Anti-actin antibodies of IgM and IgG class in chronic liver diseases detected by fluorometric immunoassay

Using a sensitive fluoroimmunoassay, anti-actin antibodies (AA) of the IgM and IgG classes were measured in 240 patients with various chronic liver diseases and in 211 patients with non-hepatic autoimmune muscle, heart, malignant and inflammatory bowel diseases. Thirty-two out of 40 patients (80%) with autoimmune chronic active hepatitis (CAH) had AA only of the IgG class (geom. mean X = 1.78, SEM +/- 0.07) and only three patients (8%) had both IgG and IgM AA, the latter in lower titres. In patients with primary biliary cirrhosis (PBC) and AMA-positive cholestatic CAH, AA of both IgM and IgG classes were equally represented (60% IgG and 64% IgM AA in PBC, 73% IgG and 51% IgM AA in cholestatic CAH) but the titres were very low (geom. mean IgG AA in PBC 1.035, SEM +/- 0.03, in cholestatic CAH 1.18, SEM +/- 0.02). In contrast to autoimmune (lupoid) CAH, AA were rare in HBsAg positive CAH (9/43, 21%) and only present in low titres. However, in six out of 21 patients with anti-HBs and anti-HBc-positive chronic active hepatitis, high AA of IgG class were found, suggesting the autoimmune type of liver disease. In NANB virus-induced chronic liver disease after blood transfusion, AA were only occasionally found (IgG antibodies 1/19, IgM antibodies 3/19) and none were found in the eight patients with sporadic NANB hepatitis. They were also rare in 30 patients with alcoholic liver disease (3/30, 10%).(ABSTRACT TRUNCATED AT 250 WORDS)     

Lymphocytotoxicity against autologous hepatocytes and membrane-bound IgG in viral and autoimmune chronic active hepatitis

ABSTRACT— Membrane-bound IgG and lymphocytotoxic activity of total, T-enriched and T-depleted lymphocytes, using autologous hepatocytes have been evaluated in: (a) 31 patients with chronic active hepatitis (CAH) (six autoimmune and 25 hepatitis B virus - HBV-related); (b) five patients with inactive alcoholic cirrhosis; and (c) nine subjects with normal hepatic histology. Lymphocytotoxicity was positive in 83% of autoimmune CAH and 68% of HBV-related cases; it was confined to the T-depleted subpopulation in the first group, while it was present in both the T-enriched and T-depleted subpopulations in 81% of HBV-related cases. Membrane-bound IgG was present in 58% of group (a) and in none of the other groups. A linear pattern was found in four out of five autoimmune CAH patients with positive lymphocytotoxic activity. The autoimmune patient with lymphocytotoxic activity within the normal range did not show any membrane fluorescence. Among HBV-related CAH patients, 13 presented a granular pattern, two an associated granular and linear pattern and ten were negative. These data suggest that different lymphocytotoxic mechanisms are involved in the two forms of CAH studied.     

Antinuclear autoantibodies in chronic liver diseases

Circulating autoantibodies are often observed in liver disorders, especially in those thought to have an autoimmune etiology-such as primary biliary cirrhosis (PBC) and chronic active hepatitis (CAH). The pathophysiologic role of these antibodies, however, remains obscure. The present study was performed to evaluate the incidence and diagnostic value of different antinuclear antibodies in chronic liver diseases, and to assess whether the antibodies are a non-specific expression of the hypergammaglobulinemia observed in these disorders. We measured six different antinuclear and closely related antibodies (against ssDNA, dsDNA, Poly (I), Poly (dT), RNA and cardiolipin) and their IgG, IgA and IgM isotypes in the sera of 86 patients with autoimmune, as well as other chronic liver diseases--namely, PBC, CAH, alcoholic (AC) and cryptogenic cirrhosis (CC). Antibodies against all the various nuclear antigens were detected in all diseases studied. The incidence ranged from 4% (anti-cardiolipin-IgG in CC) to 74% (anti-Poly (dT)-IgM in PBC). Although the antibody profiles differed among the various disease entities, they were not distinct enough to be of any clinical diagnostic value. In alcoholic cirrhosis antibody levels correlated with corresponding immunoglobulin isotype levels (notably IgA), suggesting a non-specific expression of hypergammaglobulinemia. In the other liver diseases such a correlation was lacking, favoring the existence of an underlying specific antigenic stimulation, or some other more specific immune dysfunction.     

