Роль адипокинов и цитокинов в патогенезе псориаза у пациентов с сопутствующими метаболическими нарушениями
Оригинальные статьи
Дата публикации: апреля 11, 2018
Ключевые слова
псориаз
метаболические нарушения
патогенез
адипокины
цитокины.
метаболические нарушения
патогенез
адипокины
цитокины.
Как цитировать
Хобейш М., Сысоев К., Соколовский Е., Лапин С. Роль адипокинов и цитокинов в патогенезе псориаза у пациентов с сопутствующими метаболическими нарушениями // Кремлевская медицина. Клинический вестник. 2018. Т. № 1. С. 26-35.
Аннотация
Актуальность. Псориаз - системное иммуноассоциированное заболевание с характерным коморбидным фоном. Проявления метаболического синдрома у пациентов с псориазом - это изменения, развивающиеся на фоне системного иммуно- ассоциированного воспалительного процесса и, в свою очередь, способствующие прогрессированию хронического воспаления. Материал и методы. Под наблюдением находилось 36 пациентов с псориазом. Целью исследования было определение содержания основных адипокинов, цитокинов в сыворотке периферической крови и проведение корреляционного ана- лиза со степенью тяжести, активностью псориаза, характером метаболических нарушений. Результаты исследования и выводы. Полученные данные позволили судить об адипокинах как посредниках между иммунной и эндокринной системами. Нарушение баланса между провоспалительными и противовоспалительными эффектами адипокинов, наблюдаемое при псориазе, демонстрирует дисфункцию липидного обмена как один из возможных провоцирующих факторов хронического воспаления, определяющих тяжесть основного заболевания. Уровни адипокинов и цитокинов при этом, вероятно, являются ранними биологическими маркерами тяжести процесса у пациентов с метаболическим синдромом и псориазом, контроль за которыми можно использовать для оптимизации терапии.Литература
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2. E. Daude´ n et al. Clinical practice guideline for anintegrated approach to comorbidity in patients with psoriasis.JEADV 2013; 27: 1387–1404.
3. Gisondi P., Del Giglio M., Di Francesco V. et al. Weightloss improves the response of obese patients with moderate-toseverechronic plaque psoriasis to low-dose cyclosporine therapy:a randomized, controlled, investigator-blinded clinical trial.Am. J. Clin. Nutr. 2008; 88: 1242–1247.
4. Armstrong A.W., Gelfand J.M., Boehncke W.H.,Armstrong E.J. Cardiovascular comorbidities of psoriasis andpsoriatic arthritis: a report from the GRAPPA 2012 annualmeeting. J. Rheumatol. 2013; 40(8): 1434-1437.
5. Buckley C., Cavill C., Taylor G. et al. Mortality inpsoriatic arthritis - a single-center study from the UK. J.Rheumatol. 2010; 37: 2141–2144.
6. Tam L.S., Tomlinson B., Chu T.T. et al. Cardiovascularrisk proile of patients with psoriatic arthritis compared tocontrols—the role of inlammation. Rheumatology (Oxford).2008; 47: 718–723.
7. Lin H.W., Wang K.H., Lin H.C. Increased risk ofacute myocardial infarction in patients with psoriasis: a 5-yearpopulation-based study in Taiwan. J. Am. Acad. Dermatol.2011; 64(3): 495–501.
8. Клинические рекомендации. Псориаз. Российскоеобщество дерматовенерологов и косметологов. М.: 2016.47
9. Клинические рекомендации. Псориатический артрит. Российское общество дерматовенерологов и косметологов. Ассоциация ревматологов России. М.: 2016.59
10. Wahren J., K. Ekberg, J. Johansson et al., Role ofC-peptide in human physiology, Am. J. Physiol. 2000; 278(5):E759–E768.
11. Luppi P., X. Geng, V. Cifarelli, P. Drain, and M.Trucco, C-peptide is internalised in human endothelial andvascular smooth muscle cells via early endosomes. Diabetologia.2009; 52(10): 2218–2228.
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13. Walcher D., M. Aleksic, V. Jerg et al. C-peptideinduces chemotaxis of human CD4-positive cells: involvementof pertussis toxin-sensitive G-proteins and phosphoinositide3-kinase. Diabetes. 2004; 53(7): 1664–1670.
14. Walker J.N., Ramracheya R., Zhang Q. et al. Regulationof glucagon secretion by glucose: paracrine, intrinsic or both?Diabetes Obes Metab. 2011; 13(Suppl. 1): 95–105.
15. Wahren J., Larsson C. C-peptide: New findings andtherapeutic possibilities. Diabetes Res. Clin. Pract. 2015; 107:309–319.
