icon_folder.gif   Conference Reports for NATAP  
 
  7th International Workshop on
Adverse Drug Reactions and Lipodystrophy in HIV
November 13-17, 2005
Dublin, Ireland
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Endothelial function is impaired in non-alcoholic steatohepatitis
 
 
  Abstracts presented at the 7th International Workshop on Adverse Drug Reactions and Lipodystrophy in HIV 13-16 November 2005, Dublin, Ireland
 
SS Shankar, N Chalasani and HO Steinberg Indiana University School of Medicine, Indianapolis, IN, USA
 
ABSTRACT 57
Antiviral Therapy 2005; 10:L36
 
Background: Endothelial vascular function, an independent risk factor for cardiovascular disease, is impaired in insulin-resistant states. Non-alcoholic steatohepatitis (NASH) is associated with insulin resistance. However, it is unknown whether subjects with NASH exhibit impaired endothelial function.
 
Hypothesis: We tested the hypothesis that NASH impairs endothelial function. To test this hypothesis, we assessed endothelial function, as well as insulin sensitivity, in subjects with biopsy-proven NASH and controls matched for body mass index (BMI).
 
Materials and methods: We studied four biopsy-proven NASH and six control subjects matched for age, gender and BMI. We assessed lipid parameters by standard procedures and insulin sensitivity using the euglycaemic hyperinsulinaemic clamp technique (120 mu/m2/min). Endothelial vascular function was determined by measuring changes in leg blood flow (LBF) in response to graded intrafemoral arterial infusions of the endothelium dependent vasodilator methacholine (MCh). Results are expressed as mean ±SEM. Comparison between groups was done by unpaired t-test and significance was accepted at a level of P<0.03.
 
Results: BMI was 36.5±4.7 and 36.9±4.8 (kg/m2) in NASH and controls, respectively (P=NS). Total cholesterol was 224±36 vs 177±42mg/dl in NASH and controls, respectively (P=0.05). LDL-cholesterol was 151±30 and 103±29mg/dl NASH and controls, respectively (P=0.05). Triglyceride and HDL-cholesterol levels did not differ between groups. Glucose disposal rates were 3.9 ±1.3 and 6.2±1.9 mg/kg/min NASH and controls, respectively (P=NS). Maximal increments in LBF in response to intraarterial MCh, expressed as a percentage of baseline, were 34±17 vs 193±58% in NASH and controls, respectively (P<0.05).
 
Conclusions: Endothelial function is impaired in subjects with NASH. This impairment is over and above that associated with the obesity of NASH. Whether the endothelial dysfunction is attributable to the elevated LDL-cholesterol levels, or the differences in insulin sensitivity, or to the intrinsic process of NASH itself, requires further investigation.