Soluble interleukin 2 receptor in acute viral hepatitis and chronic liver disease

Serum levels of soluble interleukin 2 receptor were determined in patients with acute viral hepatitis and patients with various chronic liver diseases. In addition, the ability of peripheral blood mononuclear cells of patients with alcoholic cirrhosis to generate soluble interleukin 2 receptor following mitogenic stimulation was studied in vitro. Serum soluble interleukin 2 receptor concentrations in all patients with acute viral hepatitis were found to be significantly elevated (1,319 +/- 527 units per ml) during the first week after onset of disease, as compared to healthy control individuals (375 +/- 102 units per ml; p less than 0.0005) and declined toward normal levels during the course of the illness. Similarly, patients suffering from chronic liver disease such as alcoholic liver cirrhosis (1,172 +/- 507 units per ml), primary biliary cirrhosis (619 +/- 190 units per ml) or chronic active HBsAg+ hepatitis (941 +/- 357 units per ml) showed increased serum soluble interleukin 2 receptor concentrations (p less than 0.0005 vs. controls, respectively). In vitro mitogen stimulation of peripheral mononuclear cells derived from patients with alcoholic cirrhosis resulted in a soluble interleukin 2 receptor production not different from that seen in healthy individuals, suggesting that elevated soluble interleukin 2 receptor serum levels seen in this disease are not the result of an increased synthesis by circulating lymphocytes. Due to the ability of soluble interleukin 2 receptor to bind free interleukin 2--thus making it a potential immunoregulatory molecule--its high serum levels could explain some of the immunologic abnormalities observed in acute and chronic liver disease.     

Clinical Significance of Serum and Urinary Neopterin Levels in Patients with Various Liver Diseases

Serum and urinary neopterin levels were measured by radioimmunoassay in 120 healthy controls, 16 asymptomatic HBsAg carriers, 12 patients with acute hepatitis, 13 with chronic inactive hepatitis, 35 with chronic active hepatitis, 46 with liver cirrhosis, 18 with hepatocellular carcinoma, and 6 with alcoholic liver disease. Serum and urinary neopterin levels were significantly higher in almost all patients than in normal subjects. Neopterin levels were highest in acute hepatitis and correlated with the results of liver function tests, but did not show this correlation in chronic liver disease. In chronic liver disease, the levels of serum neopterin in non-A non-B viral patients was significantly increased, compared with those in B viral and alcoholic patients. The rate of abnormal urinary neopterin levels in chronic liver disease was higher than the rate of abnormal serum neopterin levels, but no difference was observed between the rates of abnormal serum and urinary levels in acute hepatitis and asymptomatic HBsAg carriers. These results indicate that serum and urinary neopterin levels may be useful markers for cell-mediated immunity in liver disease, and that the immune system response in chronic liver disease may be different for different pathogens.     

Clinical significance of serum procalcitonin levels in patients with acute or chronic liver disease

OBJECTIVE: To evaluate the diagnostic value of serum procalcitonin levels in patients with acute or chronic liver disease, with or without bacterial infections and to correlate the results with the clinical outcome and the laboratory findings for these patients. METHODS: One hundred and six consecutive hospitalized patients with liver disease were evaluated for procalcitonin levels on admission. Fifteen of them (14.2%) had acute alcoholic hepatitis on cirrhotic background (group A), 20 (18.9%) had alcoholic cirrhosis without hepatitis and/or bacterial infection (group B), 16 (15.1%) had decompensated cirrhosis with proved bacterial infection (group C), 42 (39.6%) had uncomplicated viral hepatitis-related cirrhosis (group D) and 13 (12.3%) had acute icteric viral hepatitis (group E). Serum procalcitonin levels were measured using an immunoluminometric assay. Statistical analysis was based on Student's t-test and the non-parametric Kruskall-Wallis test (P<0.05). RESULTS: Serum procalcitonin levels were significantly higher in cirrhotic patients with bacterial infection (9.80+/-16.80 ng/ml) than in those without bacterial infection (0.21+/-0.13 ng/ml, P=0.001), whereas they were within normal range (<0.5 ng/ml) in all patients with uncomplicated cirrhosis, irrespective of the cause of cirrhosis. Seven of 15 group A patients (46.2%) and 4/13 group E patients (30.8%), all of them cirrhotics, had procalcitonin levels higher than 0.5 ng/ml on admission, without established bacterial infection. CONCLUSION: Serum procalcitonin levels remain below the threshold of 0.5 ng/ml in all patients with uncomplicated cirrhosis, irrespective of the cause of the disease, while they are significantly elevated when bacterial infection complicates the course of the disease. A significant proportion of patients with acute alcoholic hepatitis on a cirrhotic background as well as of patients with acute on chronic viral hepatitis, without bacterial infection, exhibit serum procalcitonin levels above 0.5 ng/ml, suggesting that this cut-off value is probably not enough to discriminate between patients with or without bacterial infection within these subgroups of patients with liver disease.     

