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Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Systematic screening of forty-seven haemophiliacs in Sheffield revealed abnormal liver-function tests in thirty-six (77%), with a tendency for these abnormalities to persist. To assess the importance of these abnormalities, percutaneous liver biopsy was carried out on eight symptom-free patients under factor-VIII cover. A wide spectrum of chronic liver disease was demonstrated, including chronic aggressive hepatitis and cirrhosis. The liver pathology bore no relation to clinical history or to biochemical findings. Hepatitis-B-virus markers were common, but evidence suggests that this is not the only factor contributing to the development of liver disease. The high incidence of chronic liver disease seems to be a recent development and is probably related to factor-concentrate replacement therapy.
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PMID:Percutaneous liver biopsy and chronic liver disease in haemophiliacs. 8 May 24

5% of 2612 homosexual males attending genitourinary clinics were found to be hepatitis-B surface-antigen (HBsAg) positive. Liver biopsy was done in 25 who had abnormal liver-function tests but no symptoms or signs of liver disease, and 14 (56%) of these proved to have chronic active hepatitis or active cirrhosis. Neither the liver-function tests nor the viral markers in serum reflected the severity of the liver disease. 38% of a group of 118 HBsAg positive patients were HBeAg positive, and sexual contacts of these individuals may be at serious risk of infection.
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PMID:Liver disease among homosexual males. 8 69

To clarify the aetiology of an outbreak of HBsAg-negative acute hepatitis in the renal unit at Fulham Hospital in 1968--70, serological tests for antibody to hepatitis-A virus (anti-H.A.V.) were done retrospectively on serum samples obtained at the time of the outbreak. 7 patients had had two previous episodes of clinical HBsAg-negative hepatitis. Serum samples were available from 24 of the 29 infected patients, and these were paired in 12 instances. There was a slight increase in the titre of anti-H.A.V. in 1 patient, and a further 2 patients who subsequently developed chronic hepatitis showed a decrease in titre, but no changes in titre were detected in the remaining 21 cases. These findings do not provide evidence for the involvement of hepatitis-A virus in the outbreak of hepatitis and effectively exclude a role for this virus in the chrnoic liver disease which developed subsequently in 8 (28%) of the patients. This outbreak is therefore probably non-A non-B hepatitis, which has not been reported previously in Great Britain in a haemodialysis unit. The results confirm that this form of hepatitis may be related to a high frequency of persistent hepatic dysfunction.
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PMID:Non-A non-B hepatitis associated with chronic liver disease in a haemodialysis unit. 8 18

Two groups of patients were observed for evidence of acute radiation hepatitis during "high dose" radiation to the liver. The first group of 18 patients with metastatic liver disease received an average of 4,050 rad to the whole liver. Half received anticoagulation with warfarin. One patient on anticoagulation developed evidence of acute radiation hepatitis while 2 patients did so without anticoagulation. Eleven patients with Hodgkin's disease received 4,000 rad to the left lobe of the liver during extended field radiation. Four of these 11 patients were anticoagulated to therapeutic range. Only one of the fully anticoagulated patients showed changes on liver scan consistent with radiation hepatitis whereas three did so without anticoagulation. No serious sequelae from anticoagulation occurred in either group. These preliminary data suggest that anticoagulation may be safely administered with high dose hepatic radiation and that further trials with anticoagulation are warranted.
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PMID:Anticoagulation and high dose liver radiation: a preliminary report. 10 86

Serum and plasma samples concentrated 8 to 10 times with polyethylene glycol (PEG) having a molecular weight of 6,000 were examined by micro-Ouchterlony (MO) analysis with a view to increasing the detection sensitivity for HBe antigen (HBeAg), one of the hepatitis B virus associated antigens, and HBe antibody (HBeAb). The subjects of this investigation consisted of 82 symptom-free HBsAg carriers and 59 patients with B hepatitis. HBeAg was detected in 22 (26.8%) and HBeAb in 43 (52.4%) of 82 asymptomatic HBsAg carriers, and 17 (20.7%) were negative for both HBeAg and HBeAb. The corresponding values for the liver disease patients were 7 (11.9%), 16 (22.1%) and 36 (61.0%). Histologically, the rate of detection for HBeAg was higher in the cases of a mild disturbance.
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PMID:Detection of HBe antigen in sera from HBs antigen asymptomatic carrier and hepatitis patients using polyethylene glycol (PEG). 10 43

Liver dysfunction was observed in 33% of patients treated by hemodialysis and kidney transplantation. Fifty-eight percent of these cases of hepatitis occurred in patients with past or present HBs antigenemia, and 77% of HBsAg-positive patients showed evidence of LD. However, during the course of a program conducted from 1969 to 1976 and involving 267 patients, the decrease in the prevalence of HBs antigenemia observed during the last two years did not lead to any reduction in LD incidence. In a small number of patients, potentially hepatotoxic drugs could be incriminated, but in our experience azathioprine never appeared to be involved. In a few patients, LD was due to granulomatous disease of the liver, such as tuberculosis and schistosomiasis. Twenty-one (7%) of the 267 patients at risk developed chronic hepatitis, which contributed to death in nine patients. In 12 cases (three deaths), this form of hepatitis occurred in HBsAg-positive patients, and in nine cases (six deaths), in HBsAg-negative patients. In three of these latter individuals, cytomegalovirus could be incriminated. Routine monthly screening for CMV in kidney recipients confirmed the high incidence of this viral infection in such patients. Studies on murine CMV infection have demonstrated that this infection can be enhanced by histoincompatible graft or by cyclophosphamide in a model that is very close to the kidney recipient. As in mice, CMV infection in kidney recipients apparently results from reactivation of a latent infection. It seems to play a major role in the LD observed and could apparently lead to chronic hepatitis and even to cirrhosis of the liver. Finally, the occurrence of LD in HBsAg-, anti-HBs- and antiCMV-negative patients would suggest the responsibility of other viruses for the pathogenesis of liver disease in patients treated by hemodialysis and kidney transplantation. Besides Epstein-Barr virus, other viruses, such as hepatitis C virus, should be thoroughly scrutinized.
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PMID:Liver disease in patients undergoing hemodialysis and kidney transplantation. 11 44

