-77.
32.    Tarantino G, Riccio A. HCV-infection and chronic arthritis: Does viral replication matter? Hepat Res. 2006;35:238-241.
33.    Weng WK, Levy S. Hepatitis Ñ virus (HCV) and lymphomage­nesis. Leukemia Lymphoma. 2003;44:1113-1120.
34.    Younossi ZM, Stepanova M, Afdhal N et al. Improvement of health-related quality of life and work productivity in chronic hepatitis C patients with early and advanced fibrosis treated with ledipasvir and sofosbuvir. J Hepatol. 2015;63(2):337-345.

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12. Reviews


Etiology, pathogenesis and prevention of sudden cardiac death in patients with myocardial infarction

M.P. Kopytsya, A.V. Kobets

SI «National Institute of Therapy named after L.T. Mala of NAMS of Ukraine», Kharkiv

Sudden cardiac death (SCD) is a leading cause of death all over the world. Presence of cardiovascular pathology (myocardial infarction (MI), heart failure, decreased ejection fraction, cardiac arrest, etc.) significantly increases the risk of its development, though SCD is frequently the first but fatal manifestation of cardiovascular system disease.
It has been shown in various studies, that in early post-infarction period, the mechanic complications are the most frequent reason of death, while arrhythmia becomes more often cause over several hours. The post-infarction arrhythmias, recorded in patients in the first 24–48 hours after MI, do not indicate the high arrhythmia risk in the remote period.  The presence of arrhythmia will be diagnostically significant after formation of changes in area of post-infarction damage few weeks later.
SCD, manifested as arrhythmia, can be prevented by application of cardioverter defibrillators, which are several types: implantable, wearable, subcutaneous, each of them has advantages and disadvantages.
The early identification of patients with high SCD risk is very important to define effective preventive method and to choose optimal treatment strategy.

Keywords: sudden cardiac death, myocardial infarction.