Autoantibody against a 78 kDa membrane protein of HepG2 cell in the sera of patients with alcoholic liver diseases

Sera from 14 normal control subjects, 30 patients with alcoholic liver diseases (fatty liver,n=8; hepatitis,n=13; liver cirrhosis,n=9), 7 controls with chronic hepatitis B, and 8 controls with chronic hepatitis C were masured for their concentrations of antibodies against HepG2 membrane protein by a binding assay utilizing¹²⁵I-labeled protein A. When the cut-off level was set as the mean value plus 2 SD of normal control subjects, the incidence of positivity was 75%, 69.2%, and 77.8% in patients with alcoholic fatty liver, alcoholic hepatitis, and alcoholic cirrhosis, respectively. Both the mean serum antibody values and the positive incidence were significantly higher in patients with alcoholic liver diseases than in either the normal controls or in the control patients with chronic hepatitis. Sodium dodecylsulfate polyacrylamide gel electrophoresis of¹²⁵I-labeled HepG2 membrane protein precipitated with IgG from patients with alcoholic liver diseases revealed an immunoreactive band at a molecular weight of 78 000 daltons (gp78). The antibody activity remained after immunoabsorption by human liver-specific lipoprotein (LSP) but decreased when HepG2 cells were pre-treated with trypsin or neuraminidase. Consequently, gp78 appears to be a glycoprotein distinct from LSP, and is specifically recognized by IgG from patients with alcoholic liver diseases. This assay may provide a new system to measure autoantibody to hepatocytes in alcoholic liver diseases.     

Anti-actin antibodies of IgM and IgG class in chronic liver diseases detected by fluorometric immunoassay*

ABSTRACT— Using a sensitive fluoroimmunoassay, anti-actin antibodies (AA) of the IgM and IgG classes were measured in 240 patients with various chronic liver diseases and in 211 patients with non-hepatic autoimmune muscle, heart, malignant and inflammatory bowel diseases. Thirty-two out of 40 patients (80%) with autoimmune chronic active hepatitis (CAH) had AA only of the IgG class (geom. mean X = 1.78, SEM±0.07) and only three patients (8%) had both IgG and IgM AA, the latter in lower titres. In patients with primary biliary cirrhosis (PBC) and AMA-positive cholestatic CAH, AA of both IgM and IgG classes were equally represented (60% IgG and 64% IgM AA in PBC, 73% IgG and 51% IgM AA in cholestatic CAH) but the titres were very low (geom. mean IgG AA in PBC 1.035, SEM±0.03, in cholestatic CAH 1.18, SEM±0.02). In contrast to autoimmune (lupoid) CAH, AA were rare in HBsAg positive CAH (9/43, 21%) and only present in low titres. However, in six out of 21 patients with anti-HBs and anti-HBc-positive chronic active hepatitis, high AA of IgG class were found, suggesting the autoimmune type of liver disease. In NANB virus-induced chronic liver disease after blood transfusion, AA were only occasionally found (IgG antibodies 1/19, IgM antibodies 3/19) and none were found in the eight patients with sporadic NANB hepatitis. They were also rare in 30 patients with alcoholic liver disease (3/30, 10%). Of 211 patients with non-hepatic disorders, only 13 patients (6%) had AA (geom. mean of positive titres 0.076, SEM±0.01). We conclude therefore that high titre AA of the IgG class are reliable serological markers for the diagnosis of an autoimmune liver disease.     

Value of serum immunoglobulins in the diagnosis of liver disease

Serum immunoglobulins were determined in 145 consecutive patients with biopsy-proven steatosis, alcoholic hepatitis, alcoholic hepatitis with fibrosis, alcoholic hepatitis with cirrhosis, inactive cirrhosis, chronic active alcoholic hepatitis, chronic active hepatitis, primary biliary cirrhosis and nonspecific hepatitis. IgM was both a sensitive (90.5%) and specific (86.2%) marker for primary biliary cirrhosis, and mean IgM levels were higher in primary biliary cirrhosis than in other diagnostic categories (p less than 0.05). IgA levels were most commonly elevated in alcoholic liver disease (p less than 0.005). IgA detected 95% of alcoholic disease, but was poorly specific (41.1%). A trend of rising IgA with increasing severity of alcoholic injury was observed, but the differences were not significant. IgG was most commonly elevated in chronic active hepatitis and alcoholic hepatitis with cirrhosis, but the IgG values did not differ significantly from those found in other diagnostic categories. Our results substantiate assertions of a diagnostic sensitivity for elevated IgA in alcoholic liver disease and IgM in primary biliary cirrhosis. With the exception of IgM in primary biliary cirrhosis, however, serum immunoglobulins are not specific markers of liver histology.     

