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Twenty male athletes, mean age 26 years, were studied by a work load test with cycle-ergometer, with increasing power output for 60 minutes until an intensity corresponding to 70% of the individual maximal heart rate was achieved. Ten of them had familial hyperbilirubinemia (Gilbert's syndrome) and ten had been considered as healthy controls. The diagnosis of Gilbert's syndrome was made using the following criteria: unconjugated hyperbilirubinemia, no systemic symptoms, no overt or clinically recognizable haemolysis, normal liver function tests. Blood levels of free fatty acids (FFA) showed a progressive significant increase after muscular exercise in both healthy and Gilbert's syndrome subjects (p < 0.001). The increase was more evident in controls compared to Gilbert's syndrome subjects (p < 0.05). Total and fractionated bilirubin showed no change in both groups. In conclusion, a competitive mechanism between bilirubin and FFA is probably responsible for the lower increase in plasma FFA in Gilbert's syndrome.

To assess the value of type III procollagen peptide (sPIIIP) as a marker of hepatic fibrosis, sera from 73 patients with alcohol-related liver disease and 30 patients with idiopathic hemochromatosis (IHC) were studied by a specific radioimmunoassay. sPIIIP was increased in 87% of 30 patients with cirrhosis, in 16% of 32 with steatofibrosis but in none of 11 with steatosis. There was a significant correlation with histologic hepatocellular necroinflammation (r = 0.42, p less than 0.01), but not with hepatic fibrosis. sPIIP was increased in 33% of 30 patients with IHC, whether or not they had cirrhosis or fibrosis, and whatever the level of iron overload or the extent of the hepatic deterioration. IHC patients with increased levels of sPIIIP had a higher prevalence of superimposed hepatic damage than did those with normal procollagen levels (p less than 0.05). Our findings, therefore, weaken the diagnostic value of sPIIIP as an index of connective tissue deposition in the liver, and suggest that, at least in alcohol-related liver disease and IHC, hepatocellular necroinflammation influences the results.