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Ранняя диагностика печеночно-клеточного повреждения и воспаления при неалкогольном стеатогепатите слабой активности
Ранняя диагностика печеночно-клеточного повреждения и воспаления при неалкогольном стеатогепатите слабой активности
Дуданова О.П., Шиповская А.А., Курбатова И.В., Ларина Н.А. Ранняя диагностика печеночно-клеточного повреждения и воспаления при неалкогольном стеатогепатите слабой активности. Гастроэнтерология. Хирургия. Интенсивная терапия. Consilium Medicum. 2018; 2: 15–20. DOI: 10.26442/26583739.2018.2.000007
DOI: 10.26442/26583739.2018.2.000007
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DOI: 10.26442/26583739.2018.2.000007
Материалы доступны только для специалистов сферы здравоохранения. Авторизуйтесь или зарегистрируйтесь.
Аннотация
Цель исследования – ранняя диагностика печеночного повреждения и воспаления при неалкогольном стеатогепатите (НАСГ) слабой активности.
Материалы и методы. Обследованы 173 пациента с НАСГ: 118 (68,2%) мужчин, 55 (31,8%) женщин, возраст 47,0±10,8 года, индекс массы тела 33,0±5,2 кг/м2. Определялся маркер апоптоза гепатоцитов – фрагменты цитокератина-18 – ФЦК-18 (TPS ELISA, Biotech, Швеция), фактор некроза опухоли α – ФНО-α (Human TNF-alpha Platinum ELISA, eBioscience, Австрия), инсулин (Insulin Test System, США), индекс инсулинорезистентности (HOMA-IR), индекс фиброза.
Результаты. Уровень ФЦК-18 при НАСГ составил 268,4±102,1 Ед/л, более чем в 4 раза превышая таковой в контрольной группе – 62,1±15,0 Ед/л (p<0,05), в то время как уровень аланинаминотрансферазы (АЛТ) повышался только в 2 раза. Уровень ФЦК-18 коррелировал с АЛТ (r=0,26; p<0,05), аспартатаминотрансферазой (r=0,32; p<0,05), числом лейкоцитов (r=0,23; p<0,05). У пациентов с высоким уровнем ФЦК-18 выше были уровни аминотрансфераз, триглицеридов, HOMA-IR. ФНО-α при НАСГ был увеличен – 6,4±2,3 пг/мл против 4,3±1,3 пг/мл (p<0,01) у здоровых лиц. Он коррелировал с окружностью талии (r=0,33; р<0,05), АЛТ (r=0,23; p<0,05). У пациентов с высоким ФНО-α были выше антропометрические показатели, уровень триглицеридов, ФЦК-18, HOMA-IR.
Заключение. Применение новых маркеров печеночно-клеточного повреждения и воспаления позволило у больных НАСГ слабой активности выявлять субклинический, латентно текущий воспалительный процесс в печени, не идентифицируемый традиционными лабораторными тестами.
Ключевые слова: неалкогольный стеатогепатит, апоптоз, фрагменты цитокератина-18, фактор некроза опухоли α, инсулинорезистентность, фиброз.
Materials and methods. 173 patients of NASH were examined: men – 118 (68.2%), women – 55 (31.8%), age of 47.0±10.8 years, body mass index – 33.0±5.2 kg/m2. A marker of hepatocyte apoptosis was determined – fragments of cytokeratin-18 – FCK-18 (TPS ELISA, Biotech, Sweden), tumor necrosis factor a (Human TNF-alpha Platinum ELISA, eBioscience, Austria), insulin (Insulin Test System, USA), insulin resistance index (HOMA-IR), fibrosis index NAFLD FS.