Clinical evaluation of the liver cell membrane autoantibody assay

To evaluate the clinical significance of the liver cell membrane autoantibody (LMA) assay, we studied the presence, titre and immunoglobulin classes of LMA in 162 patients with various liver diseases and 156 controls. LMA was detected predominantly in patients with HBsAg-negative chronic active hepatitis (73% of 26 patients), but was also found in lower prevalences in other liver diseases, such as primary biliary cirrhosis syndrome (43% of 28 patients). LMA-positive primary biliary cirrhosis patients could be distinguished from LMA-positive patients with other liver diseases by the virtual absence of IgG class LMA. The LMA assay adds to the panel of assays for non-organ-specific autoantibodies in that it is more specific for autoimmune liver disease and in that it increases the diagnostic yield of autoantibody assays, e.g. in HBsAg-negative chronic active hepatitis from 77 to 92%. Immunosuppressive therapy status and biochemical parameters of disease activity, such as transaminase values, did not show a statistically significant relationship with the prevalence, the titre and the immunoglobulin class of LMA. It is concluded, that LMA is a sensitive and specific diagnostic marker for autoimmune liver disease.     

Autoimmunity to a liver membrane lipoprotein and liver damage in alcoholic liver disease.

Antibodies reacting with a liver membrane lipoprotein (LSP) have been detected by radioimmunoassay in the sera of 15 (27%) of 55 patients with alcohol-related liver lesions. There was a close association between the presence of the anti-LSP antibody and the findings on liver biopsy of a lymphocytic infiltrate in the portal tracts together with piecemeal necrosis of periportal hepatocytes. These histological features are characteristically found in the autoimmune disorder of chronic active hepatitis, in which anti-LSP antibodies are almost invariably present. It is suggested that in these cases of alcoholic liver disease there is loss of tolerance, and continued production of anti-LSP could promote periportal inflammation and accelerate the progression to cirrhosis. In the cases of acute alcoholic hepatitis without periportal inflammation studied, anti-LSP was not detected demonstrating that production of this autoantibody is not simply secondary to liver damage.     

Antibody to liver-specific lipoprotein in acute and chronic liver diseases. Its quantitative assay with monoclonal antibody, but without the use of liver-specific lipoprotein

A double-antibody radioimmunoassay was developed to detect antibody to human liver-specific membrane lipoprotein (anti-LSP antibody) in patients' serum. Anti-human LSP monoclonal antibody was labeled with 125I and anti-anti-LSP antiserum raised in rabbits was used as the first antibody in the assay. Anti-LSP antibody level was quantitatively measured and the assay was shown to be specific. Anti-LSP antibody was found in 5/8 patients with type B acute viral hepatitis (AVH), 3/7 patients with type A AVH, 1/6 patients with non-A, non-B AVH, 10/17 patients with chronic active hepatitis (CAH), 6/16 patients with chronic persistent hepatitis, 13/16 patients with active cirrhosis of the liver and 7/19 patients with primary nonhepatic autoimmune diseases such as glomerulonephritis, systemic lupus erythematosus and rheumatoid arthritis. The mean levels of anti-LSP were increased in patients with cirrhosis of the liver (p less than 0.01), CAH (p less than 0.05) and AVH (p less than 0.05) when compared with that of normal individuals. However, the frequencies of anti-LSP did not depend on HBsAg status. The data showed that anti-LSP antibody can be detected without the use of LSP preparation although it is also found in patients with primary nonhepatic autoimmune diseases.     

Occurrence and significance of antibody to liver-specific membrane lipoprotein by double-antibody immunoprecipitation method in sera of patients with acute and chronic liver diseases.