Based on hepatitis-associated antigen carrier status as a model liver disease, level of vitamin A can be a useful diagnostic indicator in mentally retarded individuals. It was found that vitamin A levels and age were linearly related by the equation A = (B + CD), where A is the plasma vitamin A in mugms per 100 mls of plasma, B is the sex dependent constant of 25.9 for males and 28.4 for females, C is a sex dependent constant of 0.64 for males and 0.77 for females, and D is age in years. Above age 20, D becomes a constant with a value of 20. With this equation, if the observed vitamin A value is less than 79 percent of the predicted value, then liver damage should be suspected. This information presented graphically allows one to predict liver damage by observing the plasma vitamin A levels and then locating the point on the appropriate graph.
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PMID:Plasma vitamin A levels--a diagnostic indicator of hepatitis in an institutionalized mentally retarded population. 13 10

A histopathological study was carried out on 27 patients with chronic inflammatory liver disease and clinical and/or biochemical evidence of cholestasis who had either mitochondrial antibodies against mitochondrial antigen fractions of 1.19 density ("PBC antigen"; 14 cases) or of 1.13 density ("CAH-PBC mixed-type antigen"; 13 cases). For comparison, the liver biopsies of 17 patients with chronic-aggressive hepatitis (CAH) and antinuclear and/or anti-smooth muscle antibodies but without cholestasis and mitochondrial antibodies, were evaluated. The 14 patients with mitochondrial antibodies against the PBC antigen showed the typical histological features of primary biliary cirrhosis (PBC). The 13 patients with mitochondrial antibodies against the CAH-PBC mixed-type antigen had heterogenous liver alterations. In 11 cases highly active CAH and/or active postnecrotic cirrhosis (AC) were found both with augmented ductular proliferation. Some of these cases showed distinct criteria of PBC as early bile duct lesions or absence of regular bile ducts. The liver histology of one case corresponded to classical PBC; another case to chronic persistent hepatitis. The CAH-patients without cholestasis and mitochondrial antibodies only occasionally showed bile duct proliferation. In conclusion, a high correlation was found between mitochondrial antibodies against the CAH-PBC mixed-type antigen and highly active CAH or early AC with augmented ductular proliferation. This represents an overlapping of CAH and PBC. In contrast, the cases with antibodies reacting to the PBC antigen showed the slowly progressive liver changes of typical PBC.
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PMID:Histopathological features in mixed types of chronic aggressive hepatitis and primary biliary cirrhosis. Correlations of liver histology with mitochondrial antibodies of different specificity. 13 50

Alpha1-antitrypsin deficiency (AATD), in addition to its association with chronic pulmonary disease, is reported with liver disease. Twenty per cent of Pi-type ZZ AATD infants present with a cholestatic type of neonatal hepatitis and develop a slowly progressive cirrhosis, and most die before adult life. Ten per cent of Pi-type ZZ adults develop cirrhosis. They have an increased frequency of primary liver carcinoma. In Z homozygotes and heterozygotes specific globules, due to accumulation of a type of alpha1-antitrypsin, are seen in liver cells. They are thought not to be hepatotoxic but to render the liver cell more susceptible to damage by an additional factor.
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PMID:Liver pathology in alpha1-antitrypsin deficiency. A review. 16 55

The frequency of occurrence of hepatitis B antigen (HBAg) and certain tissue autoantibodies [antinuclear antibody (ANA), smooth muscle antibody (SMA) and mitochondrial antibody (MIA)] were studied with the microtiter complement fixation and immunofluorescence techniques respectively in a group of patients suffering from chronic liver diseases. These were chronic hepatitis (30), cirrhosis of the liver (66) and hepatocellular carcinoma, mostly with underlying cirrhosis (100). A group of closely matched hospital in-patients served as controls. HBAg was found in high frequency in the patients with liver disease (60% in chronic hepatitis, 36.4% in cirrhosis and 49% in hepatocellular carcinoma) whereas tissue auto-antibodies were found in lower frequencies (16.7%, 10.6% and 13% in the three groups respectively). However, in both the frequency was significantly higher than that in the controls (9.2% for HBAg and 0.8% for auto-antibodies). There was a negative correlation between HBAg and tissue auto-antibodies in the group of patients with liver disease when taken as a whole (x2=14.3, P less than 0.001). These results suggest a possible aetiological role played by hepatitis virus B in hepatocellular carcinoma through chronic hepatitis and cirrhosis in Hong Kong while the mutual exclusion between HBAg and auto-antibodies supports the hypothesis of heterogeneity in the aetiology of chronic liver diseases. The patients with auto-antibodies may belong to the auto-immune category but no definate conclusion can be reached until the role played by hepatitis virus A in chronic liver diseases is clarified when more reliable techniques for its identification are available.
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PMID:Hepatitis B antigen and auto-antibodies in chronic liver diseases in Hong Kong. 16 80


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