Иммунологические механизмы развития неалкогольной жировой болезни печени у больных подагрой и псевдоподагрой: обзор литературы
https://doi.org/10.14412/1995-4484-2017-560-565
Аннотация
Современные представления о подагре включают в себя как традиционную метаболическую теорию нарушения пуринового обмена и внешнесредового воздействия, так и участие в патологическом процессе иммуновоспалительных факторов. Воспаление является отличительной чертой острой тканевой реакции на кристаллы моноурата натрия при подагре и пирофосфата кальция – при псевдоподагре. Кристаллы взаимодействуют с мембранами плазматических клеток, с активацией NLRP3, протеолитическим расщеплением проинтерлейкина 1β и секрецией зрелого интерлейкина 1β, который модулирует ряд событий, приводящих к активации эндотелиальных клеток и нейтрофилов, что также предшествует жировой дистрофии печени. В данном обзоре подробно рассмотрены последние данные по патогенетическим механизмам, служащим в качестве предикторов развития метаболических сдвигов и неалкогольной жировой болезни печени у больных подагрой.
Об авторе
Д. А. Набиева
Ташкентская медицинская академия
Узбекистан
Узбекистан
100109 Республика Узбекистан, Ташкент, ул. Фараби, 2
Список литературы
1. Ватутин НТ, Смирнова АС, Гриценко ЮП. Диагностика, лечение и профилактика подагры: международные клинические рекомендации 2014 г. Современная ревматология. 2015;9(3):70-2 [Vatutin NT, Smirnova AS, Gritsenko YuP. The diagnosis, treatment and prevention of gout: The 2014 international clinical guidelines. Sovremennaya Revmatologiya = Modern Rheumatology Journal. 2015;9(3):70-2 (In Russ.)]. doi: 10.14412/1996-7012-2015-3-70-72
2. Kuo CF, Grainge MJ, Zhang W, et al. Global epidemiology of gout: prevalence, incidence and risk factors. Nat Rev Rheumatol. 2015;11:649-62. doi: 10.1038/nrrheum.2015.91
3. Martinon F, Glimcher LH. Gout: new insights into an old disease. J Clin Invest. 2006;116(8):2073-5. doi: 10.1172/JCI29404
4. Shih MH, Lazo M, Liu SH, et al. Association between serum uric acid and nonalcoholic fatty liver disease in the US population. J Formos Med Assoc. 2015;114:314-20. doi: 10.1016/j.jfma.2012.11.014
5. Richette P, Doherty M, Pascual E, et al. 2016 updated EULAR evidence-based recommendations for the management of gout. Ann Rheum Dis. 2017;76:29-42. doi: 10.1136/annrheumdis-2016-209707
6. Fattahi MR. The prevalence of metabolic syndrome in non-alcoholic fatty liver disease; a population-based study. Middle East J Digest Dis. 2016,8:131-7. doi: 10.15171/mejdd.2016.18
7. Feldman A, Eder SK, Felder TK, et al. Clinical and metabolic characterization of lean caucasian subjects with non-alcoholic fatty liver. Am J Gastroenterol. 2017;112(1):102-10. doi: 10.1038/ajg.2016.318
8. Busso N, So A. Mechanisms of inflammation in gout. Arthritis Res Ther. 2010;12:206. doi: 10.1186/ar2952
9. Andres M, Quintanilla MA, Sivera F, et al. Silent monosodium urate crystal deposits are associated with severe coronary calcification in asymptomatic hyperuricemia: an exploratory study. Arthritis Rheum. 2016;68:1531-9. doi: 10.1002/art.39581
10. Ларина BH, Барт БЯ, Бродский MC. Клиническое и прогностическое значение гиперурикемии при хронической сердечной недостаточности у больных пожилого возраста. Cердечная недостаточность. 2011;5(67):277-81 [Larina BH, Bart BYa, Brodskii MC. Clinical and prognostic value of hyperuricemia in chronic heart failure in elderly patients. Serdechnaya Nedostatochnost'. 2011;5(67):277-81 (In Russ.)].
