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)

The apparent well-being of some children who as neonates were believed to have obstructive jaundice prompted us to study the clinical course, histologic features and possible etiologic factors in 17 children with cholestasis in the neonatal period. During a follow-up period of five months to 22 years, all had signs of chronic cholestasis, but only four died (two from nonhepatic causes); the others live remarkably normal lives. Serial hepatic biopsies in 11 showed a variety of initial lesions, which progressed to hypoplasia of the intrahepatic bile ducts, increasing portal fibrosis and eventual cirrhosis. Although evidence of possible viral infection was found in only 10 cases, a hepatitis, beginning either before or after birth, appears to be a likely original cause. The histologic changes seen may represent different stages of one process, starting as cholestasis with or without evidence of hepatitis and progressing to obliteration or failure of normal growth of the intrahepatic bile ducts.
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PMID:Intrahepatic cholestasis in childhood. 95 76

A sensitive radioimmunoassay for cholylglycine, chenodeoxycholylglycine, deoxycholylglycine, and sulfolithocholylglycine was established using antibodies obtained from rabbits injected with albumin conjugates of these bile acids. Glycine-conjugated bile acid levels were measured in sera from 25 control subjects and 110 patients who had hepatic disease (alcoholic cirrhosis, hepatitis, cholestasis, and hepatic malignancy). Sulfolithocholylglycine was elevated in the sera of all 110 patients with hepatic disease. Cholylglucine was within normal range in only three. Chenodeoxycholylglycine was elevated in most sera of patients who had hepatitis, cholestasis, or hepatic malignancy. It was normal in most sera of patients who had alcoholic cirrhosis, suggesting that chenodeoxycholic acid may be subject to further biotransformations in these patients. Deoxycholylglycine was elevated in a minority of patients, none of whom had cholestasis. The data suggest that serum bile acids, particularly sulfolithocholylglycine, are a highly sensitive index for hepatic dysfunction.
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PMID:Levels of immunoreactive glycine-conjugated bile acids in health and hepatobiliary disease. 98 91

The authors report a case of neonatal hepatitis with alpha-1-antitrypsin occuring in a child of ZZ phenotype. The anatomopathological study carried out on two liver biopsies showed changes of common cholestatic hepatitis developing into cirrhosis, as well as intrahepatocytary globulins. Moreover, these globulins, P.A.S. positive after treatment by alphaamylase, fix an antialpha-1-antitrypsine antiserum. Ultrastructural analysis shows them to be masses of amorphous material, feebly osmiophilic, outlined by a unitary membrane the moniliform aspect of which recalls the ergastoplasmic membrane. These findings are identical to those already made in cases of cirrhogenous neonatal hepatitis by alpha-1-antitrypsine deficit reported in the literature. They point out the irreversibility of the affection which, after a stage of cholestatic hepatitis with or without inflammatory portal fibrosis, develops into cirrhosis. At this stage cholestasis has regressed or disappeared whereas portal sclerosis, often infiltrated with free elements, surrounds hepatic lobules and biliary neocanaliculi. But the globulins are still present and appear to be the specific feature of this deficit. By their ultrastructural and immuno-histochemical features, these globulins would represent a form of accumulation of alpha-1-antitrypsin in the hepatocytes which normally carry out the synthesis of this antienzyme. Accumulation in the hepatocytes proves excretory disturbance of hypothetical mechanism: structural anomaly, changes in the permeability of the membrane. Its role in the occurrence of hepatitis or cirrhosis lesions is still to be demonstrated but one may think that it consists in absence of inhibition of the enzymatic factors discharged during agressions.
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PMID:[Neonatal hepatitis with alpha-1-antitrypsin deficit. Apropos of a personal case]. 108 58

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

Percutaneous transhepatic cholangiography (PTC) was performed on a 23-year-old male because of an atypical progression of hepatitis B antigen-negative hepatitis. No bile duct was entered and the procedure was uneventful. However, celiac angiography the day following PTC revealed abnormal liver vessels in the target area and the patient developed hemobilia and clinical pancreatitis, causing common bile duct obstruction. Symptomatology persisted until celiotomy 32 days after PTC. Clots were found obstructing the bile duct. This case is presented both because of the unusual complications of PTC and the unusual angiographic abnormalities. It is suggested that when there is a specific indication for the procedure either to differentiate cholestatic jaundice from extrahepatic jaundice or to localize a site of abstruction before surgical intervention.
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PMID:Hemobilia and pancreatitis as complication of a percutaneous transhepatic cholangiogram. 114 93

Carbenicillin disodium was temporally associated with eight episodes of a mild reversible anicteric hepatitis characterized by nausea, vomiting, and a tender, somewhat enlarged liver. Serum glutamic and oxaloacetic transaminase as well as alkaline phosphatase levels rose, but serum bilirubin values remained normal. There usually were no signs of concomitant allergy to penicillin, and other penicillins could be given subsequently without ill effects. Biopsy specimens of the liver showed spotty liver cell necrosis with no cholestasis.
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PMID:Anicteric carbenicillin hepatitis. Eight episodes in four patients. 117 85

Among liver biopsies from 91 children between the age of 36 hrs and 2 years, puncture or excision was done for clarification in 64 cases. The morphological differential diagnosis between the various forms of intra- and extrahepatic bile duct dysplasias and their define characteristics related to hepatitis is presented. Morphological changes have given the basis for our grouping of diseases with cholestasis in early childhood. Our conclusions were summarized and proved in some schematic tables. Particular emphasis was given to comparative time observations for bioptic examined children over longer periods. Hereby results prognostic knowledge which should stimulate our therapeutic handling.
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PMID:[Differential diagnosis and follow-up studies in sucklings and infants with continuous cholestasis (author's transl)]. 118 21


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