A double-antibody immunoprecipitation method was developed for detecting antibody to liver-specific membrane lipoprotein (anti-LSP) in sera of patients with various liver diseases and primary nonhepatic autoimmune diseases. Liver-specific membrane lipoprotein prepared from normal rat livers was labeled with 125I (chloramine-T) and monospecific antibody raised in rabbits. Cross-reactivity and absorption studies demonstrated that the assay used was highly specific. The frequency and titer of anti-LSP were similar for HBsAg-positive and -negative patients with both acute and chronic liver diseases. Patients with chronic active hepatitis had the highest frequenzy (25 of 44 cases, 57%) when compared with those with chronic persistent hepatitis (5 of 23 cases, 22%) and nonalcoholic cirrhosis (8 of 21 cases, 38%). Of the anti-LSP positive cases, the mean titer in patients with chronic active hepatitis tended to be the highest. In patients recovered from acute viral hepatitis, anti-LSP was transiently positive (7 of 20 cases, 35%) in the acute phase. In those who progressed to chronic hepatitis, a late rise as well as an early rise occurred in 6 of 10 patients before the diagnosis was made. Two of 6 patients with primary biliary cirrhosis had anti-LSP, but none of 41 patients with other nonviral liver diseases and none of 60 patients with primary nonhepatic autoimmune diseases. These data indicate that an autoimmune reaction directed against LSP can be initiated during the acute phase of viral hepatitis and it may persist in chronic hepatitis in both HBsAg-positive and -negative cases.     

Prevalence of Anti-HCV in Cryptogenic Cirrhosis in a Suburban Detroit Community

To assess the role of the hepatitis C virus in patients with unexplained chronic liver disease, we tested for the presence of anti-hepatitis C antibody (anti-HCV) in the stored serum of patients with cryptogenic cirrhosis and a variety of other chronic liver diseases. The anti-HCV assay was performed by both the enzyme-linked and recombinant immunoblot methods in 16 patients with cryptogenic cirrhosis. Eight of these 16 patients (50%) were seropositive. Six of these eight patients were born outside of the United States, compared with only one of eight seronegative patients (p = 0.021). Of the anti-HCV-positive cryptogenic cirrhotic patients, 50% also had markers of previous hepatitis B infection, compared with only 12.5% of seronegative patients. Evidence of anti-HCV positivity was found in 10%, 19%, 0%, and 0% in patients with alcoholic cirrhosis, autoimmune hepatitis, primary biliary cirrhosis, and primary sclerosing cholangitis, respectively. We conclude that in a suburban American population, hepatitis C accounts for a significant percentage of patients with presumed cryptogenic cirrhosis. Unrecognized risk factors may account for a higher prevalence of HCV in foreign-born patients with cryptogenic cirrhosis. A low prevalence of anti-HCV positivity is found in other forms of chronic liver disease.     

Clinical evaluation of autoantibodies to liver cell membrane specific antigen, liver specific lipoprotein, and Tamm-Horsfall glycoprotein in autoimmune chronic active hepatitis

An enzyme-linked immunosorbent assay was developed to detect circulating autoantibodies to three liver cell membrane surface antigens, i.e., liver cell membrane specific antigen (LCM), liver specific lipoprotein (LSP), and Tamm-Horsfall glycoprotein (THGP). In autoimmune chronic active hepatitis (autoimmune CAH), the positive rate and mean titer (normal range, less than 5.5 units) for anti-LCM were 100% and 13.5 units before corticosteroid treatment and 100% and 9.9 units during the treatment. The corresponding values for anti-LSP were 84% and 11.8 units, and 81% and 8.9 units, and those for anti-THGP were 84% and 12.3 units, and 81% and 7.9 units. In an autoimmune CAH patient, elevation of the plasma levels of autoantibodies during the treatment apparently preceded the elevation of alanine aminotransferase (ALT). However, the ALT elevation induced by transcatheter arterial embolization was not associated with the elevation of these autoantibodies in an autoimmune CAH patient with hepatocellular carcinoma. In primary biliary cirrhosis, drug-induced hepatitis, and non-hepatic immunological disorders, the production of the three autoantibodies did not directly correlate with liver cell damage. These findings suggest that the elevation of autoantibodies against LCM, LSP, and THGP can be a useful guide for the prednisolone treatment of autoimmune CAH.     

Heterozygous MZ alpha-1-antitrypsin deficiency in adults with chronic liver disease

Pi phenotype was determined in 335 patients with liver diseases and compared with the results in 2830 healthy blood donors. Eleven of 335 patients had phenotype MZ (3.3%, compared with 2.9% in healthy blood donors (NS]. None of 53 patients with autoimmune chronic active hepatitis had the MZ phenotype, but it was found in 2 of 18 patients (11.1%) with cryptogenic cirrhosis, 3 of 78 (3.8%) with alcoholic liver cirrhosis, 2 of 36 (5.6%) with primary sclerosing cholangitis, and 1 of 26 (3.9%) with primary biliary cirrhosis. Altogether, 3 of 335 patients were homozygous for Pi ZZ and had cirrhosis. One of them (a male) developed a hepatoma and died. We conclude that the reported association between Pi MZ phenotype and chronic non-B active hepatitis does not seem to include patients with autoimmune chronic active hepatitis, whereas the possibility of an association between cryptogenic cirrhosis and the MZ phenotype cannot be excluded.     