11. Kanbay M, Jensen T, Solak Y, et al. Uric acid in metabolic syndrome: from an innocent bystander to a central player. Eur J Intern Med. 2016;29:3-8. doi: 10.1016/j.ejim.2015.11.026
12. Kuo CF, See LC, Luo SF, et al. Gout: an independent risk factor for all-cause and cardiovascular mortality. Rheumatology (Oxford). 2010;49:141-6. doi: 10.1093/rheumatology/kep364
13. Wu SJ, Zhu GQ, Ye BZ, et al. Association between sex-specific serum uric acid and non- alcoholic fatty liver disease in Chinese adults: a large population-based study. Medicine (Baltimore). 2015;94(17):e802. doi: 10.1097/MD.0000000000000802
14. Martinon F. Mechanisms of uric acid crystal-mediated autoinflammation. Immunol Rev. 2010;233:218-32. doi: 10.1111/j.0105-2896.2009.00860.x
15. Насонов ЕЛ, Елисеев МС. Роль интерлейкина 1 в развитии заболеваний человека. Научно-практическая ревматология. 2016;54(1):60-77 [Nasonov EL, Eliseev MS. Role of interleukin 1 in the development of human diseases. Nauchno-Prakticheskaya Revmatologiya = Rheumatology Science and Practice. 2016;54(1):60-77 (In Russ.)]. doi: 10.14412/1995-4484-2016-60-77
16. Perez-Ruiz F, Herrero-Beites AM, Carmona L. A two-stage approach to the treatment of hyperuricemia in gout: The «dirty dish» hypothesis. Arthritis Rheum. 2011;63:4002-6. doi: 10.1002/art.30649
17. Duewell P, Kono H, Rayner KJ, et al. NLRP3 inflammasomes are required for atherogenesis and activated by cholesterol crystals. Nature. 2010;464:1357-61. doi: 10.1038/nature08938
18. Brydges SD, Broderick L, Mcgeough MD, et al. Divergence of IL-1, IL-18, and cell death in NLRP3 inflammasomopathies. J Clin Invest. 2013;123:4695-705. doi: 10.1172/JCI71543
19. Guo H, Callaway JB, Ting JP. Inflammasomes: mechanism of action, role in disease, and therapeutics. Nat Med. 2015;21:677-87. doi: 10.1038/nm.3893
20. Lanaspa MA, Sanchez-Lozada LG, Cicerchi C, et al. Uric acid stimulates fructokinase and accelerates fructosemetabolism in the development of fatty liver. PLoS One. 2012;7 e47948. doi: 10.1371/journal.pone.0047948
21. Kahlenberg JM, Thacker SG, Berthier CC, et al. Inflammasome activation of IL-18 results in endothelial progenitor cell dysfunction in systemic lupus erythematosus. J Immunol. 2011;187:6143- 56. doi: 10.4049/jimmunol.1101284
22. Martin WJ, Shaw O, Liu X, et al. 2011. MSU crystal-recruited non-inflammatory monocytes differentiate into M1-like proinflammatory macrophages in a peritoneal murine model of gout. Arthritis Rheum. 2011;63:1322-32. doi: 10.1002/art.30249
23. Conforti-Andreoni C, Spreafico R, Qian HL, et al. Uric aciddriven Th17 differentiation requires inflammasome-derived IL-1 and IL-18. J Immunol. 2011;187(11):5842-50. doi: 10.4049/jimmunol. 1101408
24. Schauer C, Janko C, Munoz L, et al. Aggregated neutrophil extracellular traps limit inflammation by degrading cytokines and chemokines. Nat Med. 2014;20:511-7. doi: 10.1038/nm.3547
25. Farina G, York M, Collins C, Lafyatis R. dsRNA activation of endothelin-1 and markers of vascular activation in endothelial cells and fibroblasts. Ann Rheum Dis. 2011;70:544-50. doi: 10.1136/ard.2010.132464
26. Perez-Ruiz F, Becker MA. Inflammation: a possible mechanism for a causative role of hyperuricemia/gout in cardiovascular disease. Curr Med Res Opin. 2015;31(Suppl 2):9-14. doi: 10.1185/03007995.2015.1087980
27. Денисов ИС, Елисеев МС, Барскова ВГ. Исходы подагры. Обзор литературы. Часть II. Коморбидные заболевания, риск развития сердечно-сосудистых катастроф и смерти при подагре. Научно-практическая ревматология. 2013;51(6):703-10 [Denisov IS, Eliseev MS, Barskova VG. Gout outcomes. Literature review. Part II. Comorbid diseases, risk of developing cardiovascular catastrophes and death in gout patients. Nauchno- Prakticheskaya Revmatologiya = Rheumatology Science and Practice. 2013;51(6):703-10 (In Russ.)]. doi: 10.14412/1995-4484-2013-703-10
28. Kim SJ, Chae S, Kim H, et al. A protein profile of visceral adipose tissues linked to early pathogenesis of type 2 diabetes mellitus. Mol Cell Proteomics. 2014;13:811-22. doi: 10.1074/mcp.M113.035501
