Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019158 (hepatitis)
 30,205 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

Four compounds, prednisolone, sodium phenobarbitone, azathioprine and orotic acid, were tested for their ability to inhibit galactosamine induced hepatitis in the rat. Prednisolone offered total protection at doses of 100 mg/kg and above; sodium phenobarbitone and orotic acid modified the response to galactosamine and azathioprine was without effect.
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PMID:Inhibition, by drugs, of galactosamine induced hepatitis in the rat. 124 44

A retrospective study concerning ten patients with autoimmune hepatitis (AiH), diagnosed during a 2 1/2-year period is presented. The age of the patients ranged from 25 to 82 years and nine of the patients were women. Their symptoms included jaundice, pruritus, fever, anorexia and fatigue during a few weeks to years. Seven patients had increased serum aspartate aminotransferase (ASAT) levels. The three patients with normal ASAT levels had hypoalbuminaemia, decreased level of prothrombin or high levels of serum immunoglobulin G. Moderate or high levels of smooth muscle antibody titer were detected in nine patients, while none had increased levels of anti-nuclear antibody titer. Histological features of moderate or severe chronic active hepatitis were demonstrated in nine patients. One patient presented with clinical and histological features of acute hepatitis. Prednisolone therapy was followed by biochemical improvement in all the patients. In one patient, maintenance therapy with prednisolone was combined with azathioprine.
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PMID:[Autoimmune hepatitis. Forms of manifestation, diagnosis and treatment]. 141 30

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

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

Among 169 patients treated for superficial bladder tumors with intravesical instillations of 150 mg BCG-Pasteur, five developed BCG-itis--a severe systemic infection with bronchopulmonary lesions and granulomatous hepatitis. In four cases, the complication appeared early during treatment (after three, six, six and eight instillations respectively). In one case, BCG-itis appeared 6 months after completion of 2 years monthly maintenance therapy. In addition to pulmonary basal infiltration and granulomatous hepatitis, intramedullary granulomatosis was observed. In three patients, the role of trauma has to be considered, as BCG-itis appeared after a traumatic instillation with bleeding. All patients were cured by combined treatment with Rifampicin, Isoniazid and Prednisolone.
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PMID:Systemic bacillus Calmette-Guerin infection in patients treated by intravesical BCG therapy for superficial bladder cancer. 267 20

Chronic hepatitis is defined as diffuse chronic liver disease existing for at least 6 months. Cirrhosis is a sequel. It is of multiple etiology. Liver biopsy is essential for diagnosis and prognosis. Hepatitis B-related chronic hepatitis is slowly progressive. Corticosteroid therapy is disappointing. Current antiviral therapy converts the hepatitis B e antigen-positive patient to anti-HBe in about 50%. Non-A, non-B virus hepatitis-related chronic hepatitis suffers from lack of a diagnostic marker. No current therapy is of proven benefit. Autoimmune lupoid chronic active hepatitis presents a very active biochemical and immunological picture. Prednisolone therapy prolongs life but does not prevent the development of cirrhosis. Drug-related liver disease is recognized by its associations. Recovery follows withdrawal of the drug. Deaths often follow continuation of the drug. Indications of progression to a terminal state with likelihood of less than a 6-month survival are detailed. These are helpful in deciding on hepatic transplantation before the patient becomes moribund.
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PMID:Chronic hepatitis and cirrhosis. 642 Mar 7


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