Hepatitis C as a risk factor of diabetes mellitus type 2

• Published in: Revista clínica espanõla Vol. 206; no. 4; p. 167
• Main Authors: Vírseda Chamorro, I, Vírseda Chamorro, M, Prieto Carbajo, R I, Jaqueti Aroca, J
• Format: Journal Article
• Language: Spanish
• Published: Spain 01.04.2006
• Subjects: Diabetes Mellitus, Type 2 - blood; Diabetes Mellitus, Type 2 - etiology; Female; Ferritins - blood; Hepatitis C - blood; Hepatitis C - complications; Humans; Male; Middle Aged; Risk Factors
• ISSN: 0014-2565
• DOI: 10.1157/13086795

Hepatitis C virus (HCV) has been implicated as a risk factor for the development of diabetes mellitus, type 2 (DM2). Our aim is to check if HCV infection in our patients is a risk for the development of DM2. In that case, we study if the possible pathogenic mechanism could be related with an increase in iron deposits. A consecutive series of 305 patients that attended to our service for measurement of anti-HCV antibodies was collected. HCV-antibodies were identified by second generation ELISA and confirmed by immunoblot. We detected viral RNA in 56% of these patients by polymerase chain reaction. The control group was made up of 137 patients. In every case, we analyzed the plasma levels of glucose, ferritin and other biochemical parameters. We found 13% of diabetics in the patient with viral RNA, 9.3% in the infected patients without RNA and 3.9% in the controls. The average of the ferritin level for the infected patients was 256 mg/l and for the controls was 151 mg/l (p = 0.01). The diabetic patients had ferritin levels of 346 mg/l and non-diabetic patients had 218 mg/l (p = 0.038). The presence of HCV-antibodies showed a 2.78 odds ratio for diabetes risk. Our results showed a relationship between HCV infection and diabetes mellitus type 2, so that the percentage of diabetics increased parallelly with the degree of viral activity and the variable "presence of HCV-antibodies" was the one that most contributed to the risk. Although our results would support the role of the iron metabolism in the development of diabetes, follow-up studies of a cohort of patients infected by HCV would be necessary to contrast this statement.