Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019163 (hepatitis B)
 38,309 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Most of the knowledge of post-hepatitic cirrhosis comes from studies performed in the last five years on the hepatitis B antigen-related variety. The position of other types of hepatitis (particularly type A) as an aetiological factor in cirrhosis remains conjectural. In general, the post-hepatitic cirrhosis develops insidiously after a mild or unrecognised acute episode of hepatitis. General progress is slow. Early deaths are due to liver failure. Later, primary hepatocellular carcinoma assumes increasing importance. Needle biopsy of the liver is usually necessary to confirm the diagnosis of cirrhosis and to estimate the degree of activity. Sampling errors when such a small specimen of liver is obtained must be taken into account, when formulating a diagnosis and prognosis. Prednisolone therapy is usually given if the patient is symptomatic, biochemical tests are abnormal and the liver biopsy confirms active chronic hepatitis with or without cirrhosis. The evidence of benefit is not so strong as for other forms of active hepatitis and cirrhosis such as the lupoid type. The management of the cirrhosis is otherwise along orthodox lines.
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PMID:Viral hepatitis and cirrhosis. 16 21

Two chimpanzees with low levels of anti-HBs developed increased antibody titres but showed no antigenemia after i.v. administration of 10 ml infective chimpanzee serum. Treatment of a chimpanzee (also possessing anti-HBs) i.m. with Cyclophosphamide plus Prednisolone for 3 weeks starting 2 days before the challenge with infective serum resulted in detectable circulating HBsAg by day 67. By day 95, the HBsAg concentration had increased to 17 times a human Ag reference plasma and low titres of anti-HBc were also present, but liver enzyme levels did not become abnormal until day 107. Since the circulating HBsAg concentration decreased gradually to 2 times the reference plasma by day 168, the animal was again immunosuppressed using oral Prednisolone alone for 7 weeks and then sacrificed. The liver yielded useful quantities of purified HBcAg while the plasma was an excellent source of Dane particles and HBsAg (41 X human reference plasma). This success could not be reproduced in 4 immunosuppressed cynomolgus monkeys. Our studies, therefore, demonstrate the value of the immunosuppressed high-order primate in the initiation and modulation of hepatitis B.
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PMID:Hepatitis B core antigen in the immunosuppressed chimpanzee. 120 61

A case of polymyositis associated with chronic active hepatitis was reported. A 53-year-old man, who had no previous history of blood transfusion nor hepatitis, noticed proximal dominant muscle weakness on January 29, 1985. He was admitted to Kyoto National Hospital on February 7, and laboratory studies disclosed the elevation of serum enzyme levels; creatine kinase (CK) 9845 IU/L (normal 54-263), glutamate oxaloacetate transaminase (GOT) 834 IU/L (9-31), glutamate pyruvate transaminase (GPT) 491 IU/L (4-34), lactate dehydrogenase (LDH) 2135 IU/L (248-464). Also serum gamma globulin was high (1.8 g/dl) and LE-like cell was found. The diagnosis of polymyositis was made and prednisolone therapy (60 mg/day) was started on February 23. The elevated serum enzymes decreased gradually, but severe muscle weakness persisted for about one month. On April 3, he was admitted to our hospital. Physical examination revealed moderate proximal dominant muscle weakness without skin eruption, jaundice or hepatosplenomegaly. The serum enzymes were still high; CK 1826, GOT 173, GPT 232 (GOT less than GPT), LDH 1548. However, alkaline phosphatase (ALP) and bilirubin were normal. Hepatitis B surface antigen (HBsAg) was not detected. Antinuclear antibody was positive. The electromyogram study showed myopathic change, and the muscle biopsy demonstrated myopathic change and cell infiltration, compatible with polymyositis. These results suggested liver dysfunction associated with polymyositis. Prednisolone therapy was continued and muscle weakness decreased. From December, 1985, serum enzymes (CK, GOT, GPT, LDH) elevated again and muscle weakness also slightly increased. Anti-smooth muscle antibody was positive. It was suggested that both polymyositis and liver dysfunction deteriorated.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A case of polymyositis associated with chronic active hepatitis]. 218 64

