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)

Over a period of 18 months the development of hepatitis after intake of oxyphenisatin, a laxative, was established in 14 patients by re-exposure to the drug. The characteristic feature was nonspecific upper abdominal pain up to colic-like pain, lact of appetite, nausea or vomiting, and pruritus. The biochemical changes were those of chronic hepatitis with varying severity of biliary stasis and abnormal immunofluorescence. On re-exposure there was a particularly remarkable rise in GLDH activity. The histological picture showed acute inflammatory changes in the biliary passages on re-exposure, while the liver cells were clearly involved only secondarily. At a latter point the histological picture became non-specific. At laparoscopy there were different stages of minor periportal hepatic fibrosis to marked postnecrotic liver scars with portal hypertension and decompensation. Early diagnosis is difficult but crucial to the patient's fate, because this form of hepatitis regresses completely after oxyphenisatin has been stopped. Laxatives containing this drug should be withdrawn from the market.
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PMID:[Oxyphenisatin-induced liver disease (author's transl)]. 12 99

The authors report 3 cases and report the diagnostic usefulness of two signs of minor cholestasis described by one of them in 1966. A relative increase, in the absence of obvious virus hepatitis or cirrhosis, of the serum bilirubin, cholesterol, lipids and alkaline phosphatase, together with B.S.P. excretion. suggest minor cholestasis. The sign of "metacritical aggravation" when there is some suspicion of minor cholestasis, the supervision of the course of the disease, or a retrospective inquiry, permit, in the presence of minor symptoms, such as, pain, fever, jaundice, or pruritus, one to make the diagnosis of minor cholestasis. The latter is due either to the presence of small gall stones in the common bile duct, or to inflammation of the ampulla of Vater, or sphincter of Oddi, a Vaterian ampulloma, pancreatitis, or following damage to the common bile duct. In practice, liver biopsy confirms the diagnosis, and intravenous cholangiography, by the perfusion method, is usually able to demonstrate obstruction of the common bile duct.
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PMID:[Relative increase and metacritic aggravation in the diagnosis of anicteric cholestasis]. 16 83

15 patients with primary biliary cirrhosis (PBC) and 109 patients with chronic aggressive hepatitis (CAH) have been followed. Features of PBC, namely the generalized pruritus, massive rise in alkaline phosphatase, antimitochondrial antibodies and high levels of IgM-globulins, were present in 7 patients with CAH. This group was treated with immunosuppressive drugs for 1-2 years. Clinical, biochemical, immunological and histological parameters were used to assess the therapeutic effect. The pruritus improved and there was a statistically significant reduction in the IgG-hyperglobulinemia. Some resolution of the piecemeal necroses was seen. However, in judging these changes the sampling error must be taken into account. The unknown agent attacks both the hepatocytes and the epithelial cells of the bile ducts. The immunosuppressive treatment protects the liver cells from further damage while the progressive destruction of the bile ducts remains uninfluenced. The results suggest that the smallest possible dose sufficient to suppress the activity of CAH must be selected.
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PMID:[Combined form of chronic aggressive hepatitis primary biliary cirrhosis]. 92 35

Papular acrodermatitis of childhood is an infectious disease characterized by a non-relapsing, non-itching, monomorphic erythemato-papular dermatitis limited to the face and limbs. It is always associated with anacute hepatitis, with hepatitis B antigen in the serum and with a reactive reticulohistiocytic lymphadenitis. In childhood other types of papular or papulovesicular acro-located eruptions, itching or non-itching, associated with reactive lymphadenitis, are observed, in the course of known diseases and with unknown cause. These acro-located cutaneous eruptions of unknown origin, which show varying features, should be classified as "papulovesicular acrolocated syndrome" until their ethiopathogenesis is known.
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PMID:[Infantile papular acrodermatitis. Acrodermatitis papulosa and the infantile papulovesicular acrolocalized syndrome]. 99 19

Phenobarbital was administered to a patient with extrahepatic biliary obstruction who was initially thought to have cholestatic hepatitis. On two occasions, administration of the drug was associated with a decrease of jaundice, pruritus, and serum bile acid levels. This strongly suggests that phenobarbital may be effective not only in intrahepatic cholestasis, as reported earlier, but also in extrahepatic obstruction, and therefore cannot be used for the differention of these two types of cholestasis.
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PMID:Effect of phenobarbital in a case of extrahepatic cholestasis. 111 59