16. Khatib N., Gaidhane S., Gaidhane A.M. et al. Ghrelin:ghrelin as a regulatory peptide in growth hormone secretion. J.Clin. Diagn. Res. 2014; 8: 13-17.
17. Wittekind D.A., Kluge M. Ghrelin in psychiatricdisorders - A review. Psychoneuroendocrinology. 2015; 52: 176194.
18. Dixit V.D., Schaffer E.M., Pyle R.S. et al. Ghrelininhibits leptin- and activation-induced proinflammatorycytokine expression by human monocytes and T cells. J. Clin.Investigat. 2004; 114(1): 57–66.
19. Campbell J.E., Drucker D.J. Pharmacology, physiology,and mechanisms of incretin hormone action. Cell. Metab. 2013Jun 4; 17(6): 819-837.
20. Vykoukal D., Davies M.G.Vascular biology of metabolicsyndrome. J. Vasc. Surg. 2011; 54: 819–831.
21. Gerkowicz A., Pietrzak A., Szepietowski J.C., Radej S.,Chodorowska G. Biochemical markers of psoriasis as a metabolicdisease. Folia Histochem. Cytobiol. 2012; 50(2): 155–170.
22. Festa A., D’Agostino R. Jr., Tracy R.P., Haffner S.M.Insulin Resistance Atherosclerosis Study. Elevated levels ofacutephase proteins and plasminogen activator inhibitor-1predict the development of type 2 diabetes: the insulinresistance atherosclerosis study. Diabetes. 2002; 51: 1131–1137.
23. Trost S., Pratley R., Sobel B. Impaired fibrinolysis andrisk for cardiovascular disease in the metabolic syndrome andtype 2 diabetes. Curr. Diab. Rep. 2006; 6: 47–54.
24. Procaccini C., Pucino V., Mantzoros C.S., Matarese G.Leptin in autoimmune diseases. Metabolism. 2015; 64: 92-104.
25. Stofkova A. Leptin and adiponectin: from energy andmetabolic dysbalance to inflammation and autoimmunity.Endocr. Regul. 2009; 43: 157–168.
26. Naldi L., Chatenoud L., Linder D. et al. Cigarettesmoking, body mass index, and stressful life events as risk factorsfor psoriasis: results from an Italian case control study. J. Invest.Dermatol. 2005; 125: 61–67.
27. Cerman A.A., Bozkurt S., Sav A. et al. Serum leptinlevels, skin leptin and leptin receptor expression in psoriasis. Br.J. Dermatol. 2008; 159: 820–826.
28. Johnston A., Arnadottir S., Gudjonsson J.E. et al.Obesity in psoriasis: leptin and resistin as mediators of cutaneousinflammation. Br. J. Dermatol. 2008; 159: 342–350.
29. Cerman A.A., Bozkurt S., Sav A. et al. Serum leptinlevels, skin leptin and leptin receptor expression in psoriasis. Br.J. Dermatol. 2008; 159: 820–826
30. Kang S-W., Kim M.S., Kim H-S. et al. Celastrolattenuates adipokineresistinassociated matrix interaction andmigration of vascular smooth muscle cells. J. Cell. Biochem.2013; 114(2): 398–408.
31. Verma S., Li S.H., Wang C.H. et al. Resistin promotesendothelial cell activation: further evidence of adipokineendothelialinteraction. Circulation. 2003; 108: 736-740.
32. Silswal N., Singh A.K., Aruna B. et al. Human resistinstimulates the proinflammatory cytokines TNF-alpha and IL-12in macrophages by NF-kappa B-dependent pathway. Biochem.Biophys. Res. Commun. 2005; 334: 1092-1101.
33. Osawa H., Onuma H., Ochi M. et al. Resistin SNP420 determines its monocyte mRNA and serum levels inducingtype 2 diabetes. Biochem. Biophys. Res. Commun. 2005; 335:596–602.
34. Minn A.H., Patterson N.B., Pack S. et al. Resistin isexpressed in pancreatic islets. Biochem. Biophys. Res. Commun.2003; 310: 641–645.
35. Versini M., Jeandel P.-Y., Rosenthal E., ShoenfeldY. Obesity in autoimmune diseases: Not a passive bystander.Autoimmun. Rev. 2014; 13: 981–1000.
36. Brown J.E., Onyango D.J., Ramanjaneya M. et al.Visfatin regulates insulin secretion, insulin receptor signallingand mRNA expression of diabetes-related genes in mousepancreatic beta-cells. J. Mol. Endocrinol. 2010; 44(3): 171–178.
37. Coimbra S., Figueiredo A., Castro E. et al. The rolesof cells and cytokines in the pathogenesis of psoriasis. Int. J.Dermatol. 2012; 51(4): 389–395.