Nonalcoholic liver disease. Overlooked causes of liver injury in patients with heavy alcohol consumption.

Alcoholic subjects with abnormal liver chemistry studies are often assumed to have alcoholic liver disease, even though the diagnosis is not established by liver biopsy. To determine the magnitude of nonalcoholic liver disease in patients with heavy alcohol consumption, the data on 145 consecutive patients judged to consume at least 80 g of alcohol daily for prolonged periods, and who underwent liver biopsy at the University of Chicago, were reviewed. Nonalcoholic liver disease was suspected clinically and confirmed by liver biopsy in 40 (28 per cent), whereas alcoholic liver disease was suspected in 105 but confirmed in only 83 (80 per cent). The remaining 22 patients had liver disorders, including cholangitis or pericholangitis, acute hepatitis or some form of chronic hepatitis, for which they required appropriate therapy. Neither clinical features, hepatitis B surface antigen (HBsAg), anti-HBsAg nor serum glutamic oxaloacetic transaminase to serum glutamic pyruvic transaminase (SGOT:SGPT) ratios distinguished these 22 patients from those with alcoholic liver disease. Thus, liver biopsy is necessary for the identification of nonalcoholic liver disease in patients suspected of harboring alcoholic liver disease, since other clinical features do not allow identification of these patients.     

Significance of plasma glutathione determination in patients with alcoholic and non-alcoholic liver disease

Plasma glutathione levels were determined in 79 patients with various types of liver disease and 18 healthy controls in order to study their significance in the course of liver disease. Plasma was taken at the time of needle liver biopsy. A positive linear correlation was found between plasma and hepatic glutathione concentrations, as has been suggested in experimental animals. In patients with acute viral hepatitis, chronic hepatitis, non-alcoholic liver cirrhosis and alcoholic liver disease, plasma glutathione levels were significantly decreased compared with those in controls. Of importance is the fact that the plasma levels increased after recovery in patients with acute viral hepatitis and after abstinence from alcohol intake in patients with alcoholic liver disease. Determination of plasma glutathione may be valuable in the evaluation of liver disease, particularly in acute viral hepatitis and alcoholic liver disease in which the hepatic content of glutathione is suggested to be decreased. Such patients may be susceptible to oxidative stress and radical-related hepatic injury.     

Serum levels of cytokeratin-18 (tissue polypeptide-specific antigen) in liver diseases.

OBJECTIVE: The tissue polypeptide-specific antigen (TPS, cytokeratin-18, a normal constituent of the hepatocyte cytoskeleton) is a standard tumour marker. This study aimed to evaluate serum TPS levels in patients with liver disease. METHODS: Serum TPS was measured with a commercial immunoassay in 884 individuals (753 outpatients from a liver disease clinic, 131 patients admitted to the hospital with acute liver disease). RESULTS: Abnormally high (> 80 U/l) TPS levels were found in 57.7% (95% CI 54.0-61.3%) of outpatients with liver disease. Elevated TPS levels were observed for all liver diseases, including fatty liver, alcoholic disease, chronic viral hepatitis, autoimmune hepatitis, cholestasis, transplantation, and hepatocarcinoma. TPS levels correlated with liver markers, particularly serum AST. In addition, TPS levels correlated with Knodell's score in patients with chronic hepatitis. TPS was increased in one-third of patients with normal liver enzyme values. Serum TPS levels decreased after specific therapy in patients with hepatitis C and autoimmune hepatitis. Abnormally high TPS levels were found in the vast majority of patients admitted to the hospital, with markedly high (> 800 U/l) values being observed in 47.5% (95% CI 36.1-55.7%) of patients with alcoholic liver disease and in 80.8% (95% CI 60.0-92.7%) of patients with acute hepatitis. CONCLUSIONS: Serum TPS (cytokeratin-18) is elevated in patients with non-malignant liver diseases, particularly in those with prominent cytolysis. Further studies are needed to evaluate the use of TPS as a marker of liver disease.     