Twenty patients with hepatitis B e antigen (HBeAg) -positive chronic hepatitis, who received 40 mg of prednisolone per day for three weeks followed by withdrawal, were studied for changes in alanine aminotransferase (ALT), triiodothyronine (T3), thyroxine (T4), and hepatitis B virus DNA polymerase (HBV-DNAp) levels determined before and during prednisolone treatment and after its withdrawal. A decreased HBV-DNAp level of less than 100 cpm/ml three to five weeks after withdrawal was considered a sign of efficacy and was shown in 10 patients (50%). Significant differences were found between ALT levels, between T3 levels, and between the T3/T4 ratios assayed in the third and fourth weeks in total (P less than 0.02) and in the group in which efficacy was demonstrated (P less than 0.01). The T3/T4 ratio in the third week in the effectively treated group was significantly less than that in the noneffectively treated group (P less than 0.05). Prednisolone withdrawal effective for HBV-DNAp was shown in the patients with a decreased T3 level and the T3/T4 ratio at the third week and an increase in the ATL level after the withdrawal. The ALT level increased after the T3 level decreased. Changes in the T3 level or the T3/T4 ratio represent a marker for effectiveness of prednisolone withdrawal and for determination of combination therapy after steroid withdrawal.
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PMID:Triiodothyronine level and triiodothyronine/thyroxine ratio in HBeAg-positive chronic hepatitis patients treated with prednisolone withdrawal. 239 Sep 25

Chronic hepatitis is defined as chronic liver disease of at least 6 months' duration. Liver biopsy is essential for diagnosis and allows classification into chronic persistent hepatitis and chronic active hepatitis. Chronic persistent hepatitis is associated with hepatitis B infection or with infection with the non A non B viruses. The prognosis is good and it requires no treatment. Autoimmune chronic active hepatitis presents a very active clinical, biochemical and immunological picture. Prednisolone therapy is of benefit in prolonging life. Steroid therapy is disappointing in hepatitis B related chronic active hepatitis. Superinfection with delta agent may affect HBsAg positive patients: it appears to cause activation of disease and progression towards cirrhosis. Hepatocarcinoma is another complication of chronic B infection. Chronic active non A non B hepatitis is diagnosed by elimination since there is no specific diagnostic test.
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PMID:[Value of puncture biopsy of the liver during diagnostic and follow-up examinations (clinical aspects, immunological markers, images) in chronic hepatitis]. 242 1

Ten patients with severe chronic type B hepatitis confirmed by liver biopsy were treated with prednisolone for eight weeks and followed up for more than one year. The patients were comprised of 6 males and 4 females, ages 17 to 45 (mean 32) yrs. Serum alanine aminotransferase (ALT) was elevated more than one month before the treatment in all (mean: 379 U/L, range: 87 to 772 U/L). Initial serological tests showed hepatitis B surface antigen (HBsAg) and hepatitis B e antigen (HBeAg) in all and hepatitis B virus DNA (HBV-DNA) in 7/10 (70%). Liver biopsy showed severe chronic active hepatitis with confluent necrosis or acinar hepatitis in all. Prednisolone, 60 mg/day, was administered initially and the dose was tapered every 2 weeks over the 8 weeks period. Two to six months after cessation of treatment, 5 of 10 patients showed a disappearance of HBeAg and serum HBV-DNA and return of serum ALT level to normal (responders). The initial serum ALT level in responders was slightly higher than that of non-responders (mean: 404 vs. 355 U/L), but there was no statistical significance. Among 5 responders, serum HBV-DNA was detected in three patients initially and was transiently detected in one patient during treatment. In non-responders, HBeAg persisted during and after the treatment and serum HBV-DNA persisted in three, but serum ALT was decreased in all. One patient who did not show any clinical or serological improvement, died of jaundice, ascites and hepatic encephalopathy 4 months later.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of short-term prednisolone therapy in patients with severe chronic type B hepatitis. 248 9

