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)

Absolute numbers of T and B lymphocytes as well as active E rosette-forming cells were measured in twenty-seven patients with chronic active hepatitis (CAH), and in thirty control patients. In patients with CAH without cirrhosis, active E rosette-forming cells (a subpopulation of T lymphocytes considered to be actively involved in cell-mediated immune reactions) as well as lymphocytes with surface markers for IgA, IgM and IgG were increased. In patients with CAH and cirrhosis, total T lymphocytes were decreased. These results emphasize the significance of lymphocytes in CAH, and suggest the importance of monitoring T- and B-cell populations in patients with this disease.
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PMID:T and B lymphocytes in patients with chronic active hepatitis (CAH). 30 78

Total lymphocyte counts, B-, T-, C'3 receptor-bearing lymphocytes, and K-cell activity were studied in peripheral blood in patients with Crohn's disease and inflammatory liver disease. Patients with active untreated Crohn's disease and acute virus B hepatitis exhibited a markedly increased K-cell activity measured in a plaque assay when compared with normal controls (P less than 0.01). Patients with immunosuppressive treated Crohn's disease, HBsAg-positive chronic active hepatitis, and cirrhosis of the liver showed only a slight increase of K-cell activity (P less than 0.01). In the postacute phase of hepatitis (four to 12 weeks from onset) K-cell activity fell to normal levels. The number of B-lymphocytes showed a relative and absolute decrease in all groups of patients. With the exception of patients with acute HBsAg-positive hepatitis and the post-acute phase of hepatitis all the other groups showed statistically decreased absolute numbers for C'3 receptor-bearing lymphocytes. The significant decrease in K-cell activity and the number of T-lymphocytes in Crohn's disease treated with immunosuppressive drugs was interpreted as an effect of azathioprine and prednisone on these lymphocyte subpopulations.
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PMID:K-lymphocytes (killer-cells) in Crohn's disease and acute virus B-hepatitis. 30 25

A Farr technique has been used to assay antibodies to double-stranded DNA in the serum of patients with acute and chronic liver disease and carriers of HBsAg from the United Kingdom and Iraq. These antibodies were found in all groups from both countries. The highest levels were found in chronic active hepatitis and cirrhosis. In the Iraqi patients there was a strongly positive correlation between DNA-binding antibody levels and the presence of hepatitis B markers but not with disease activity. In the patients from the United Kingdom there was little correlation with disease activity and none with autoantibodies. Ninety-five per cent of asymptomatic carriers of HBsAG had elevated DNA-binding antibodies. It is suggested that hepatitis B-specific DNA might be one trigger to DNA antibody formation, though in liver disease a variety of factors are clearly operative.
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PMID:DNA-binding antibodies and hepatitis B markers in acute and chronic liver disease. 30 8

Results in 44 patients with esophageal bleeding who underwent a mesocaval shunt utilizing a prosthetic graft are presented. Portal hypertension was secondary to alcoholic cirrhosis in 30 patients, to chronic active hepatitis in eight, to primary biliary cirrhosis in four, to cirrhosis secondary to inflammatory bowel disease in one, and to portal vein thrombosis following splenectomy in one. Thirty-six shunts were performed during the emergent or semiemergent time period, and only eight were performed electively. Sixteen of the patients were Child's class A, 16 were class B, and 12 were class C. There were no hospital deaths in the emergency shunt group (of eight patients); there was a 12% mortality rate for patients undergoing semiemergency shunts (two of 17 patients) and a 42% mortality rate for patients who had emergency shunts (eight of 19 patients). Death was related more closely to hepatic reserve, however, than to timing of the shunt. Among the 32 class A and B patients, there were only three deaths in hospital (9%), as compared with seven deaths among the 12 class C patients (58%). Portal-systemic encephalopathy was high in the period immediately after operation (13 of 34 patients, 38%), but it was a chronic problem following discharge from the hospital in only three of 34 patients (9%). The mesocaval shunt is a safe, effective procedure for the control of variceal bleeding in class A and class B patients in any time period, but it carries a high operative mortality risk in the class C patient when it is performed as an emergency operation.
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PMID:Mesocaval shunts for the control of bleeding esophageal varices. 31 25

In patients who have impaired hepatic reserve, the Warren shunt has been proposed as an effective operation because it decompresses the esophageal varices without disturbing portal perfusion of the liver. However, early reports of high operative mortality and technical difficulties have impeded acceptance of the procedure. The operation was done in a series of 17 patients. All patients in whom elective variceal decompression with a patent splenic vein was required and without clinical ascites were candidates for this operation. Follow-up ranged from 2 to 48 months. Six patients had alcoholic cirrhosis, two had primary biliary cirrhosis and seven had postnecrotic cirrhosis; in two the cause of the liver disease was unknown. Five patients were categorized as Child's class A, nine as class B and three as class C. No intraoperative or early postoperative deaths owing to hemorrhage occurred. However, there was one death two weeks postoperatively from pulmonary sepsis and one death five weeks postoperatively due to antigen-positive hepatitis. Two patients died from hepatic failure six weeks and five months after operation, respectively; in the first of these, chronic active hepatitis was diagnosed at the time of operation. In one patient hemorrhage recurred and transfusion was required. Although ascites, which eventually resolved, developed in eight patients after operation, the results in 76 percent of patients have been good without new episodes of hemorrhage or encephalopathy. We conclude that the Warren shunt is a safe and effective elective operation for the treatment of patients in whom hemorrhage from esophageal varices has occurred.
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PMID:The Warren shunt in treating bleeding esophageal varices. 31 64