Results. The patients of NASH had a high FCK-18 – 268.4±102.1 U/l, more than 4 times higher than that in the control group – 62.1±15.0 U/l (p<0,05), while the level of alanine aminotransferase (ALT) exceeded the norm only by 2 times. The level of FCK-18 correlated with ALT (r=0.26; p<0.05), aspartate aminotransferase (r=0.32; p<0.05) and leukocyte count (r=0.23; p<0.05). In patients with a high level of FCK-18, the level of aminotransferases, triglycerides, HOMA-IR were higher. The level of TNF-a was significantly increased – 6.4±2.3 pg/ml vs. 4.3±1.3 pg/ml (p<0.01) in healthy individuals. It correlated with the circumference of the waist (r=0.33; p<0.05), ALT (r=0,23; p<0.05). In patients with a high level of TNF-a anthropometric indices, levels of triglycerides, FCK-18, HOMA-IR were higher than those in patients with normal TNF-a levels.
Conclusion. The use of new markers of hepatic cell damage and inflammation allowed in NASH of weak activity to detect a subclinical, latent current inflammatory process in the liver that is not identified by traditional laboratory tests.
Key words: non-alcoholic steatohepatitis, apoptosis, fragments of cytokeratin-18, tumor necrotic factor-alpha, insulin resistance, fibrosis.
Материалы и методы. Обследованы 173 пациента с НАСГ: 118 (68,2%) мужчин, 55 (31,8%) женщин, возраст 47,0±10,8 года, индекс массы тела 33,0±5,2 кг/м2. Определялся маркер апоптоза гепатоцитов – фрагменты цитокератина-18 – ФЦК-18 (TPS ELISA, Biotech, Швеция), фактор некроза опухоли α – ФНО-α (Human TNF-alpha Platinum ELISA, eBioscience, Австрия), инсулин (Insulin Test System, США), индекс инсулинорезистентности (HOMA-IR), индекс фиброза.
Результаты. Уровень ФЦК-18 при НАСГ составил 268,4±102,1 Ед/л, более чем в 4 раза превышая таковой в контрольной группе – 62,1±15,0 Ед/л (p<0,05), в то время как уровень аланинаминотрансферазы (АЛТ) повышался только в 2 раза. Уровень ФЦК-18 коррелировал с АЛТ (r=0,26; p<0,05), аспартатаминотрансферазой (r=0,32; p<0,05), числом лейкоцитов (r=0,23; p<0,05). У пациентов с высоким уровнем ФЦК-18 выше были уровни аминотрансфераз, триглицеридов, HOMA-IR. ФНО-α при НАСГ был увеличен – 6,4±2,3 пг/мл против 4,3±1,3 пг/мл (p<0,01) у здоровых лиц. Он коррелировал с окружностью талии (r=0,33; р<0,05), АЛТ (r=0,23; p<0,05). У пациентов с высоким ФНО-α были выше антропометрические показатели, уровень триглицеридов, ФЦК-18, HOMA-IR.
Заключение. Применение новых маркеров печеночно-клеточного повреждения и воспаления позволило у больных НАСГ слабой активности выявлять субклинический, латентно текущий воспалительный процесс в печени, не идентифицируемый традиционными лабораторными тестами.
Ключевые слова: неалкогольный стеатогепатит, апоптоз, фрагменты цитокератина-18, фактор некроза опухоли α, инсулинорезистентность, фиброз.
________________________________________________
Materials and methods. 173 patients of NASH were examined: men – 118 (68.2%), women – 55 (31.8%), age of 47.0±10.8 years, body mass index – 33.0±5.2 kg/m2. A marker of hepatocyte apoptosis was determined – fragments of cytokeratin-18 – FCK-18 (TPS ELISA, Biotech, Sweden), tumor necrosis factor a (Human TNF-alpha Platinum ELISA, eBioscience, Austria), insulin (Insulin Test System, USA), insulin resistance index (HOMA-IR), fibrosis index NAFLD FS.
