Zaigham Abbas, Naila Tariq, Masood Iqbal, Mashoor Alam Shah.
Insulin and C Peptide response, and Antiphospholipid Antibody levels in Hepatitis C related Chronic Liver Disease.
J Coll Physicians Surg Pak Jan ;12(2):67-70.

Objective: Patients with cirrhosis due to hepatitis C (HC) have an increased prevalence of diabetes mellitus. The pathogenic mechanism by which HC predisposes to DM is not clear. The objective of this study was to determine the insulin and C-peptide response to 75 gram oral glucose load and measure anti phospholipid antibody levels in patients with chronic liver disease due to HC. Design: A prospective study. Place and Duration of Study: This study was conducted at the Department of Medicine, Jinnah Postgraduate Medical Centre over a period of three months. Subjects and Methods: An analytical case control study was carried out on 37 patients (M=18, F=19); none of these patients had received interferon. They were divided into four groups; (A) HC cirrhosis with DM (n=9), (B) HC cirrhosis without DM (n=11), (C) Hepatitis B (HB) cirrhosis without DM (n=7), (D) chronic hepatitis C without DM (n=10). Group C and D were taken as controls. Fasting blood samples were taken and repeated after 2 hours of 75-gram oral glucose load (2 hPG). Results: Mean ages of group A, B, C and D were (yr±SD) 51.3±7.6, 48.9±2.4, 33.7±10.8 and 31.7±8.8 respectively. There was no statistically significant difference in the age, Pugh score and body mass index of HC cirrhotic patients with and without DM. Patients of group A had higher fasting and 2 h PG glucose levels (p=0.003 and 0.000) and higher fasting insulin level (p=0.045). However, increments in insulin and C peptide levels 2 h PG were much less (p=0.048 and 0.003). HB cirrhotics without diabetes (group C) behaved just like HC cirrhotic without diabetes (group B). Patients of group D had normal glucose tolerance and insulin and C peptide levels. All four groups had normal antiphospholipid antibody levels. Conclusion: Patients with cirrhosis due to HC and HB show evidence of glucose intolerance in spite of hyperinsulinemia probably due to insulin resistance. HC cirrhotics with diabetes have fasting hyperglycemia in spite of higher insulin levels. They have blunt insulin and C-peptide responses with marked 2 h PG hyperglycemia, which indicates subnormal secretion of insulin and pancreatic islets dysfunction. This response is very similar to usual non-insulin dependent diabetes mellitus.

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