Acute viral hepatitis. Course and incidence of progression to chronic hepatitis

In a prospective study, 53 consecutive patients with biopsyproved acute viral hepatitis were observed serially and treated identically during a 15 week period following the onset of jaundice. They were divided into four groups on the basis of the presence or absence of hepatitis-associated antigen (HAA) and the presence or absence of parenteral exposure to a potential source of HAA. Even though the degree of hepatocellular necrosis was greater in the HAA-positive group, irrespective of the portal of entry of HAA, 89.2 per cent of HAA-positive and 83.3 per cent of HAA-negative subjects made equally rapid and complete recovery within 6 weeks after the onset of illness. The development of chronic active hepatitis in the remainder was associated with either the persistence of HAA in the serum beyond the 13th week of illness or the presence of a positive lupus erythematosus test during the first and subsequent weeks of illness. We conclude from this study that in the majority of patients with acute viral hepatitis recovery is complete but that chronic active hepatitis will develop in patients in whom HAA persists beyond 13 weeks of illness or in whom the lupus erythematosus test is positive and antinuclear antibody (ANA) is present at the onset of illness (11.3 per cent).     

Serum activity of mitochondrial aspartate aminotransferase: a sensitive marker of alcoholism with or without alcoholic hepatitis

Serum activity of the mitochondrial isoenzyme of aspartate aminotransferase (mAST) was measured with an immunological method in 74 subjects. Fourty-six were chronic alcoholics with (30) or without (16) obvious alcoholic liver disease; 28 were nonalcoholic controls among whom 14 had acute or chronic viral hepatitis, the remaining 14 being healthy individuals. Mean mAST activity was much higher in all the alcoholic subjects, with or without liver disease, 10.4 and 1.95 units per liter, respectively, than in the healthy controls (0.43, p less than 0.001). The mean mAST to total AST ratio was similar in the healthy controls and in the patients with viral hepatitis (2.98 and 3.19%, NS), whereas it was about 4 times higher in the alcoholics with a sensitivity which reached 93% in the patients with alcoholic liver disease and 100% in those without. Both gamma-glutamyl transpeptidase and glutamate dehydrogenase serum activities were far less sensitive and specific. As almost all chronic alcoholics had similar abnormal values of mAST/total AST ratio, this leads to question whether "normal" liver may really exist in any of such subjects.     

血清蛋白电泳、免疫球蛋白及其轻链测定对肝病患者的临床意义

目的探讨血清中免疫球蛋白和轻链测定以及血清蛋白电泳在肝病患者中的临床应用价值。方法用免疫散射比浊法在特定蛋白分析仪上检测92例肝病患者(包括急性肝炎患者28例、慢性肝炎患者33例、肝硬化患者31例)及45例健康者血清中免疫球蛋白IgG、IgA、IgM以及κ轻链和λ轻链的水平;用琼脂糖凝胶电泳法对所有样本进行血清蛋白电泳检测。结果与对照组相比,急性肝炎组以IgM升高为主,差异有统计学意义(P<0.05);两组κ轻链和λ轻链水平比较,差异无统计学意义(P>0.05)。急性肝炎组和肝硬化组IgG、IgA水平均高于对照组,差异有统计学意义(P<0.05);两组κ轻链和λ轻链水平分别与对照组比较,差异均有统计学意义(P<0.05)。血清蛋白电泳结果显示,急性肝炎组与对照组相比,两组γ区球蛋白含量比较,差异无统计学意义(P>0.05);慢性肝炎组和肝硬化组γ区球蛋白含量与对照组比较,差异有统计学意义(P<0.05)。结论血清中免疫球蛋白及其轻链的含量与肝脏疾病密切相关,慢性肝炎肝硬化患者血清蛋白电泳呈现典型的多克隆增殖图谱。血清蛋白电泳、免疫球蛋白和轻链水平的测定可作为肝脏功能监测的辅助指标。     

Serum immunoglobulins (IgG, IgA, IgM) in chronic hepatitis C. A comparison with non-cirrhotic alcoholic liver disease