Results. The patients of NASH had a high FCK-18 – 268.4±102.1 U/l, more than 4 times higher than that in the control group – 62.1±15.0 U/l (p<0,05), while the level of alanine aminotransferase (ALT) exceeded the norm only by 2 times. The level of FCK-18 correlated with ALT (r=0.26; p<0.05), aspartate aminotransferase (r=0.32; p<0.05) and leukocyte count (r=0.23; p<0.05). In patients with a high level of FCK-18, the level of aminotransferases, triglycerides, HOMA-IR were higher. The level of TNF-a was significantly increased – 6.4±2.3 pg/ml vs. 4.3±1.3 pg/ml (p<0.01) in healthy individuals. It correlated with the circumference of the waist (r=0.33; p<0.05), ALT (r=0,23; p<0.05). In patients with a high level of TNF-a anthropometric indices, levels of triglycerides, FCK-18, HOMA-IR were higher than those in patients with normal TNF-a levels.
Conclusion. The use of new markers of hepatic cell damage and inflammation allowed in NASH of weak activity to detect a subclinical, latent current inflammatory process in the liver that is not identified by traditional laboratory tests.
Key words: non-alcoholic steatohepatitis, apoptosis, fragments of cytokeratin-18, tumor necrotic factor-alpha, insulin resistance, fibrosis.
Полный текст
Список литературы
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11. Kawanaka M, Nishino K, Nakamura J et al. Correlation between serum cytokeratin-18 and the progression or regression of non-alcoholic fatty liver disease. Ann Hepatol 2015; 14 (6): 837–44.
12. Rahman T, Islam S, Ferdoushi S et al. Association of Serum Cytokeratin-18 Fragment Concentration in Patients with Different Types of Nonalcoholic Fatty Liver Disease. Gastroenterol Hepatol Open Access 2015; 2 (2): 00037.
13. He L, Deng L, Zhang Q et al. Diagnostic Value of CK-18, FGF-21, and Related Biomarker Panel in Nonalcoholic Fatty Liver Disease: A Systematic Review and Meta-Analysis. Biomed Res Int 2017; 2017: 9729107.
14. Bratoeva K, Nikolova S, Merdzhanova A et al. Association Between Serum CK-18 Levels and the Degree of Liver Damage in Fructose-Induced Metabolic Syndrome. Metab Syndr Relat Disord 2018; 16 (7): 350–7.
15. Tilg H. The role of cytokines in non-alcoholic fatty liver disease. Dig Dis 2010; 28 (1): 179–85.
16. Pacifico L, Ferraro F, Bonci E et al. Upper limit of normal for alanine aminotransferase: quo vadis? Clin Chim Acta 2013; 422: 29–39.
17. Wang K. Molecular mechanisms of hepatic apoptosis. Cell Death Dis 2014; 5: e996.
18. Gucciardi ME, Malhi H, Mott JL, Gores GJ. Apoptosis and Necrosis in the Liver. Compr Physiol 2013; 3 (2): 977–1010. DOI: 10.1002/cphy.c120020
19. Chen Z, Yu R, Xiong Y et al. A vicious circle between insulin resistance and inflammation in nonalcoholic fatty liver disease. Lipids Health Dis 2017; 16 (1): 203.
20. Asrih M, Jornayvaz FR. Metabolic syndrome and nonalcoholic fatty liver disease: Is insulin resistance the link? Mol Cell Endocrinol 2015; 418: 55–65.
21. Atay K, Canbakan B, Koroglu E et al. Apoptosis and Disease Severity is Associated with Insulin Resistance in Non-alcoholic Fatty Liver Disease. Acta Gastroenterol Belg 2017; 80 (2): 271–7.
22. Jamali R, Arj A, Razavizade M, Aarabi MH. Prediction of Nonalcoholic Fatty Liver Disease Via a Novel Panel of Serum Adipokines. Medicine (Baltimore) 2016; 95 (5): 2630.
2. Perumpail BJ, Khan MA, Yoo ER et al. Clinical epidemiology and disease burden of nonalcoholic fatty liver disease. World J Gastroenterol 2017; 23 (47): 8263–76.
3. Ivashkin V.T., Drapkina O.M., Maev I.V. i dr. Rasprostranennost' nealkogol'noi zhirovoi bolezni pecheni u patsientov ambulatorno-poliklinicheskoi praktiki v Rossiiskoi Federatsii: rezul'taty issledovaniia DIREG 2. Ros. zhurn. gastroenterologii, gepatologii, koloproktologii. 2015; 6: 31–41. [in Russian]
4. Hernaez R, Lazo M, Bonekamp S et al. Diagnostic accuracy and reliability of ultrasonography for the detection of fatty liver: a meta-analysis. Hepatology 2011; 54: 1082–90.