29. Елисеев МС, Барскова ВГ, Насонов ЕЛ. Канакинумаб (ингибитор интерлейкина 1β – прорыв в возможностях противовоспалительной терапии при подагре. Научно- практическая ревматология. 2013;51(4):428-31 [Eliseev MS, Barskova VG, Nasonov EL. Canakinumab (an interleukin 1β inhibitor) is a breakthrough in the possibilities of anti- inflammatory therapy for gout. Nauchno-Prakticheskaya Revmatologiya = Rheumatology Science and Practice. 2013;51(4):428-31 (In Russ.)]. doi: 10.14412/1995-4484-2013-1255
30. Van Bon L, Cossu M, Lof A, et al. Proteomic analysis of plasma identifies the Toll-like receptor agonists S100A8/A9 as a novel possible marker for systemic sclerosis phenotype. Ann Rheum Dis. 2014;73:1585-9. doi: 10.1136/annrheumdis-2013-205013
31. Lupattelli G, de Vuono S, Boni M, et al. Insulin resistance and not BMI is the major determinant of early vascular impairment in patients with morbid obesity. J Atheroscler Thromb. 2013;20:924- 33. doi: 10.5551/jat.18663
32. Petta S, Craxi A. Hepatocellular carcinoma and non-alcoholic fatty liver disease: from a clinical to a molecular association. Curr Pharm Des. 2010;16:741-52. doi: 10.2174/138161210790883787
33. Ekstedt M, Hagstrom H, Nasr P, et al. Fibrosis stage is the strongest predictor for disease-specific mortality in NAFLD after up to 33 years of follow-up. Hepatology. 2015;61(5):1547-54. doi: 10.1002/hep.27368
34. Bass M, Merriman R. Fatty acid metabolism and lipotoxicity in the pathogenesis of NAFLD/NASH. Fatty Liver Disease: NASH and Related Disorders. J Gastroenterol Hepatol. 2010;21:109-22.
35. Otokozawa S, Ai M, Diffenderfer MR, et al. Fasting and postprandial apolipoprotein B-48 levels in healthy, obese, and hyperlipidemic subjects. Metabolism. 2009;58:1536-42. doi: 10.1016/j.metabol.2009.04.040
36. Petta S, Tripodo C, Grimaudo S, et al. High liver RBP4 protein content is associated with histological features in patients with genotype 1 chronic hepatitis C and with nonalcoholic steatohepatitis. Dig Liver Dis. 2011;43:404-10. doi: 10.1016/j.dld.2010.12.013
37. Bedossa P; FLIP Pathology Consortium. Utility and appropriateness of the fatty liver inhibition of progression (FLIP) algorithm and steatosis, activity, and fibrosis (SAF) score in the evaluation of biopsies of nonalcoholic fatty liver disease. Hepatology. 2014;60:565-75. doi: 10.1002/hep.27173
38. Afzali A, Weiss NS, Boyko EJ, et al. Association between serum uric acid level and chronic liver disease in the United States. Hepatology. 2010;52:578-89. doi: 10.1002/hep.23717
39. Mosca A, Nobili V, De Vito R, et al. Serum uric acid concentrations and fructose consumption are independently associated with NASH in children and adolescents. J Hepatol. 2017;66(5):1031-6. doi: 10.1016/j.jhep.2016.12.025
40. Targher G, Marra F, Marchesini G. Increased risk of cardiovascular disease in non- alcoholic fatty liver disease: causal effect or epiphenomenon? Diabetologia. 2008;51:1947- 53. doi: 10.1007/s00125-008-1135-4
41. Yamada T, Suzuki S, Fukatsu M, et al. Elevated serum uric acid is an independent risk factor for nonalcoholic fatty liver disease in Japanese undergoing a health checkup. Acta Gastroenterol Belg. 2010;73:12-7.
42. Hwang IC, Suh SY, Suh AR, et al. The relationship between normal serum uric acid and nonalcoholic fatty liver disease. J Korean Med Sci. 2011;26:386-91. doi: 10.3346/jkms.2011.26.3.386
Рецензия
Для цитирования:
Набиева Д.А. Иммунологические механизмы развития неалкогольной жировой болезни печени у больных подагрой и псевдоподагрой: обзор литературы. Научно-практическая ревматология. 2017;55(5):560-565. https://doi.org/10.14412/1995-4484-2017-560-565
For citation:
Nabieva D.A. IMMUNOLOGICAL MECHANISMS FOR THE DEVELOPMENT OF NONALCOHOLIC FATTY LIVER DISEASE IN PATIENTS WITH GOUT AND PSEUDOGOUT: A REVIEW OF LITERATURE. Rheumatology Science and Practice. 2017;55(5):560-565. (In Russ.) https://doi.org/10.14412/1995-4484-2017-560-565
Просмотров: 666
Послать статью по эл. почте 