List of references:
1.    Bokeriya LA, Bokeriya OL, Bazarsadaeva TS. Novyie prediktori vnezapnoy serdechnoy smerti. Annalyi aritmologii. 2009;6(4):41-49
2.    Bokeriya OL, Ahobekov AA. Vnezapnaya serdechnaya smert: mehanizmyi vozniknoveniya i stratifikatsiya riska. Annali aritmologii. 2012;9(3):32-40.
3.    Bokeriya OL, Biniashvili MB. Vnezapnaya serdechnaya smert i ishemicheskaya bolezn serdtsa. Neinvazivnaya aritmologiya. 2013;10(2):38-43.
4.    Kornatskiy VM. Problema bolezney sistemy krovoobrascheniya i puti ee minimizatsii v Ukraine. Kardiologiya. 2013;5(7):25-29.
5.    Sichov OS, Korkushko OV, Bobrov VO et al. Likuvannya shlunochkovih porushenü sertsya ta profilaktika raptovoyi ser­tsevoyi smerti. Rekomendatsiyi AsotsIatsiyi kardiologiv Ukrayini.Kiev;2009.
6.    Yurchenko VD, Krilyuk VO, Burchinskiy VG, Kuzminskiy IV, Krilyuk OE. Raptova sertseva smert - vazhliva sotsIalno-ekonomIchna problema v UkraYinI. Ekstrena meditsina: vid nauki do praktiki. 2013;5(6):150-156.
7.    Adabag AS, Therneau TM, Gersh BJ, Weston SA, Roger VL. Sudden death after myocardial infarction. JAMA. 2012;300:2022–2029.
8.    Bunch TJ, Hohnloser SH, Gersh BG. Mechanisms of Sudden Cardiac Death in Myocardial Infarction Survivors Insights From the Randomized Trials of Implantable Cardioverter-Defibrillators. Circulation. 2007;115:2451-2457.
9.    Chung MK, Szymkiewicz SJ, Shao M et al. Aggregate national experience with the wearable car-dioverter-defibrillator: event rates, compliance, and survival. J Am Coll Cardiol. 2010;56:194-203.
10.    Dickstein K, Kjekshus J. Optimaal steering committee of the optimaal study group. Effects of losartan and captopril on mortality and morbidity in high-risk patients after acute myocardial infarction: the optimaal randomised trial: Optimal Trial in Myocardial Infarction with Angiotensin II Antagonist Losartan. Lancet. 2007;360:752-760.
11.    Dillon KA, Szymkiewicz SJ, Kaib TE. Evaluation of the effectiveness of a wearable cardioverter defibrillator detection algorithm. J Electrocardiol. 2012;43:63-67.
12.    Dorian P, Hohnloser SH, Thorpe KE et al. Mechanisms underlying the lack of effect of implantable cardioverter-defibrillator therapy on mortality in high-risk patients with recent myocardial infarction: insights from the Defibrillation in Acute Myocardial Infarction Trial (DINAMIT). Circulation. 2012;122:2645-2652.
13.    Fishman GI, Chugh SS, Dimarco JP et al. Sudden cardiac death prediction and prevention: report from a National Heart, Lung, and Blood Institute and Heart Rhythm Society Workshop. Circulation. 2012;122(22):2335-2348.
14.    Goldenberg I, Moss AJ, Hall WJ. Multicenter Automatic Defibrillator Implantation Trial (MADIT) II Investigators. Causes and consequences of heart failure after prophylactic implantation of a defibrillator in the Multicenter Automatic Defibrillator Implantation Trial II. Circulation. 2006;113:2810-2817.
15.    Hohnloser SH, Kuck KH, Dorian P et al. Dinamit Investigators. Prophylactic use of an implantable cardioverter-defibrillator after acute myocardial infarction. N Engl J Med. 2004;351:2481-2488.
16.    Hsieh CH, Chia EM, Huang K, Lu J et al. Evolution of ventricular tachycardia and its electro-physiological substrate early after myocardial infarction: an ovine model. Circ Arrhythm Electrophysiol. 2013;6:1010-1017.
17.    Jarman JW, Lascelles K, Wong T, Markides V, Clague JR, Till J. Clinical experience of entirely subcutaneous implantable cardioverter-defibrillators in children and adults: cause for caution. Eur Heart J. 2012;33:1351-1359.
18.    Liew R, Chiam P. Risk Stratification for Sudden Cardiac Death after Acute Myocardial Infarction. Annals Academy of Medicine. 2010;39(3):134-139.
19.    Klein HU, Goldenberg I, Moss AJ. Risk stratification for implantable cardioverter defibrillator therapy: the role of the wearable cardioverter-defibrillator. Eur Heart J. 2013;34:2230-2242.
20.    Myerburg RG, Junttila MJ. Sudden Cardiac Death Caused by Coronary Heart Disease. Circulation. 2012;125:1043-1052.
21.    Ottervanger JP, Ramdat Misier AR, Dambrink JH et al. Zwolle Myocardial Infarction Study Group. Mortality in patients with left ventricular ejection fraction 22.    Piccini JP, Al-Khatib SM, Hellkamp AS et al. Mortality benefits from implantable cardioverter-defibrillator therapy are not restricted to patients with remote myocardial infarction: an analysis from the Sudden Cardiac Death in Heart Failure Trial (SCD-HeFT). Heart Rhythm. 2011;8:393-400.
23.    Pouleur AC, Barkoudah E, Uno H et al. Valiant Investigators. Pathogenesis of sudden unexpected death in a clinical trial of patients with myocardial infarction and left ventricular dysfunction, heart failure, or both. Circulation. 2012;122:597-602.
24.    Russo AM, Stainback RF, Bailey SR et al. ACCF/HRS/AHA/ ASE/HFSA/SCAI/SCCT/SCMR 2013 appropriate use criteria for implantable cardioverter-defibrillators and cardiac resynchronization therapy... Heart Rhythm. 2013;10:e11-e58.12.
25.    Solomon SD, Zelenkofske S, McMurray JJ et al. Valsartan in Acute Myocardial Infarction Trial (VALIANT) Investigators. Sudden death in patients with myocardial infarction and left ventricular dysfunction, heart failure, or both. N Engl J Med. 2005;352:2581-2588.
26.    Wellens HJJ, Schwartz PJ, Lindemans FW. et al. Risk stratification for sudden cardiac death: current status and challenges for the future. Eur. Heart J. 2014;35(25):1642-1651.
27.    Zaman S, Kovoor Pr. Sudden Cardiac Death Early After Myocardial Infarction: Pathogenesis, Risk Stratification, and Primary Prevention. Circulation. 2014;129:2426-2435.
28.    Zaman S, Narayan A, Thiagalingam A et al. What is the optimal left ventricular ejection fraction cut-off for risk stratification for primary prevention of sudden cardiac death early after myocardial infarction? Europace Advance Access. 2014;3:432-439.

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Atypical course of sarcoidosis with injury of liver and abdominal lymph nodes

I.P. Jerko1, A.A. Moloshok2, Ju.V. Rudich2, L.V. Sheremok2

1 Regional Oncology Center, Chernihiv
2 Regional Autopsy Bureau, Chernihiv

Sarcoidosis is a systemic granulomatous disease of unknown etiology with a benign course and a tendency to spontaneous healing. The paper presents a case of sarcoidosis in a patients with Epstein—Barr virus, with injury of liver and abdominal lymph nodes, that was difficult for clinical diagnosis.

Keywords: sarcoidosis, liver, lymph nodes, the Epstein—Barr virus.

List of references:
1.    Vizel AA, Vizel IY. Sarcoidoz:sostoyanie problemu i nereshennue zadachi (Rus). Pulmonologia i allergologia. 2010;1:6.
2.    Palzev MA, Kakturskiy LV, Zayratyanz OV . Patologycheskaya anatomia. Nasionalnoe rukovodstvo. M: GEOTAR-Media; 2011:149-154 (Rus).
3.    Chugalina AT. Respiratornaya medisina. M: GEOTAR-Media; 2007;2.
4.    Neuman LS. Åtiologies of sarcoidosis. Eur Respir Mono­grap­hy. 2005;10:23-48.
5.    Nunes H, Bouvry D, Soler P, Valeyre D. Sarcoidosis. Orphanet J Rare Dis. 2007;19(2):46.

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