The therapeutic effect of corticosteroid in hepatitis B virus (HBV) related membranous nephropathy was investigated in a 29-year-old chronic HBV carrier. Prednisolone (60 mg/day) was given for eight weeks and gradually reduced over the subsequent four months. In the renal biopsies taken before and after corticosteroid therapy, light microscopy revealed progression of sclerosis. Immunofluorescent staining showed glomerular capillary deposition of hepatitis B core antigen (HBcAg) by polyclonal antisera and hepatitis B e antigen (HBeAg) by monoclonal antibodies. Electron microscopy revealed 40-50 nm diameter virus-like particles in the glomeruli only from the biopsy performed after corticosteroid therapy. The serum concentrations of alanine aminotransferase, HBeAg, and HBV DNA increased with corticosteroid therapy suggesting active viral replication despite the absence of overt clinical hepatitis. Renal function did not improve and corticosteroid therapy was apparently not helpful in this patient. Our results conflict with the earlier notion that short-term corticosteroid does not interfere with a favorable outcome of the infection of the related renal disease.
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PMID:Replication of hepatitis B virus with corticosteroid therapy in hepatitis B virus related membranous nephropathy. 249 7

A 65 year old woman with lupoid hepatitis developed hepatocellular carcinoma which was diagnosed at an early stage. She had no history of blood transfusion and serum hepatitis B virus markers were negative. Prednisolone and 6-mercaptopurine were administered for the treatment of lupoid hepatitis. A hepatocellular carcinoma was detected by the elevation of serum alpha-fetoprotein and imaging studies. A tumour, 1.4 cm in diameter, was located in the lateral segment of the left hepatic lobe. It was resected by hepatic subsegmentectomy. Histological study showed a hepatocellular carcinoma of Edmondson type II against a background of posthepatitic cirrhosis. The patient was in good condition 2.5 years after the operation.
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PMID:Resected case of hepatocellular carcinoma associated with lupoid hepatitis. 256 48

The term chronic active hepatitis covers aetiologically different conditions with similar histological features. Autoimmune chronic active hepatitis - the type that was described originally - is the only type which responds well to prednisolone therapy. Autoimmune chronic active hepatitis can be differentiated from other types by serological and other markers. Treatment with prednisolone should be given for at least two years, with adjustment of dosage according to the serum levels of aspartate transaminase; maintenance does should be 8-12 mg a day. Azathioprine (50-100 mg a day) may be given concurrently as a corticosteroid-sparing agent. Prednisolone therapy in patients with autoimmune chronic active hepatitis enhances the quality of life and survival is prolonged greatly; currently the survival rate after 10 years for prednisolone-treated cases is at least 70%. Prednisolone is not effective in hepatitis B-associated chronic active hepatitis and may be deleterious. In cryptogenic chronic active hepatitis, in which markers of autoimmunity or hepatitis B viral infection are lacking, a trial of prednisolone therapy may be given for three months, and continued only if the indices of disease activity indicate a response. Corticosteroid agents have not proved of benefit in other liver diseases, including alcoholic hepatitis and acute liver failure, and a beneficial effect in primary biliary cirrhosis is yet to be established.
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PMID:Treatment of chronic active hepatitis and other liver diseases with corticosteroid agents. 356 Dec 94

Large doses of recombinant leukocyte A interferon were administered to 20 patients with deoxyribonucleic acid polymerase- and hepatitis B e antigen-positive chronic hepatitis B to study the maximum tolerated dose, its pharmacokinetics, and its antiviral activity. The first group of 5 patients received a constant dose of 36 X 10(6) U/day for 28 consecutive days. When it was well tolerated, the second, third, and fourth groups (5 patients each) received 50, 72, and 100 X 10(6) U/day, respectively. All 20 patients completed the 28-day treatment. Hourly and daily profile of serum interferon level showed a dose-dependent effect with an increasing dosage, and cumulative effects during the treatment. The mean peak serum interferon concentration ranged from 93 U/ml on day 1 in the first group to 1271 U/ml on day 28 in the fourth group. Inhibition of serum deoxyribonucleic acid polymerase activity and hepatitis B virus-deoxyribonucleic acid during the treatment was compared between the groups with low doses (36 and 50 X 10(6) U) and high doses (72 and 100 X 10(6) U). Low doses of interferon suppressed deoxyribonucleic acid polymerase activity to the same extent as did the high doses. Prednisolone withdrawal was combined with interferon in 5 patients. Three patients treated with such combination became seronegative for hepatitis B e antigen during the treatment, whereas all 15 with interferon alone remained seropositive. These results suggest that a maximum antiviral effect of recombinant leukocyte A interferon is below the maximum tolerated doses.
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PMID:Recombinant leukocyte a interferon treatment in patients with chronic hepatitis B virus infection. Pharmacokinetics, tolerance, and biologic effects. 397 31


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