Auto-immune features in patients with idiopathic chronic active hepatitis who are seronegative for conventional auto-antibodies

In patients with chronic active hepatitis (CAH), the absence of the conventional serum auto-antibodies (antinuclear, smooth muscle and liver-kidney microsomal) is often taken as evidence against an auto-immune aetiology and as indicative that the disease is unlikely to respond to immunosuppressive therapy. We report 12 British patients (11 female) who presented with histologically florid CAH (11 with cirrhosis or fibrosis and seven with ascites) but without significant titres of these antibodies or any other demonstrable aetiological feature (cryptogenic CAH), who have been followed up for a median of 5.25 years (range: 0.75-16 years). Ten had hypergammaglobulinaemia and/or specific elevations of serum IgG concentrations at presentation and five of 10 patients tested were found to have the HLA allotypes B8 and DR3. Remission was initially induced with prednisolone with or without azathioprine in all patients. Six patients subsequently relapsed on one or more occasions, either spontaneously while on maintenance therapy or during attempts to withdraw corticosteroids, and required increases or reintroduction of immunosuppressive therapy to regain disease control. Retrospective analysis of pretreatment samples from 11 of the patients revealed that all had been seropositive at presentation for auto-antibodies against the liver membrane lipoprotein preparation known as liver-specific membrane lipoprotein (LSP) and/or against the hepatic asialoglycoprotein receptor (ASGP-R), titres of which subsequently fluctuated in direct relation to response to treatment.(ABSTRACT TRUNCATED AT 250 WORDS)     

Antibody to liver membrane antigens in chronic active hepatitis. IV. Exclusion of specific reactivity to polypeptides and glycolipids by immunoblotting

The reactivity of sera was examined in patients with autoimmune chronic active hepatitis and other liver diseases by immunoblotting. Polypeptides and glycolipids of liver plasma membrane, liver-specific lipoprotein and kidney membrane were separated and probed with sera from patients and from a rabbit immunized with mouse liver plasma membrane. Chronic active hepatitis sera reacted with a number of polypeptides in the liver plasma membrane preparations; similar but weaker reactivity was observed with sera from patients with other diseases and in some healthy subjects. Chronic active hepatitis sera did not react with glycolipids from liver plasma membrane. The immune rabbit serum reacted with two polypeptides of 180 kd present in liver plasma membrane but absent from kidney membrane, with two polypeptides of 50 kd which were nonliver-specific but species-specific, and with three major glycolipid components of liver plasma membrane: this reactivity thus differed markedly from that of the chronic active hepatitis sera. In studies using dot-blotting, it was found that solubilization of liver plasma membrane in detergents resulted in a marked reduction of the reactivity to liver plasma membrane of chronic active hepatitis sera, but little change in the reactivity of the chronic active hepatitis and other sera with liver-specific lipoprotein by immunoblotting indicated that liver-specific lipoprotein consisted of constituents of liver plasma membrane together with intracellular proteins.(ABSTRACT TRUNCATED AT 250 WORDS)     

Differences of liver membrane antibody frequency in alcoholic liver disease

The presence of liver membrane antibody in IgG and IgA was investigated by radioimmunoassay using isolated rabbit hepatocytes as target cells. This technique was more sensitive than the immunofluorescent method. IgG liver membrane antibodies were positive in 24% of patients with alcoholic liver disease. IgA liver membrane antibodies were detected in 58% of patients with alcoholic liver disease, whereas they were detected only in 21% of those with nonalcoholic liver disease, except for cases of autoimmune chronic active hepatitis. In alcoholic liver disease, IgA liver membrane antibodies were detected at a high frequency in a group of patients with alcoholic hepatitis and active cirrhosis (94%) as compared with that of fatty liver, hepatic fibrosis, and inactive cirrhosis (42%). These results suggest that alcoholic liver disease is characterized in part by a humoral immune response of IgA liver membrane antibodies.This study was supported in part by grants 59480207 and 60304058 from the Japanese Ministry of Education, Science and Culture.     