Absolute number of T and B lymphocytes were measured in the peripheral blood of 25 patients with biopsy proven HBsAg-positive Chronic Active Hepatitis (CAH), in 9 with Chronic Persistent Hepatitis (CPH), and in 25 HBsAg-negative healthy controls. In patients with CAH and cirrhosis total T lymphocytes were decreased; no difference were found between patients with CPH and normal controls. This data emphasize the importance of monitoring T-cells population in patients with HBsAg-positive CAH.
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PMID:Alteration in cell-mediated immunity in patients with chronic active hepatitis. I. Lymphocyte subpopulations. 31 50

The characterisation of lymphocytes from liver biopsies indicates that 'activated' T lymphocytes are present in the liver in alcohol induced hepatitis, chronic active hepatitis (HBS+ve and -ve), and in primary biliary cirrhosis but not in inactive cirrhosis, chronic persistent hepatitis, extrahepatic and drug induced cholestasis. A greater percentage of lymphocytes bear Fc-receptors in chronic active hepatitis than in alcohol induced hepatitis or cholestatic liver disease. The concentration of 'activated' T cells in the peripheral blood in all groups studied was within the normal range, suggesting that the 'activated' T cells found in the liver were reacting to either native or foreign antigens within the liver. The data on Fc-receptor bearing cells are consistent with the involvement of antibody assisted K cell mediated cytotoxicity in chronic active hepatitis.
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PMID:Lymphocyte populations in liver biopsy specimens from patients with chronic liver disease. 32 39

The large number of chemical agents administered for therapeutic or diagnostic purposes can produce various types of hepatic injury by several mechanism. Acute injury may be cytotoxic, cholestatic or mixed. Cytotoxic injury may consist of necrosis or steatosis. Cholestatic injury may be cholangiolitic (hepatocanalicular) or bland (canalicular). Chronic hepatic lesions caused by medicinal agents include chronic active hepatitis, steatosis, cirrhosis, fibrosis, hepatoportal sclerosis (non-cirrhotic portal hypertension), hepatic vein thrombosis, peliosis hepatis, adenoma, carcinoma, and angiosarcoma. There is a useful relationship between the type of hepatic injury and the chemical setting in which the drugs are employed. Some agents produce the liver damage because they are intrinsic (true, predictable) hepatotoxins. Other (non-predictable "hepatotoxins"), produce hepatic injury only in the rare and unusually susceptible individual (idiosyncratic injury). Hepatotoxic agents can be recognised by their dose-dependent and experimental reproducibility, properties which are not shared by agents which produce hepatic injury only in idiosyncratic hosts. Intrinsic hepatotoxins may be categorised as direct or indirect. Direct hepatotoxins injure the hepatocyte by direct physiochemical alteration and as a consequence produce metabolic defects. Indirect hepatotoxins selectively block metabolic pathways and, by producing a precise biochemical lesion, lead to structural changes. They may lead to hepatic steatosis or necrosis (cytotoxic indirect hepatotoxins) or block bile flow (cholestatic indirect hepatotoxins). Direct hepatotoxins are rarely encountered as drugs. Overdoses of some drugs and antineoplastic agents appear to be indirect cytotoxic hepatotoxins, and the C-17 alkylated anabolic and contraceptive steroids are indirect, cholestatic hepatotoxins. Idiosyncracy of the host is the mechanism for most types of drug-induced hepatic injury. It may reflect allergy to the drug or a metabolic aberration of the host permitting the production of hepatotoxic metabolites.
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PMID:Drug-induced liver disease. 35 64

The classification, clinical course, etiology and treatment of chronic hepatitis are discussed. The clinical manifestations of chronic hepatitis are of limited diagnostic use. Diagnosis must be made by liver biopsy. The disease is classified as chronic persistent or chronic active hepatitis. The prognosis for chronic persistent hepatitis is excellent, and no treatment is required. Chronic active hepatitis may progress to cirrhosis and is associated with a poor prognosis if untreated. Recognized causes of chronic active hepatitis are hepatitis-B virus infection, post-transfusion hepatitis not associated with hepatitis-B virus, and certain drugs. For drug-induced hepatitis, discontinuation of the medication is indicated. For other types of chronic active hepatitis the recommended treatment is prednisone 10 mg and azathioprine 50 mg daily.
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PMID:Drug therapy reviews: chronic hepatitis. 35 29

A patient suffering from chronic active hepatitis with macronodular cirrhosis, positive for hepatitis B surface antigen (HBsAg), was treated with an orthotopic liver allograft. The HBs antigenemia, as measured with several precipitation tests and by complement fixation, became negative after transplantation and remained so for about 2 1/2 months. During the interval, very low titers of the antigen were detectable by radioimmunoassay. At about three months after transplantation, she had an attack of acute hepatitis, at which time HBsAg became detectable by all tests. She recovered, but progressive liver disease developed during the remaining 1 1/2 years of her life. She died of disseminated nocardiosis and candidiasis with deteriorating hepatic function. The homograft at autopsy showed no evidence of rejection, but was the site of chronic active liver disease, although of a different pathologic pattern than that affecting her native liver. The differences in histology may reflect the influence of chronic immunosuppression on the features of chronic active hepatitis.
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PMID:Liver allograft. Its use in chronic active hepatitis with macronodular cirrhosis, hepatitis B surface antigen. 36 34


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