Nonalcoholic steatohepatities in type 2 diabetes mellitus

The present study was conducted on 22 females with type 2 diabetes mellitus and hepatomegaly in whom ultrasonography showed bright hepatomegaly, in addition to 20 healthy controls of comparable age and sex. Patients with evidence of hepatitis C, B, metabolic liver disease or autoimmune hepatitis were excluded. None of the patients and controls was alcohol drinker. In all patients and controls, fasting and two-hour postprandial plasma glucose, HbA1c, bilirubin, aspartate aminotransferase [AST], alanine aminotransferase [ALT], alkaline phosphatase, cholesterol and triglyceride were done. Liver biopsy using Baxter cut needle [G14] was done in patients only. It can be concluded that nonalcoholic steatohepatitis [macrovesicular steatosis and lobular inflammation alone] occurs in 31.8% of patients with hepatic steatosis in type 2 diabetes mellitus. Hepatocyte necrosis and progression to hepatic fibrosis may occur in some cases. Progression to fibrosis may occur in patients with inadequate glycemic control

presence of multiple autoantibodies and its relation to the control of diabetic patients under therapy

The presence of multiple autoantibodies to different islet cell antigen including those to insulin autoantibodies [IAA] islet cell cytoplasm [ICA] and glutamic acid decarboxylase [GAD-Ab] were studied in 70 diabetic patients [30 cases of type I diabetes [IDDM], 30 cases of type II [NIDDM], 10 cases shifted from oral hypoglycemic therapy to insulin, in addition to 20 normal healthy controls]. All were subjected to fasting and postprandial plasma glucose, C-peptide level, glycosylated hemoglobin, insulin antibodies, islet cell cytoplasmic antibodies and glutamic acid decarboxylase antibodies. The obtained results showed that in IDDM group, 23.3% were positive for ICA, 40% were positive for GAD-Ab and 60% were positive for IAA. In NIDDM group, 23.7% were positive for ICA, 36.7% positive for GAD-Ab and 50% were positive for IAA. In the group of patients who shifted recently to insulin therapy, 30% were positive for ICA, 30% positive for GAD-Ab and 90% were positive for IAA. There was a positive correlation between glycosylated hemoglobin with the number of positive antibodies. Cases with no positive antibodies had a significant lower glycosylated hemoglobin level than those with one or more positive antibodies. It was concluded that the presence of both ICA and GAD-Ab was a stronger predictor of rapid B cell loss; hence, there was a more need for insulin therapy