Growth hormone-stimulated IGF-1 generation in cirrhosis reflects hepatocellular dysfunction

Abstract

Previous studies reported decreased serum IGF-1 levels in cirrhosis. We aimed to correlate GH-stimulated IGF-1 responses with both MELD and Child-Pugh scores and determine the impact of portal hypertension and nutrition on IGF-1 responses. Fifty-three patients (56+/-2 yrs) with cirrhosis were enrolled. Serum IGF-1 levels were measured by RIA before and 24h after a single injection of GH (0.06 mg/kg). Compared to controls, basal IGF-1 levels were significantly decreased in patients with cirrhosis (17.3+/-6.3 vs 13.6+/-5.1, P<0.001). Increments in IGF-1 levels were significantly lower in cirrhotic patients (controls: 133% vs 49% in MELD score <10, 38% in MELD score 11-18, and 13% in MELD score 19-24, p<0.001). 37% of patients had blunted IGF-1 responses. Increments in IGF-1 levels correlated with albumin (r=0.6), portal congestive index (r=0.4), and MAMC (r=0.25). By multivariate analysis, only CP (OR 5.7) and MELD scores (OR 4.5) accurately differentiated between blunted or non-blunted IGF-1 responses and not portal hypertension (OR 0.9) or malnutrition (OR 1.35). Cirrhosis is associated with low IGF-1 levels and an attenuated response to exogenous GH. These findings correlate better with the extent of hepatic dysfunction rather than the presence of portal hypertension or malnutrition.