BACKGROUND/AIMS: Serum immunoglobulin concentrations are commonly elevated in patients with liver cirrhosis. Immunoglobulin class increase may vary depending on the cause of liver disease. Hepatitis C virus is, together with alcohol, a leading cause of chronic liver disease. The present study aimed to evaluate serum IgG, IgA and IgM levels in chronic hepatitis C. Results were compared with those of patients with non-cirrhotic alcoholic liver disease and healthy controls. Special attention was given to cases with minimal liver disease, as an approach to evaluate if the causing agent, independently of liver damage, influences serum immunoglobulin levels. METHODOLOGY: A total of 274 patients with histologically-proven chronic hepatitis C, 121 alcoholics with non-cirrhotic liver disease (steatosis or alcoholic hepatitis), and 75 healthy controls were studied. Serum IgG, IgA, and IgM were assayed by nephelometry. RESULTS: Serum IgG was increased in patients with chronic hepatitis C with respect to both alcoholics (p < 0.001) and healthy controls (p < 0.001). IgG levels were similar in alcoholics and in controls. IgA was increased in patients with non-cirrhotic alcoholic liver disease with respect to both chronic hepatitis C patients (p < 0.001) and controls (p < 0.001). IgA values were similar in subjects with chronic hepatitis C and controls. Selective IgG or IgA alteration was present in cases with minimal liver disease (chronic hepatitis C with a Knodell index equal or lower than 3, and alcoholics with liver steatosis, respectively). CONCLUSIONS: Hepatitis C virus and alcohol are linked to a selective increase of serum IgG and IgA, respectively, even in cases with mild or minimal liver disease.     

Measurement of carboxy terminal peptide of type I procollagen in sera of patients with viral hepatitis and liver cirrhosis

In the present investigation, a radioimmunoassay for carboxy terminal peptide of human type I procollagen (type 1 C-peptide) was developed. Its clinical implication for serodiagnosis of hepatic fibrosis in 85 patients with viral hepatitis, 45 patients with post-hepatitic liver cirrhosis and 37 patients with alcoholic liver diseases was evaluated in comparison with that of the previously established amino terminal peptide (type III N-peptide) assay. Anti-sera against type I procollagen was obtained by immunization of rabbit with purified type I procollagen from culture medium of IMR-90. The serum level of type I C-peptide in normal subjects was found to be 42 ng/ml (s.d. = 19). Type I C-peptide levels in patients with acute hepatitis were within normal range, while in chronic hepatitis, the mean type I C-peptide level increased as the grade of fibrosis advanced from grade I to III. However, there was no statistically significant difference between the mean type I C-peptide level of grade III and that of liver cirrhosis. Increments of type I C-peptide levels were also observed in alcoholic liver fibrosis (fatty liver with fibrosis and liver cirrhosis). On the other hand, type III N-peptide assay appeared to reflect not only the degree of hepatic fibrosis, but also the degree of hepatic inflammation, giving the high levels in acute viral hepatitis. Collectively, the results indicate the usefulness of type I C-peptide assay for monitoring hepatic fibrosis in viral hepatitis as well as in alcoholic liver disease.     

Hyperimmunoglobulinemia associated with narcotic addiction. Effects of methadone maintenance treatment

Increased serum immunoglobulins were common in narcotic addicts. Immunoglobulin M (IgM) levels were high in 75 per cent of 46 adult addicts and in 65 per cent of 63 adolescent addicts seeking methadone maintenance or detoxification. Isolated hypermacroglobulinemia was found in 56 per cent. During methadone maintenance or abstinence high IgM levels were much less frequent. History of overt hepatitis, manifest liver disease, serum glutamic oxaloacetic transaminase (SGOT) or alkaline phosphatase levels did not correlate with the presence of high serum IgM levels. Serum immunoglobulin G (IgG) was more variably and less frequently increased than IgM in the untreated addicts, but was commonly increased in the patients maintained on methadone. Prospective studies of 21 patients starting methadone maintenance showed a decrease in mean serum IgM during treatment. The incidence of normal IgM levels in these patients rose to 48 per cent after one year compared to 24 per cent before treatment. The pattern of immunoglobulin changes in narcotic addiction is significantly altered during methadone maintenance treatment, perhaps as a result in the reduction of drug abuse.     

