Liver membrane antibodies in alcoholic liver disease.
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Autoantibodies↗
Biomedical subjects
K Krogsgaard
Publications and source records attributed to K Krogsgaard.
Characterisation of Liver membrane autoantibodies determined by indirect immunofluorescence.
Indirect immunofluorescence studies were performed using sera and IgG-Fab2 fragments from patients with chronic active hepatitis (CAH) who were positive for a liver membrane antibody (LMA). The specificity was investigated using hepatocytes from humans as well as rabbit, rat, guinea pig and monkey. Only sera also positive for smooth muscle antibody gave staining of lymphocytes and absorption with F-actin from rabbit muscle abolished this as well as all other smooth muscle staining without influencing LMA. It was concluded that LMA, routinely detected by indirect immunofluorescence using rabbit hepatocytes, represents specific binding to non-species-specific membrane antigens which are normal constituents of human hepatocytes. The antigen is separately located, and not cross-reactive with F-actin.
Animals↗
Localisation of immunoglobulin on the liver cell surface in primary biliary cirrhosis.
Direct immunofluorescence studies were performed on isolated liver cells in order to detect surface localisation of IgG in acute and chronic hepatitis and primary biliary cirrhosis. Membrane-bound IgG was demonstrated in nine patients. Six of eight patients with primary biliary cirrhosis showed granular fluorescence on their liver cell surfaces suggesting that an antibody or immune complex-mediated cytotoxicity might be involved in the pathogenesis of this disease.
Cell Membrane↗
[Liver involvement after treatment with naproxen].
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Chemical and Drug Induced Liver Injury↗
Correlation between liver morphology and portal pressure in alcoholic liver disease.
In 14 alcoholic patients, the degree of hepatic architectural destruction was graded (preserved architecture; nodules alternating with preserved architecture; totally destroyed architecture) and related to portal pressure. A positive correlation was found between the degree of architectural destruction and both wedged hepatic vein pressure (r = 0.72, p less than 0.01) and wedged-to-free hepatic vein pressure (r = 0.67, p less than 0.02). Degree of fatty change, fibrosis, inflammation, necrosis and occurrence of Mallory bodies showed no correlation with portal pressure. After morphometrical evaluation of liver biopsies, no significant correlation was found between mean hepatocyte volume or relative sinusoidal vascular volume and portal pressure. To test whether an increase in hepatocyte volume compresses the vascular structures and causes portal hypertension, the ratio of relative sinusoidal vascular volume to mean hepatocyte volume, which expresses the compression of the vascular structures exerted by enlargement of hepatocytes, was related to portal pressure. No significant correlation was found. Further, mean hepatocyte volume was not significantly correlated to relative sinusoidal vascular volume. The present findings are in accordance with the hypothesis that elevated hepatic vascular resistance and portal pressure in alcoholic liver disease are in part determined by the severity of the hepatic architectural destruction and subsequent distorsion and compression of the efferent vein system. Parenchymal changes, including changes in hepatocyte volume, seem to be of minor importance.
Adult↗
Hepatitis B virus DNA in serum from patients with acute hepatitis B.
Sera from 77 consecutive patients with acute type B hepatitis were examined for hepatitis B virus DNA (HBV DNA) by a spot hybridization method. The median follow-up time was 8 months (range, 1 week to 3 years). HBV DNA was detected in 26 (34%) patients on admission to the hospital. A significant positive correlation was found between short duration of symptoms and the presence of HBV DNA (p less than 0.025). Twenty-four (46%) of 52 HBeAg-positive patients were HBV DNA positive compared to 2 HBV DNA-positive patients of 25 HBeAg-negative patients (8%) (p less than 0.001). Four HBeAg-negative patients had serum HBV DNA initially or during follow-up; three had anti-HBe. Six of 77 patients with acute type B hepatitis (8%) became chronic HBsAg carriers, and HBV DNA was detectable from 5 months to more than 3 years after onset of symptoms. The presence of serum HBV DNA for more than 8 weeks after initial symptoms may predict development of a chronic HBsAg carrier state. In none of the chronic carriers was serum HBV DNA present after clearing of HBeAg.
