Markers of inflammation in patents with type 2 diabetes and cardiovascular form of diabetic autonomous neuropathy
https://doi.org/10.14341/2072-0351-5705
Abstract
Aim.
To determine the level of inflammation markers and their relation to endothelial dysfunction and insulin resistance in patents with type 2 diabetesmellitus and cardiovascular form of diabetic autonomous neuropathy.
Materials and methods.
A total of 87 patients aged 45-66 years were examined for blood insulin level, insulin resistance index (HOMA-IR), CRP,and anti-inflammatory cytokine (TNF-a, IL-1-beta, IL-6) levels. Endothelial dysfunction was estimated based on quantitative Willebrand factorassay. Vegetative disorders were detected from reflex cardiovascular ECG data.
Results.
The development of cardiovascular form of diabetic autonomous neuropathy in patents with type 2 diabetes depended on diabetes duration,quality of carbohydrate metabolism compensation, levels of hyperinsulinemia and insulin resistance. Mean levels of Willebrand factors andinflammation markers in patents with type 2 diabetes and overt vegetative dysfunction were significantly higher than in diabetic patients withoutautonomous neuropathy. Correlation analysis revealed significant correlation of CRP and IL-6 levels with results of standard ECG tests.
Conclusion.
Results of the study demonstrate chronic inflammation in patents with type 2 diabetes and cardiovascular form of diabetic autonomousneuropathy. Increased level of inflammation markers and its relation to severity of vegetative disorders and endothelial dysfunction confirm the roleof inflammation in pathogenesis of nervous co-morbidity in patents with type 2 diabetes.
To determine the level of inflammation markers and their relation to endothelial dysfunction and insulin resistance in patents with type 2 diabetesmellitus and cardiovascular form of diabetic autonomous neuropathy.
Materials and methods.
A total of 87 patients aged 45-66 years were examined for blood insulin level, insulin resistance index (HOMA-IR), CRP,and anti-inflammatory cytokine (TNF-a, IL-1-beta, IL-6) levels. Endothelial dysfunction was estimated based on quantitative Willebrand factorassay. Vegetative disorders were detected from reflex cardiovascular ECG data.
Results.
The development of cardiovascular form of diabetic autonomous neuropathy in patents with type 2 diabetes depended on diabetes duration,quality of carbohydrate metabolism compensation, levels of hyperinsulinemia and insulin resistance. Mean levels of Willebrand factors andinflammation markers in patents with type 2 diabetes and overt vegetative dysfunction were significantly higher than in diabetic patients withoutautonomous neuropathy. Correlation analysis revealed significant correlation of CRP and IL-6 levels with results of standard ECG tests.
Conclusion.
Results of the study demonstrate chronic inflammation in patents with type 2 diabetes and cardiovascular form of diabetic autonomousneuropathy. Increased level of inflammation markers and its relation to severity of vegetative disorders and endothelial dysfunction confirm the roleof inflammation in pathogenesis of nervous co-morbidity in patents with type 2 diabetes.
About the Authors
Irina Arkad'evna Bondar'
State Medical University, Novosibirsk; Novosibirsk Regional Clinical Hospital, Novosibirsk
Olesya Yur'evna Shabel'nikova
State Medical University, Novosibirsk; Novosibirsk Regional Clinical Hospital, Novosibirsk
References
1. Верткин А.Л., Ткачева О.Н., Новикова И.М. Безболевая ишемия и диабетическая автономная нейропатия // Рус. мед. журнал. - 2005. - Т. 13. № 5. - С. 1036-1038.
2. Бондарь И.А., Демин А.А., Королева Е.А. Диабетическая автономная нейропатия. Новосибирск: Изд-во НГТУ. - 2006. - C. 164.
3. Tesfaye S., Chaturvedi N., Eaton S.E. et al. EURODIAB Prospectiv Complications Study Grup. Vascular risk factors and diabetic neuropathy //N. Engl. J. Med. - 2005. - Vol. 352. - № 4. -P. 341-50.
4. Vinik Aaron I., et al., Diabetic Autonomic Neuropathy // Diabetes Care. - 2003. - Vol. 26. - P. 1553-1579.
5. Katz S.D., Rao R., Berman J. et al. A simple bedside test of 1-minute heart rate variability during deep breathing as a prognostic index after myocardial infarction // Circulation. - 1994. - Vol. 90. - P. 12-16.
6. Anderson E.A., Balon T.W. Hoffman R.P. et al. Insulin increases sympathetic activity but not blood pressure in borderline hypertensive humans // Hypertension. - 1992. - Vol. 19. - P. 321-327.
