Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023890 (cirrhosis)
 42,195 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

A 62-year-old woman presented with uveitis and abnormal chest X-ray (bilateral hilar adenopathy). Skin biopsy in 1983 had revealed non-caseating epithelioid cell granuloma consistent with sarcoidosis. Her serum biochemical investigations and exploratory laparoscopy suggested nodular liver cirrhosis, but biopsy was not performed. Both blood urea nitrogen (BUN) and serum creatinine values were within normal limits. She received prednisolone therapy of 15 mg daily initially, and later a maintenance dose of 5 mg daily. In 1985, she complained of skin itching and her laboratory data revealed severe renal insufficiency (BUN 97 mg/dl, serum creatinine 12.2 mg/dl) and hypercalcemia (corrected serum calcium level: 11.5 mg/dl). Prednisolone treatment (40 mg daily) resulted in a dramatic improvement of renal function as well as other clinical abnormalities due to sarcoidosis, without any significant changes in liver function. She died of cerebral infarction in 1989. Autopsy showed interstitial nephritis with tubular calcinosis and hyalinized glomeruli. It is postulated that hypercalcemia due to sarcoidosis contributed to the renal failure in this patient. This case suggests that renal damage due to sarcoidosis may be reversible with appropriate corticosteroid therapy.
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PMID:[An autopsy case of sarcoidosis associated with renal failure]. 140 82

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

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

Primary biliary cirrhosis is a chronic, progressive, cholestatic liver disease thought to be related to abnormalities in immune regulation. The disease is associated with granulomatous bile duct destruction, cholestasis, hepatic copper overloading and the development of hepatic fibrosis or cirrhosis or both. There have been numerous therapeutic trials evaluating immunosuppressive, antifibrotic and cupruretic agents. Prednisolone, D-penicillamine, azathioprine, colchicine and chlorambucil have been evaluated in controlled clinical trials, and biochemical improvement of liver function has been noted with all of the agents, except D-penicillamine. Improved survival has also been reported in patients treated long-term with azathioprine and colchicine. However, none of the therapeutic agents has been demonstrated to halt histologic progression of the disease or to induce a complete clinical, biochemical and histologic remission as has been reported in patients with autoimmune chronic active hepatitis treated with corticosteroids. Many of the trials did not use a double-blind design, failed to use the "intent to treat" rule or failed to define an objective time to analyze results. Many of the studies involved small numbers of patients with short-term follow-up and thus potentially were inadequate to appreciate drug effects that might be of clinical benefit. Currently, there is no totally effective therapy for primary biliary cirrhosis. We believe that well-designed clinical trials can provide important information to better understand this disease until a totally effective therapy is available. New clinical trials should use well-established methodologic guidelines in study design and well-accepted statistical standards in the analysis and interpretation of results.
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PMID:Clinical and statistical analyses of new and evolving therapies for primary biliary cirrhosis. 328 61

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

A long-term follow-up of at least 10 years or until death of 44 patients taking part in a controlled prospective trial of prednisolone therapy in hepatitis B antigen negative chronic active hepatitis (lupoid hepatitis) has been performed at the Royal Free Hospital, London. Patients presenting between 1963 and 1967 were randomly allocated into control and treatment groups. Ten year life table survival curves showed a significantly improved survival in the treatment group where 63% of patients were alive at 10 years compared with only 27% in the control group (log rank test, P = 0.03). The median survival in the treatment group was 12.2 years compared with 3.3 years in the control group. The mean duration of treatment was 4.5 years. Age, presence of antinuclear factor, cirrhosis, or level of serum transaminases at presentation did not appear to affect survival. Male patients if untreated had a poorer prognosis than females (P = 0.02). The natural history of chronic active hepatitis appeared from clinical, biochemical, and histological findings to be from an active hepatitis or cirrhosis to inactive macronodular cirrhosis. Prednisolone therapy significantly improved survival by reducing mortality in the early active phase of the disease.
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PMID:Late results of the Royal Free Hospital prospective controlled trial of prednisolone therapy in hepatitis B surface antigen negative chronic active hepatitis. 698 4