HB virus infection and delta surinfection in Sahelian Africa

78 hospitalized patients were selected when presenting with at least one of these signs: hepatomegaly, jaundice, ascites, oesophageal varices, abdominal venous pattern, splenomegaly. All had radioimmunoassays for hepatitis B surface antigen (HBsAg) and antidelta antibody (78/78). Acute or chronic hepatic disease was diagnosed in 56 patients: 7 acute viral hepatitis, 13 chronic hepatitis, 23 non alcoholic hepatic cirrhosis, and 13 hepatocellular carcinoma. Twenty-two patients with other diagnoses served as controls. Serum antidelta was present in each group: acute viral hepatitis (2/7), chronic hepatitis (2/13), non alcoholic hepatic cirrhosis (9/23), hepatocellular carcinoma (3/13), controls (2/22). Every patient with acute or chronic hepatic disease and positive serum anti-delta was positive for serum HBsAg. Amony controls, 2 patients with positive serum antidelta were negative for serum HBsAg but positive for antiHBs. Delta superinfection is present in the sahelian region; Patients with acute viral hepatitis, chronic hepatitis, non alcoholic hepatic cirrhosis, and hepatocellular carcinoma are electively infected. Patients with acute or chronic hepatitis and positive serum antidelta have hepatitis B virus evolutive infection (positive serum HBsAg).     

Inhibitors of leukocyte chemotaxis in alcoholic liver disease

Twenty-one of 42 patients (50 per cent) with alcoholic liver disease showed serum chemotactic inhibitory activity (CIA). CIA was not related to any single biochemical or histologic feature in the patients studied. The frequency of CIA was greatest in those with active infection. Serial studies demonstrated that CIA may be a transient phenomenon, associated with active alcoholic liver disease or appearance of infection. Nine of 15 patients showed skin test anergy; CIA was present in 8 of these 9 patients. Serum immunoglobulin A (IgA) and G (IgG) concentrations were significantly higher in patients with CIA when compared to those without CIA.Sucrose density gradient centrifugation of serums showing CIA yielded three peaks of inhibitory activity. Two had sedimentation coefficients of 10.7S and 6.8S, and the third was approximately 3S. The two higher molecular weight inhibitors were predominant in the 50 per cent ammonium sulfate precipitate. Immunoabsorption by anti-IgA but not by anti-IgG or IgM columns removed the ammonium sulfate precipitable chemotactic inhibitors. The appearance of chemotactic inhibitors in patients with alcoholic liver disease may have relevance to their apparent susceptibility to serious infections.     

Serum autoantibodies and immunoglobulins in hepatitis-associated antigen (HAA)-positive and -negative liver disease

Serum immunoglobulin G, A, and M and serum antinuclear, mitochondrial, and smooth muscle antibody have been measured in 223 patients with hepatitis-associated antigen (HAA)-positive and -negative acute and chronic liver disease. In patients with acute hepatitis, chronic persistent hepatitis, and primary liver cell carcinoma, these indices failed to show any significant differences. However, in the group with chronic aggressive hepatitis the patients who were HAA negative had significantly higher levels of serum IgG, much higher titres of smooth muscle antibody, and often antinuclear and mitochondrial antibodies which were not found in the HAA-positive patients from this group. This suggests that different pathogenic mechanisms may be operative in HAA-positive and -negative chronic aggressive hepatitis.     

Alcoholic liver disease absence of alpha-fetoprotein elevations in the recovery phase

Serum alpha-fetoprotein (AFP) may be detected in patients with nonneoplastic liver diseases such as massive hepatic necrosis, viral hepatitis, and experimental liver injury. AFP levels have not been serially assessed in patients with alcoholic liver disease, with or without cirrhosis, during the period following cessation of alcohol. Thirty-two such patients sere studied with weekly AFP determinations, an average of five such measurements being obtained per patient. The severity of alcoholic liver disease in this group varied from mild alcoholic hepatitits to advanced cirrhosis, and overall mortality was 31%. Thirty-one of the 32 patients had consistently negative AFP determinations. One patient with persistently elevated AFP levels proved to have hepatoma at autopsy. This study failed to detect AFP elevations in a group of patients with alcoholic liver disease and suggests that positive AFP determinations in such patients should raise the question of underlying hepatocellular carcinoma.     

Serum alpha 1-antitrypsin levels in alcoholic hepatitis.

Serum alpha 1-antitrypsin concentrations have been measured in 68 patients with liver disease. High mean values (359 +/- 18.0) were found in patients with alcoholic hepatitis whereas patients with acute viral hepatitis and chronic active hepatitis did not show any significant differences from the controls. In a group of patients with both alcoholic hepatitis and acute pancreatitis the mean value (218 +/- 5.8) was significantly lower than in the control group. The mechanism for the reduction of serum alpha 1-antitrypsin levels in this group remains to be clarified but low serum alpha 1-antitrypsin may be due to increased proteolytic enzyme concentrations in acute pancreatitis.     

