QUANTIFICATION OF APOLIPOPROTEIN-A-I AND APOLIPOPROTEIN-B MESSENGER-RNA IN HEAVY DRINKERS ACCORDING TO LIVER-DISEASE

It has previously been shown that, in heavy drinkers, serum apolipopro tein A-I (ApoA-I) levels are closely related to the degree of Liver in jury: they are at a maximum in patients with steatosis, begin to decre ase in patients with fibrosis, and reach a minimum in patients with se vere cirrhosis. In contrast with serum ApoA-I variations, serum apolip oprotein B (ApoB) levels are stable. The assessment of messenger RNA ( mRNA) levels of ApoA-I and ApoB using a quantitative competitive polym erase chain reaction (PCR) method was performed in 18 alcoholic patien ts: 8 with normal livers or steatosis (group I), 6 with fibrosis or no nsevere cirrhosis (group II), and 4 with severe cirrhosis (group III). For ApoA-I; group I had higher serum levels (208.4 +/- 37.6 mg/dL mea n +/- SE) and mRNA levels (0.51 +/- 0.12) than group II (serum 116 +/- 19 mg/dL;, P < .01, mRNA 0.40 +/- 0.11, P < .09) or group III (serum 56.5 +/- 28.6 mg/dL, P < .01, mRNA 0.27 +/- .02, P = .008). For ApoB, the three groups had similar serum ApoB levels: 129.9 +/- 37.7, 121 +/ - 51, 120.7 +/- 57.4 mg/dL. Group I presented higher levels of ApoB mR NA than those of group III (0.68 +/- 0.21 vs. 0.41 +/- 0.18, P < .06). There was a significant correlation between serum and mRNA levels of ApoA-I (r = .65, P = .003) but no correlation between serum and mRNA l evels of ApoB (r = .19, NS). We suggest that (1) steatosis is associat ed with increased ApoAI mRNA; (2) fibrosis is associated with decrease d serum ApoA-I, probably caused by a posttranscriptional mechanism; (3 ) severe alcohol-induced cirrhosis is associated with a nonspecific de crease in ApoA-I and ApoB mRNA; and (4) in contrast to ApoA-I mRNA, th e ApoB mRNA level makes a slight contribution to the ApoB serum concen tration.