5. Charlton MR, Burns JM, Pedersen RA et al. Frequency and outcomes of liver transplantation for nonalcoholic steatohepatitis in the United States. Gastroenterology 2011; 141: 1249–53.
6. Estes C, Razavi H, Loomba R et al. Modeling the epidemic of nonalcoholic fatty liver disease demonstrates an exponential increase in burden of disease. Hepatology 2018; 67 (1): 123–33.
7. Ivashkin V.T., Maevskaia M.V., Pavlov Ch.S i dr. Klinicheskie rekomendatsii po diagnostike i lecheniiu nealkogol'noi zhirovoi bolezni pecheni Rossiiskogo obshchestva po izucheniiu pecheni i Rossiiskoi gastroenterologicheskoi assotsiatsii. Ros. zhurn. gastroenterologii, gepatologii, koloproktologii. 2016; 2: 24–42. [in Russian]
8. Lazebnik L.B., Radchenko V.G., Golovanova E.V. i dr. Zhirovaia bolezn' pecheni: kliinika, diagnostika, lechenie (rekomendatsii dlia terapevtov, 2-ia versiia). Terapiia. 2017; 3: 6–23. [in Russian]
9. Bedossa P, Poitou C, Veyrie N et al. Histopathological algorithm and scoring system for evaluation of liver lesions in morbidly obese patients. Hepatology 2012; 56 (5): 1751–9.
10. Kanwal F, Kramer JR, Mapakshi S et al. Risk of Hepatocellular Cancer in Patients with Non-alcoholic Fatty Liver Disease. Gastroenterology 2018. pii: S0016-5085(18)34889-3. [Epub ahead of print]
11. Kawanaka M, Nishino K, Nakamura J et al. Correlation between serum cytokeratin-18 and the progression or regression of non-alcoholic fatty liver disease. Ann Hepatol 2015; 14 (6): 837–44.
12. Rahman T, Islam S, Ferdoushi S et al. Association of Serum Cytokeratin-18 Fragment Concentration in Patients with Different Types of Nonalcoholic Fatty Liver Disease. Gastroenterol Hepatol Open Access 2015; 2 (2): 00037.
13. He L, Deng L, Zhang Q et al. Diagnostic Value of CK-18, FGF-21, and Related Biomarker Panel in Nonalcoholic Fatty Liver Disease: A Systematic Review and Meta-Analysis. Biomed Res Int 2017; 2017: 9729107.
14. Bratoeva K, Nikolova S, Merdzhanova A et al. Association Between Serum CK-18 Levels and the Degree of Liver Damage in Fructose-Induced Metabolic Syndrome. Metab Syndr Relat Disord 2018; 16 (7): 350–7.
15. Tilg H. The role of cytokines in non-alcoholic fatty liver disease. Dig Dis 2010; 28 (1): 179–85.
16. Pacifico L, Ferraro F, Bonci E et al. Upper limit of normal for alanine aminotransferase: quo vadis? Clin Chim Acta 2013; 422: 29–39.
17. Wang K. Molecular mechanisms of hepatic apoptosis. Cell Death Dis 2014; 5: e996.
18. Gucciardi ME, Malhi H, Mott JL, Gores GJ. Apoptosis and Necrosis in the Liver. Compr Physiol 2013; 3 (2): 977–1010. DOI: 10.1002/cphy.c120020
19. Chen Z, Yu R, Xiong Y et al. A vicious circle between insulin resistance and inflammation in nonalcoholic fatty liver disease. Lipids Health Dis 2017; 16 (1): 203.
20. Asrih M, Jornayvaz FR. Metabolic syndrome and nonalcoholic fatty liver disease: Is insulin resistance the link? Mol Cell Endocrinol 2015; 418: 55–65.