Hypogonadism is not related to the etiology of liver cirrhosis

We investigated the clinical and laboratory findings of hypogonadism and feminization in male patients with viral or alcoholic cirrhosis to determine whether chronic liver disease plays a primary role in the development of sexual dysfunction and hormonal changes. Two groups of male patients with liver cirrhosis (23 alcoholic, 33 viral) age-and Child's gradematched, and 20 age-matched healthy men, as a control group, were included in this study. Clinical signs of hypogonadism and feminization were examined in the cirrhotic patients. Follicle-stimulating hormone, luteinizing hormone, prolactin, testosterone, free testosterone, estradiol, androstenedione, dehydroepiandrosterone sulfate, and sex hormone-binding globulin were estimated in all groups. Seminal fluid was also analyzed in 7 alcoholic and 15 viral cirrhotics. Serum levels of estradiol, androstenedione, and sex hormone-binding globulin were significantly higher, and free testosterone and dehydroepiandrosterone sulfate levels were significantly lower in both groups of cirrhotics compared with the control group. Child's C patients in both groups of cirrhotics were found to have higher estradiol and lower free testosterone levels than child's A and B patients. Alcoholic and viral cirrhotics had markedly reduced sperm motility and density. The differences between alcoholic and viral cirrhotic patients in the clinical signs of hypogonadism, serum levels of sex steroids, and the results of seminal fluid analysis were not statistically significant. These findings suggest that liver cirrhosis per se, independent of etiology, causes hypogonadism and feminization, and that the degree of hypogonadism and feminization correlates well with the severity of liver failure.     

Serum levels of tissue polypeptide specific antigen are correlated with hepatocyte cytokeratin expression in alcoholic liver disease

BACKGROUND: Serum levels of the tumor marker tissue polypeptide specific antigen (TPS, cytokeratin 18 fragments) are increased in patients with alcoholic liver disease, particularly in cases of alcoholic hepatitis. Mallory bodies, characteristic of alcoholic hepatitis, are cytokeratin 8 and 18 aggregates. The study was aimed at investigating the possible relationship of serum TPS levels with hepatocyte cytokeratin expression in patients with alcoholic liver disease. METHODS: Twenty-four patients with alcoholic liver disease were studied. Immunohistochemical staining for cytokeratins 8 and 18 was performed in liver specimens by means of CAM 5.2 monoclonal antibody. The number of hepatocytes containing CAM 5.2-reactive cytokeratin inclusions was compared with serum TPS levels. MAIN RESULTS AND CONCLUSIONS: The vast majority of alcoholics (95%) showed increased (>100 units/liter) serum TPS levels. Serum TPS levels were significantly correlated with the number of hepatocyte cytokeratin inclusions. Serum TPS levels can predict hepatocyte cytokeratin expression in patients with alcoholic liver disease.     

Infection à virus HB et surinfection delta en Afrique Sahélienne

78 hospitalized patients were selected when presenting with at least one of these signs: hepatomegaly, jaundice, ascites, oesophageal varices, abdominal venous pattern, splenomegaly. All had radioimmunoassays for hepatitis B surface antigen (HBsAg) and antidelta antibody (78/78). Acute or chronic hepatic disease was diagnosed in 56 patients: 7 acute viral hepatitis, 13 chronic hepatitis, 23 non alcoholic hepatic cirrhosis, and 13 hepatocellular carcinoma. Twenty-two patients with other diagnoses served as controls. Serum antidelta was present in each group: acute viral hepatitis (2/7), chronic hepatitis (2/13), non alcoholic hepatic cirrhosis (9/23), hepatocellular carcinoma (3/13), controls (2/22). Every patient with acute or chronic hepatic disease and positive serum anti-delta was positive for serum HBsAg. Amony controls, 2 patients with positive serum antidelta were negative for serum HBsAg but positive for antiHBs.Delta superinfection is present in the sahelian region; Patients with acute viral hepatitis, chronic hepatitis, non alcoholic hepatic cirrhosis, and hepatocellular carcinoma are electively infected. Patients with acute or chronic hepatitis and positive serum antidelta have hepatitis B virus evolutive infection (positive serum HBsAg).