Fifteen patients with cholestatic disorders were treated for 1 to 5 months with phenobarbital. Primary biliary cirrhosis was diagnosed in seven, sclerosing cholangitis in two, intrahepatic biliary hypoplasia in three, and cholestatic hepatitis in three. Except for the patients with cholestatic hepatitis, in whom marked cholestasis was virtually the only abnormality in liver biopsy specimens, serum bilirubin and bile acid concentrations were diminished during therapy, the hepatic clearance of sulfobromophthalein and 131-I-rose bengal was variably enhanced, and there was relief from pruritus. Serum cholesterol concentrations and other measures of hepatic function were not significantly changed during therapy except for serum alkaline phosphatase activity, which rose in twelve patients. Parallel changes occurred in 5'-nucleotidase, suggesting a hepatic origin for the alkaline phosphatase activity. These studies indicate that phenobarbital therapy is associated with improvement in organic anion clearance in some patients with cholestatic disorders and may be beneficial to such patients.
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PMID:Phenobarbital effects in cholestatic liver diseases. 111 64

Problems of pregnancy in patients with liver disease are discussed. The effects of pregnancy on the disease course are generally limited to triggering of intensifiying icterus and pruritus; intrahepatic cholestasis may also occur. Increased incidences of miscarriage and prematurity have been reported in patients with liver cirrhosis, chronic hepatitis, cholestasis, and Dubin-Johnson syndrome, which is hereditary, and viral hepatitis in early pregnancy (increased incidence of chromosome abnormalities). Liver diseases constitute a relative indication for abortion, depending on the general state of the mother's health and her desire for the child. Problems of diagnosis and treatment are also considered.
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PMID:[Pregnancy in liver diseases]. 112 34

7 cases of pruritus in pregnancy are reported and their laboratory findings compared with a group of normal pregnant women; then pruritus is reviewed with respect to diagnosis, pathogenesis, therapy, and prognosis. The 7 women developed pruritus in 28-38 weeks of typically the 2nd pregnancy, although during oral contraception in 1 woman. The frequency was about 2/1000 pregnancies. Lab findings suggestive of cholestasis included normal prothrombin, elevated transaminaes, alkaline phosphatase, total bilirubin, total cholesterol, and slowed BSP clearance. None of these women had any history of hepatitis, medication, or positive Australia antigen. It is important in diagnosis to rule out infections, toxic or iatrogenic hepatitis, and especially herpes gestationis, which is teratogenic. Pruritus of pregnancy is identical to that seen during oral contraception, i.e., it is a less severe form of cholestatsis than jaundice. It can be treated with cholestyramine, or will regress spontaneously after delivery, but may cause prematurity.
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PMID:[Significance of pruritus during pregnancy. Relations with the hepatic disorders of gestation]. 113 31

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

Viral A hepatitis is a self-limited infection occurring predominantly among children usually as an anicteric often subclinical illness. Adults afflicted with this virus are more likely to develop icteric hepatitis. This is exemplified in developed countries when a common source outbreak occurs among non-immune adults. Fulminant hepatitis is uncommon in the USA and hepatitis A has never been documented to evolve into chronic hepatitis. However, prolonged cholestasis and relapsing hepatitis are well described. The usual features of cholestatic viral hepatitis A are pruritus, fever, diarrhoea, and weight loss. Serum bilirubin levels are > 10 mg/dl and the clinical course lasts at least 12 weeks. Cholestasis will spontaneously resolve, although corticosteroids will hasten the resolution but may predispose the patient to develop a relapse of the hepatitis. A biphasic or relapsing form of viral hepatitis A occurs in 6 to 10% of cases. The initial episode lasts 3 to 5 weeks and is followed by a period of remission characterized by normal liver chemistries lasting 4 to 5 weeks. Relapse may mimic the initial episode of the acute hepatitis. The full duration of the illness ranges from 16 to 40 weeks from the onset and immunoglobulin M antibody to hepatitis A virus persists throughout the clinical course. Hepatitis A virus has been recovered from stools during the relapse. Extrahepatic manifestations of hepatitis A include evanescent skin rash and transient arthralgias. Documented cases of arthritis and cutaneous vasculitis have been associated with cryoglobulinaemia and are rare.
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PMID:Atypical clinical manifestations of hepatitis A. 147 99


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