7. Hausberg M., Hoffman R.P., Somers V.K., et al. Contrasting autonomic and hemodinamic effects of insulin in healthy elderly versus young subjects // Hypertension. - 1997. - Vol. 29. - P. 700-705.
8. Hasegawa G., Nakano K., Sawada M. et al. Possible role of tumor necrosis factor and interleukin-1 in the development of diabetic nephropathy // Kidney Int. - 1991. - Vol. 40. - P. 1007-1012.
9. Dalla Vestra M., Mussap M., Gallina P. et al. Acute-phase markers of inflammation and glomerular structure in patients with type 2 diabetes // J. Am. Soc. Nephrol. - 2005. - Vol. 16. - P. S78-S82.
10. Navarro J.F., Mora C., Mac'a M., et al. Inflammatory parameters are independently associated with urinary albumin excretion in type 2 diabetes mellitus // Am. J. Kidney Dis. - 2003. - Vol. 42. P. 53-61.
11. Navarro J.F., Mora C., Rivero A. et al. Urinary protein excretion and serum tumor necrosis factor in diabetic patients with advanced renal failure: Effects of pentoxifylline administration // Am. J. Kidney Dis. - 1999. - Vol. 33. - P. 458-463.
12. Joussen A.M., Poulaki V., Le M.L. et al. A central role for inflammation in the pathogenesis of diabetic retinopathy // FASEB J. - 2004. - Vol. 18. - P. 1450-1452.
13. Stehouwer C.D., Gall M.A., Twisk J.W., et al. Increased urinary albumin excretion, endothelial dysfunction, and chronic low-grade inflammation in type 2 diabetes: progressive, interrelated, and independently associated with risk of death // Diabetes. - 2002. - Vol. 51. - P. 1157- 65.
14. Ewing D.J., Martin C.N., Young R.J., Clarke B.F. The value of cardiovascular autonomic function tests: 10 years' experience in diabetes // Diabetes Care. - 1985. - Vol. 8. - P. 491-498.
15. Kemple P. Neuropathies. Pathomechanism, clinical presentation, diagnosis, therapy. Springe. - 2002. - P. 208.
16. Festa A., D'Agostino R.Jr., Howard G., et al. Chronic subclinical inflammation as part of the insulin resistance syndrome: the Insulin Resistance Atherosclerosis Study (IRAS) // Circulation - 2000. - Vol. 102. - P. 42-47.
17. Клебанова Ф.М., Балаболкин М.И., Креминская В.М. Значение жи- ровой ткани и ее гормонов в механизмах инсулиновой резистентно- сти и развитии сахарного диабета 2 типа // Клин. мед. - 2007. - №7. - С. 20-27.
18. Cersosimo E., DeFronzo R.A. Insulin resistance and endothelial dysfunction: the road map to cardiovascular diseases // Diabetes. Metab. Res. Rev. - 2006. - Vol. 22. - P. 423-436.
19. Boneu B., Abbal M., Plante J., et al. Bierme R. Factor VIII complex and endothelial damage // Lancet. - 1975. - Vol. 30. - P. 325-333.
20. Satoh J., Yagihashi S., Toyota T. The possible role of tumor necrosis factoralpha in diabetic polyneuropathy // Exp. Diabesity Res. - 2003. - Vol. 4. - P. 65-71.
21. Miranda T. Schram, Nish Chaturvedi, Casper Schalkwijk, et al. Vascular Risk Factors and Markers of Endothelial Function as Determinants of Inflammatory Markers in Type 1 Diabetes // Diabetes Care. 2003. - Vol. 6. - P. 2165-2173.
22. Weyer C., Yudkin J.S., Stehouwer C.D., et al. Humoral markers of inflammation and endothelial dysfunction in relation to adiposity and in vivo insulin action in Pima Indians // Atherosclerosis. - 2002. - Vol. 161. - P. 233-242.
23. Esler M. Magdalena R., Wiesner G et al. // Am. J. Hipertens. - 2001. - Vol. 14 - P. 304-309.
Review
For citations:
Bondar' I.A., Shabel'nikova O.Yu. Markers of inflammation in patents with type 2 diabetes and cardiovascular form of diabetic autonomous neuropathy. Diabetes mellitus. 2009;12(4):51-55. (In Russ.) https://doi.org/10.14341/2072-0351-5705
Views:
2458
This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License (CC BY-NC-ND 4.0).
Email this article 
