[Hyperammonemia induced by propranolol in cirrhotic patients. Role of the kidney and influence of the severity of the cirrhosis]. / Hyperammoniémie induite par le propranolol chez le cirrhotique. Rôle du rein et influence de la gravité de la cirrhose.

The effect of the intravenous injection of 0.1 mg/kg of propranolol on arterial ammonemia was studied in 30 patients with alcoholic cirrhosis comparatively with 10 healthy volunteers. Moreover, in 20 patients in the cirrhotic group (10 were Pugh's grade A or B and 10 others were grade C), left renal vein catheterization was performed to follow the changes in ammonemia and glutaminemia levels simultaneously with those occurring in arterial blood. After 30 min, arterial ammonemia was significantly increased in the controls (p less than 0.02) and in the cirrhotic patients (p less than 0.001). The renal venous ammonemia was also significantly increased in all of the cirrhotic patients (p less than 0.01). In the grade A and B patients, the increase in ammonemia was more marked in the renal vein as compared with that in arterial blood (p less than 0.001). In contrast, in the grade C patients, the increase in ammonemia did not differ significantly between the two sectors. The difference in ammonia concentration between arterial and renal venous blood increased significantly after 30 min in the grade A and B patients (p less than 0.001) whereas it was stable in the grade C patients. The changes of glutaminemia in arterial and renal venous blood were not significantly different in the two groups of cirrhotic patients. These data show that, in our experimental conditions, propranolol induces arterial hyperammonemia in cirrhotic patients and that the kidney could interfere with the mechanism of hyperammonemia, at least in grade A and B patients.

Relationships between 34 HLA-A, HLA-B and HLA-DR antigens and three serological markers of viral infections in alcoholic cirrhosis.

In order to study the genetic risk of alcoholic cirrhosis, the frequency of 26 HLA-A and -B antigens was compared in 184 normal controls, 175 alcoholic cirrhotic patients and 83 alcoholic patients with hepatic steatosis of carefully selected ethnic origin. Eight HLA-DR antigens were also determined in 95 subjects of the normal control group and 63 patients of the alcoholic cirrhosis group. The incidence of hepatitis B virus antibodies (anti-HBc and anti-HBs) was defined in 74 patients of the alcoholic steatosis group, 170 patients of the alcoholic cirrhosis group and 111 normal controls different from the previously mentioned normal control group. The incidence and the titers of cytomegalovirus and rubella antibodies were also determined in 93 patients of the alcoholic cirrhosis group and the 111 normal controls. Serum immunoglobulin concentrations were measured in the same 93 cirrhotic patients. Compared with the controls, the alcoholic cirrhosis group revealed a significantly higher frequency of HLA-B15 (21.7 vs. 9.8%, p less than 0.00025, corrected p less than 0.050) and HLA-DR4 (38.1 vs. 17.9%, p less than 0.005, corrected p less than 0.050) and a significantly lower frequency of HLA-B13 (2.9 vs. 11.4%, p less than 0.025, corrected p less than 0.050). As for the frequency of all other HLA antigens, there was no significant difference between the three groups (normal controls, alcoholic cirrhosis and alcoholic steatosis).(ABSTRACT TRUNCATED AT 250 WORDS)

Frequencies of glyoxalase I phenotypes as biological markers in chronic alcoholism.

Biological markers for alcoholism would be a valuable tool for early diagnosis. We have studied the phenotype frequencies of genetically determined erythrocyte enzymes in 397 alcoholics, including two populations with liver disease: steatosis (n = 86) and cirrhosis (n = 128) and a population of alcoholics without apparent liver disease (n = 183) compared to a well selected control population (n = 177). Only for Glyoxalase I (GLO) phenotypes (1,2 and 2-1) were significant differences found between the male controls and the male alcoholics. In the total male alcoholic population the frequency of phenotype 1 was significantly increased (23.2% vs. 11%, p less than 0.02), and the frequency of phenotype 2 was significantly decreased (32.3% vs. 46.3 p less than 0.02) compared to the male control population. For normal women the frequency of phenotype 1 and 2 was significantly different from normal men. (1: +177% p less than 0.001, 2: -45% p less than 0.01), but no significant differences were found between alcoholic and normal women. Our results suggest that in male subjects Glyoxalase I phenotype 1 may provide a marker for predisposition to alcoholism.

[Hepatitis B virus, serological markers of viral infections and humoral immunity in alcoholic cirrhosis]. / Virus de l'hépatite B, marqueurs sérologiques d'infections virales et immunité humorale au cours de la cirrhose alcoolique.

In order to define the role of hepatitis B virus (HBV) in alcoholic liver disease and to study the relationship between HBV and other common viruses, the serological markers of viral disease (HBV, Rubella, Polio, Herpes, and Cytomegalovirus-CMV) were compared in 163 patients with alcoholic cirrhosis (group C), 100 patients with alcoholic steatosis (group S) and in 168 non-alcoholic control subjects (group NA). A significantly increased prevalence of HBV markers in group C was related to the presence of anti-HBc antibodies, in 10.5 p. 100 of cirrhotic patients, vs. 1.2 p. 100 in group S and 1 p. 100 in group NA (p less than 0.01). In cirrhotic patients with HBV markers (HBV +) incidence of alcoholic hepatitis was 4 times lower and the total duration of alcohol overconsumption was significantly lower than in cirrhotic patients without these markers (HBV-). Hepatic function tests were not different in HBV + and HBV- cirrhotic patients, excepted for the ASAT/ALAT ratio (1.55 +/- 0.10 vs. 1.92 +/- 0.12; p less than 0.05). Prevalence of anti-CMV antibodies, and anti-herpes greater than 1/100 antibodies, was significantly increased in S and C groups (p less than 0.01). Anti-Rubella, Polio, and CMV antibody titers were higher (p less than 0.05) in HBV + than in HBV- cirrhotic patients. In cirrhotic subjects, titers of these 3 anti-virus antibodies were not related to alcoholic hepatitis or to IgG and IgM concentrations.(ABSTRACT TRUNCATED AT 250 WORDS)

[Prevalence of HLA-A and -B antigens, anti-HBc and -HBs antibodies in alcoholic hepatopathies]. / Prévalence des antigènes HLA-A et B, des anticorps anti-HBc et anti-HBs au cours des hépatopathies alcooliques.

The frequency of 26 HLA-A and B antigens and of antibodies to the hepatitis B core antigen (anti-HBc) and surface antigen (anti-HBs) has been studied in 150 alcoholic patients divided into 3 groups: I) n = 50, isolated hepatic steatosis; II) n = 50, acute alcoholic hepatitis +/- cirrhosis; III) n = 50, cirrhosis without acute alcoholic hepatitis. For the control group 184 blood donors were selected. In all these subjects, as in all the alcoholic patients, the Alsatian origin of four grand parents was proved. An increased frequency of HLA-B15 was observed in group III (34 p. 100) compared to the control group (9.8 p. 100) (corrected p less than 0.001). There was no significant difference between the four groups for all the other HLA antigens. In group III, the prevalence of anti-HBc and/or anti-HBs was higher in patients with HLA-B15 (64.7 p. 100) than in patients without this antigen (15.1 p. 100) (p less than 0.001). In groups I and II, there was no significant difference. These results suggest that there is a genetic predisposition to cirrhosis without acute alcoholic hepatitis, dependent on HLA-B15 antigen. This predisposition could involve the hepatitis B virus.