Adolescent↗
Hepatitis B virus DNA, HBeAg and delta infection during the course from acute to chronic hepatitis B virus infection.
The presence of hepatitis B virus DNA in serum was determined in 57 unselected patients during the course from acute to chronic hepatitis B infection. Forty-six (81%) patients were hepatitis B virus DNA-positive in the first available serum sample. Generally, hepatitis B virus DNA was cleared before or at the same time as HBeAg, but in two patients (4%), hepatitis B virus DNA could be demonstrated after HBeAg clearance. One of the latter patients had hepatitis B virus DNA in the presence of anti-HBe. Both patients became hepatitis B virus DNA-negative. Seven of the hepatitis B virus DNA-positive patients received long-term treatment with prednisone, and three of them continued to be hepatitis B virus DNA positive for more than 10 years. Among the untreated patients hepatitis B virus DNA could be detected for up to 7 years, and 10 patients were hepatitis B virus DNA-positive for three years or more. Twenty-four patients (42%) showed serological signs of delta agent infection. Hepatitis B virus DNA clearance was observed in a significantly higher proportion (87%) of delta-infected patients as compared to patients with no delta infection (45%) (p less than 0.05). In addition patients with delta infection had a significantly increased hepatitis B virus DNA clearance rate as compared to patients without delta markers in their serum (p less than 0.01). In one (8%) delta-infected patient, hepatitis B virus DNA clearance was followed by a fall in transaminases into the normal range as opposed to results in 86% of patients with pure hepatitis B (p less than 0.002).
Carrier State↗
The influence of HTLV-III infection on the natural history of hepatitis B virus infection in male homosexual HBsAg carriers.
The presence of antibodies to HTLV-III and markers of active hepatitis B virus replication was examined in a longitudinal study of 33 consecutive male homosexual HBsAg carriers. The mean follow-up time was 37 months (range = 4 to 109 months). All patients were initially hepatitis B virus DNA-positive and HBeAg positive. Antibodies to HTLV-III were detectable in eight patients while they were positive for both of these markers. One of them cleared hepatitis B virus DNA and seroconverted from HBeAg to anti-HBe. This corresponds to an annual clearance/seroconversion rate of 4% (95% confidence limits = 0 to 15%). In two patients, antibodies to HTLV-III appeared after clearance of hepatitis B virus DNA and HBeAg, and in one of them, hepatitis B virus DNA reappeared. Among the 25 patients negative for HTLV-III antibodies, the annual hepatitis B virus DNA clearance rate was 20% and HBeAg to anti-HBe seroconversion rate was 11% (95% confidence limits = 11 to 31% and 4 to 20% respectively). The observed hepatitis B virus DNA clearance rates in the two groups were significantly different (p less than 0.05). Disease activity, as determined by transaminase levels, was significantly lower in HTLV-III-infected individuals as compared to individuals without HTLV-III infection (p less than 0.05). Infection with HTLV-III may extend the period of active viral replication or even reactivate hepatitis B virus replication and seems to diminish inflammatory disease activity in chronic HBsAg carriers.
Acquired Immunodeficiency Syndrome↗
Delta-infection and suppression of hepatitis B virus replication in chronic HBsAg carriers.
The presence of hepatitis B virus DNA and anti-delta was examined in a longitudinal study of 24 patients known to be delta-infected during the course from acute to chronic hepatitis B virus infection. Fifteen patients (63%) were hepatitis B virus DNA positive in the first serum sample. Eleven of 14 patients, who cleared hepatitis B virus DNA, did so following or at the same time as onset of delta-infection. Duration of hepatitis B virus DNA positivity in these 11 patients was shorter than in 11 anti-delta-negative controls matched according to duration of preceding hepatitis B virus DNA positivity, but the difference was not statistically significant. Considering only patients positive for IgM anti-delta in the last serum sample (eight patients), a statistically significant shorter duration of hepatitis B virus DNA positivity was found in delta-infected patients than in the controls (p less than 0.02). The study indicates that the delta-agent may have the capacity to inhibit hepatitis B virus replication and that a chronic delta-infection may lead to a termination of the period of active viral replication.
Adolescent↗