Fiber morphometry of the external intercostal muscle. Comparison of dominant and nondominant sides in patients with severe COPD]

OBJECTIVES: Contribution of cellular immunity to the onset and perpetuation of alcohol-induced liver damage remains controversial. The aim of this work was to know whether T-cells participate in the pathogenesis of alcoholic liver injury by measuring the serum levels of sIL-2R in alcoholic patients with different degree of hepatic damage. PATIENTS AND METHODS: Fifty two patients and eighteen healthy subjects (Control group) were included. All patients were active drinkers of at least 100 grams/day of ethanol over a ten-years period. Serum sIL-2R was determined by ELISA. Liver biopsy was performed in all patients and liver function tests, serum immunoglobulins and complement proteins C3 and C4 were measured in all participants. The relationship between the sIL-2R and the severity of liver disease was studied. RESULTS: Circulating sIL-2R was higher in the group of patients than in the control (2.388 +/- 275.7 U/ml vs. 795.7 +/- 48.7 IU/mL; p < 0.001). There were not increased circulating sIL2R in those patients with alcoholic hepatitis. However, patients with cirrhosis showed increased serum sIL-2R regardless of the presence of alcoholic hepatitis. Furthermore, serum levels of sIL-2R inversely correlated with hepatic function test (r = -0.69; p < 0.001 for serum albumin; and r = -0.73; p < 0.001 for the prothrombin time) and were highest in those patients of the Child-Turcotte's class C. CONCLUSIONS: Circulating sIL-2R increases in alcoholic cirrhosis. However, our data do not support a contributory role of the cellular immunity, as assessed by circulating sIL-2R levels to the alcoholic liver damage. The increased serum sIL-2R in cirrhosis may result from defective heptic clearance of this molecule.