Patients (n = 213) with chronic hepatitis B were randomised to prednisolone (two weeks of 0.6 mg/kg/day, one week of 0.45 mg/kg/day and one week of 0.25 mg/kg/day) or placebo followed by two weeks rest, and were then given human lymphoblastoid interferon 10 MU daily for five days followed by 10 MU thrice weekly for 11 weeks. There were statistically significant effects of prednisolone pre-treatment on both HBeAg disappearance and HBeAg to anti-HBe seroconversion (log rank test statistics 5.43; p = 0.02 and 4.75; p = 0.03). HBeAg disappearance and HBeAg to anti-HBe seroconversion rates were 28 vs. 44% and 23 vs. 38% (placebo vs. prednisolone). Fifteen patients (7.5%) lost HBsAg. Three out of 22 cirrhotic patients (14%), one of whom received prednisolone pre-treatment, developed hepatic decompensation with a fatal outcome. Prednisolone pre-treatment, enhances the effect of lymphoblastoid interferon in chronic hepatitis B. Interferon treatment (with and without prednisolone) should be used with caution in patients with cirrhosis and avoided in patients with evidence of hepatic decompensation.
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PMID:[Pretreatment with prednisolone enhances the effect of human lymphoblastoid interferon in chronic hepatitis B]. 977 Oct 59

The traditional approach to alcoholism is treatment of underlying psychological and behavioral problems. Earlier and more direct avenues to prevent or counteract alcohol's effects include a focus on early detection of alcoholism, using, in part, biochemical markers of heavy drinking such as carbohydrate-deficient transferrin (CDT) and screening, among heavy users of alcohol, for signs of medical complications. Only a few heavy drinkers eventually develop liver cirrhosis. Because no practical genetic markers exist indicating who will develop fibrosis and cirrhosis, heavy drinkers who have signs of liver injury should undergo liver biopsy to determine whether they have perivenular fibrosis, a recognized precursor lesion to cirrhosis. Those who do should start intense treatment efforts, such as correction of nutritional deficits, curbing alcohol consumption, and participation in ongoing controlled trials. Some "supernutrients" have been effective in baboons, including S-adenosylmethionine for the treatment of alcohol-induced liver injury and polyenylphosphatidylcholine for the prevention of fibrosis. Both drugs are now being tested in humans. Prednisolone improves survival in patients with alcoholic hepatitis who have either spontaneous hepatic encephalopathy or a high "discriminant function."
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PMID:Alcoholic Liver Disease. 1109 76

A case of the very early phase of Pneumocystis carinii pneumonia in a human immunodeficiency virus (HIV)-negative man with alcoholic hepatitis and cirrhosis treated with steroids is presented. A 40-year-old man with a 10-year history of alcohol abuse was admitted to hospital with jaundice, fever and macrohematuria. Laboratory examinations revealed neutrophilic leukocytosis and a serum bilirubin level of 13.9 mg/dL. The serum bilirubin level rose to 28.5 mg/dL over 1 month. Prednisolone administered orally for 10 days produced a slight improvement in the jaundice and fever. After an interval of a week, it was resumed and maintained for 22 days (total dose, 1555 mg) until the patient died of a massive hemorrhage from ruptured vessels of a gastric ulcer. An autopsy disclosed P. carinii pneumonia in the lower lobe of the left lung, cytomegalovirus infection in both lungs and the esophagus, and esophageal candidiasis. To our knowledge, this is the first report of P. carinii pneumonia together with cytomegalovirus infection in an HIV-negative alcoholic patient. The present case suggests that a rare opportunistic infection such as P. carinii pneumonia might be caused by treating cirrhosis and alcoholic hepatitis with corticosteroids, even if only for a relatively short period.
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PMID:Autopsy case of alcoholic hepatitis and cirrhosis treated with corticosteroids and affected by Pneumocystis carinii and cytomegalovirus pneumonia. 1156 18


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