21. Atay K, Canbakan B, Koroglu E et al. Apoptosis and Disease Severity is Associated with Insulin Resistance in Non-alcoholic Fatty Liver Disease. Acta Gastroenterol Belg 2017; 80 (2): 271–7.
22. Jamali R, Arj A, Razavizade M, Aarabi MH. Prediction of Nonalcoholic Fatty Liver Disease Via a Novel Panel of Serum Adipokines. Medicine (Baltimore) 2016; 95 (5): 2630.
2. Perumpail BJ, Khan MA, Yoo ER et al. Clinical epidemiology and disease burden of nonalcoholic fatty liver disease. World J Gastroenterol 2017; 23 (47): 8263–76.
3. Ивашкин В.Т., Драпкина О.М., Маев И.В. и др. Распространенность неалкогольной жировой болезни печени у пациентов амбулаторно-поликлинической практики в Российской Федерации: результаты исследования DIREG 2. Рос. журн. гастроэнтерологии, гепатологии, колопроктологии. 2015; 6: 31–41. / Ivashkin V.T., Drapkina O.M., Maev I.V. i dr. Rasprostranennost' nealkogol'noi zhirovoi bolezni pecheni u patsientov ambulatorno-poliklinicheskoi praktiki v Rossiiskoi Federatsii: rezul'taty issledovaniia DIREG 2. Ros. zhurn. gastroenterologii, gepatologii, koloproktologii. 2015; 6: 31–41. [in Russian]
4. Hernaez R, Lazo M, Bonekamp S et al. Diagnostic accuracy and reliability of ultrasonography for the detection of fatty liver: a meta-analysis. Hepatology 2011; 54: 1082–90.
5. Charlton MR, Burns JM, Pedersen RA et al. Frequency and outcomes of liver transplantation for nonalcoholic steatohepatitis in the United States. Gastroenterology 2011; 141: 1249–53.
6. Estes C, Razavi H, Loomba R et al. Modeling the epidemic of nonalcoholic fatty liver disease demonstrates an exponential increase in burden of disease. Hepatology 2018; 67 (1): 123–33.
7. Ивашкин В.Т., Маевская М.В., Павлов Ч.С и др. Клинические рекомендации по диагностике и лечению неалкогольной жировой болезни печени Российского общества по изучению печени и Российской гастроэнтерологической ассоциации. Рос. журн. гастроэнтерологии, гепатологии, колопроктологии. 2016; 2: 24–42. / Ivashkin V.T., Maevskaia M.V., Pavlov Ch.S i dr. Klinicheskie rekomendatsii po diagnostike i lecheniiu nealkogol'noi zhirovoi bolezni pecheni Rossiiskogo obshchestva po izucheniiu pecheni i Rossiiskoi gastroenterologicheskoi assotsiatsii. Ros. zhurn. gastroenterologii, gepatologii, koloproktologii. 2016; 2: 24–42. [in Russian]
8. Лазебник Л.Б., Радченко В.Г., Голованова Е.В. и др. Жировая болезнь печени: клииника, диагностика, лечение (рекомендации для терапевтов, 2-я версия). Терапия. 2017; 3: 6–23. / Lazebnik L.B., Radchenko V.G., Golovanova E.V. i dr. Zhirovaia bolezn' pecheni: kliinika, diagnostika, lechenie (rekomendatsii dlia terapevtov, 2-ia versiia). Terapiia. 2017; 3: 6–23. [in Russian]
9. Bedossa P, Poitou C, Veyrie N et al. Histopathological algorithm and scoring system for evaluation of liver lesions in morbidly obese patients. Hepatology 2012; 56 (5): 1751–9.
10. Kanwal F, Kramer JR, Mapakshi S et al. Risk of Hepatocellular Cancer in Patients with Non-alcoholic Fatty Liver Disease. Gastroenterology 2018. pii: S0016-5085(18)34889-3. [Epub ahead of print]
11. Kawanaka M, Nishino K, Nakamura J et al. Correlation between serum cytokeratin-18 and the progression or regression of non-alcoholic fatty liver disease. Ann Hepatol 2015; 14 (6): 837–44.