Intrahepatic IgG/IgM plasma cells ratio helps in classifying autoimmune liver diseases

Background/AimPlasma cells infiltrate in the liver is a prototype lesion of autoimmune liver diseases. The possible role of plasma cells isotyping (IgM and IgG) in the liver in the diagnostic definition of autoimmune liver disease, and particularly in variant syndromes such as autoimmune cholangitis and the primary biliary cirrhosis/autoimmune hepatitis overlap syndrome, is less defined.MethodsWe analysed the clinical, serological and histological features of 83 patients with autoimmune liver disease (40 primary biliary cirrhosis, 20 autoimmune hepatitis, 13 primary sclerosing cholangitis, 4 autoimmune cholangitis and 6 overlap syndrome) compared to 34 patients with chronic hepatitis C and evaluated the expression of IgM and IgG plasma cells in their liver by immunostaining.ResultsBy Spearman's correlation, the mean-counts of IgM plasma cells in portal tracts were significantly correlated with female gender, serum alkaline phosphatase, gamma-glutamyl transferase and IgM values, positivity for anti-mitochondrial antibody-M2 and, on liver biopsy, with bile duct changes, orcein-positive granules and granulomas. Whereas IgG plasma cells resulted more correlated with alanine aminotransferase levels. IgG/IgM ratio lower than 1 was found no only in primary biliary cirrhosis but also in all patients with autoimmune cholangitis. Conversely, all patients with overlap syndrome showed IgG/IgM ratio higher than 1.ConclusionImmunostaining for IgM and IgG plasma cells on liver tissue can be a valuable parameter for better diagnosis of autoimmune liver disease and also for variant or mixed syndromes.     

A diagnostic marker of autoimmune chronic active hepatitis: liver plasma membrane antibody in the serum absorbed with particulate fraction of kidney homogenate

The sera absorbed with the particulate fraction of rabbit kidney homogenate (RK) were tested for the antibody against liver plasma membrane (LPM-Ab) by the radiometric assay method. After incubation of the isolated rabbit liver plasma membrane (RLPM) with appropriately diluted serum, IgG bound to RLPM (IgG-RLPM) was determined using 125I-labelled Staphylococcal protein A. IgG-RLPM in each subject tested was expressed in arbitrary units, that is, the multiple of the mean radioactivity associated with RLPM in 35 control subjects. Thus IgG-RLPM was 1.00 (mean) +/- 0.23 (SD) in the control subjects, 1.13 +/- 0.30 in 9 patients with chronic persistent hepatitis (CPH), 1.13 +/- 0.52 in 15 with chronic active hepatitis (CAH), 1.34 +/- 0.38 in 23 with liver cirrhosis (LC) and 3.45 +/- 0.73 in 5 with autoimmune CAH. F(ab')2 fragments from a patient with autoimmune CAH and a control subject decreased IgG-RLPM by 86.4 +/- 6.35 and -5.2 +/- 14.9%, respectively, in four patients with autoimmune CAH. LPM-Ab was detected in 0, 20.0 and 17.4% in the patients with CPH, CAH and LC, respectively. All of the patients with autoimmune CAH were positive for LPM-Ab. The absorption of the sera positive for LPM-Ab with RK decreased IgG-RLPM in various extents. In two of five patients with autoimmune CAH and two of seven patients with CAH or LC, the majority of LPM-Ab was cross-reactive with RK.     

Low prevalence of hepatitis C antibodies in chronic liver disease in Finland.

High prevalence of hepatitis C antibodies (anti-HCV) have been found in the Middle- and Southern European countries in connection with chronic liver diseases. In a study of Finnish chronic liver disease patients no anti-HCV antibodies were found in 22 autoimmune chronic active hepatitis, in 5 chronic persistent hepatitis and in 38 alcoholic liver disease patients. 2/30 primary biliary cirrhosis patients were anti-HCV positive. As a comparison 3/9 patients with acute community acquired non-A non-B hepatitis and 28/48 i.v. drug addicts had anti-HCV antibodies. The results indicate that HCV infections in Finnish chronic hepatitis patients are rare.     

Renal tubular acidosis and autoimmune liver disease

Forty-two patients with autoimmune liver disease have been investigated. Renal tubular acidosis was detected in 60% of the patients with primary biliary cirrhosis, in 30% with active chronic hepatitis, and in one out of seven cases with cryptogenic cirrhosis. The presence of the defect of renal acidification was not related to the level of plasma potassium, copper, or total globulin, nor to the pattern of immunological abnormalities detected in the serum. It is suggested that autoimmune liver disease and renal tubular acidosis may be part of a systemic disorder in the pathogenesis of which immunological mechanisms are involved.