12. Rahman T, Islam S, Ferdoushi S et al. Association of Serum Cytokeratin-18 Fragment Concentration in Patients with Different Types of Nonalcoholic Fatty Liver Disease. Gastroenterol Hepatol Open Access 2015; 2 (2): 00037.
13. He L, Deng L, Zhang Q et al. Diagnostic Value of CK-18, FGF-21, and Related Biomarker Panel in Nonalcoholic Fatty Liver Disease: A Systematic Review and Meta-Analysis. Biomed Res Int 2017; 2017: 9729107.
14. Bratoeva K, Nikolova S, Merdzhanova A et al. Association Between Serum CK-18 Levels and the Degree of Liver Damage in Fructose-Induced Metabolic Syndrome. Metab Syndr Relat Disord 2018; 16 (7): 350–7.
15. Tilg H. The role of cytokines in non-alcoholic fatty liver disease. Dig Dis 2010; 28 (1): 179–85.
16. Pacifico L, Ferraro F, Bonci E et al. Upper limit of normal for alanine aminotransferase: quo vadis? Clin Chim Acta 2013; 422: 29–39.
17. Wang K. Molecular mechanisms of hepatic apoptosis. Cell Death Dis 2014; 5: e996.
18. Gucciardi ME, Malhi H, Mott JL, Gores GJ. Apoptosis and Necrosis in the Liver. Compr Physiol 2013; 3 (2): 977–1010. DOI: 10.1002/cphy.c120020
19. Chen Z, Yu R, Xiong Y et al. A vicious circle between insulin resistance and inflammation in nonalcoholic fatty liver disease. Lipids Health Dis 2017; 16 (1): 203.
20. Asrih M, Jornayvaz FR. Metabolic syndrome and nonalcoholic fatty liver disease: Is insulin resistance the link? Mol Cell Endocrinol 2015; 418: 55–65.
21. Atay K, Canbakan B, Koroglu E et al. Apoptosis and Disease Severity is Associated with Insulin Resistance in Non-alcoholic Fatty Liver Disease. Acta Gastroenterol Belg 2017; 80 (2): 271–7.
22. Jamali R, Arj A, Razavizade M, Aarabi MH. Prediction of Nonalcoholic Fatty Liver Disease Via a Novel Panel of Serum Adipokines. Medicine (Baltimore) 2016; 95 (5): 2630.
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2. Perumpail BJ, Khan MA, Yoo ER et al. Clinical epidemiology and disease burden of nonalcoholic fatty liver disease. World J Gastroenterol 2017; 23 (47): 8263–76.
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Авторы
О.П.Дуданова1, А.А.Шиповская1, И.В.Курбатова2, Н.А.Ларина1
1. ФГБОУ ВО «Петрозаводский государственный университет». 185910, Россия, Петрозаводск, пр. Ленина, д. 33;
2. ФГБУН «Федеральный исследовательский центр “Карельский научный центр РАН”». 185910, Россия, Петрозаводск, ул. Пушкинская, д. 11
*odudanova@gmail.com
1. Petrozavodsk State University. 185910, Russian Federation, Petrozavodsk, pr. Lenina, d. 33;
2. Karelia Research Centre of Russian Academy of Sciences. 185910, Russian Federation, Petrozavodsk, ul. Pushkinskaia, d. 11
*odudanova@gmail.com
1. ФГБОУ ВО «Петрозаводский государственный университет». 185910, Россия, Петрозаводск, пр. Ленина, д. 33;
2. ФГБУН «Федеральный исследовательский центр “Карельский научный центр РАН”». 185910, Россия, Петрозаводск, ул. Пушкинская, д. 11
*odudanova@gmail.com
________________________________________________
1. Petrozavodsk State University. 185910, Russian Federation, Petrozavodsk, pr. Lenina, d. 33;
2. Karelia Research Centre of Russian Academy of Sciences. 185910, Russian Federation, Petrozavodsk, ul. Pushkinskaia, d. 11
*odudanova@gmail.com
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