Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0033774 (pruritus)
 14,546 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An extra- and intra-hepatic bile duct dilatation has been observed in a child in the course of scarlet fever. Manifestations of cholestasis, cytolysis and inflammation were present. Pruritus disappeared within 2 months, biological abnormalities within 3 months and ultrasonic bile duct abnormalities between 3 and 6 months, with a follow-up of 9 months. This case report suggests a relationship between a transitory obstruction, possibly toxic in origin, of the bile ducts and the scarlet fever.
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PMID:[Transient dilatation of the intra- and extra-hepatic bile ducts. A new aspect of bile duct involvement in scarlet fever]. 328 6

A computer system for probabilistic diagnosis of jaundice was tested on a patient sample from a geographical area different from that for which it was first constructed. 144 consecutive patients with jaundice seen in two Stockholm hospitals were interviewed and examined to record a total of 82 indicants from history, demographic details, physical findings and laboratory tests. Data were compared with those of 319 jaundiced patients previously interviewed and examined at different London hospitals. It was found that disease incidences were different in the two patient samples. There were more patients with acute viral hepatitis, chronic active hepatitis and primary biliary cirrhosis in the London data base whereas the Stockholm data base included significantly more patients with Gilbert's syndrome and alcoholic cirrhosis. Indicant frequencies, standardised for disease incidence, differed with respect to age (Stockholm patients were on average six years older), time from onset of first symptom to hospital admission (Stockholm patients had on average a two-week shorter history of disease) and a number of symptoms such as nausea, vomiting, anorexia, weight loss, itching, pale stools and dark urine which were more frequent among the London patients. Differences in hospital admission policy was regarded as an important reason for the differences in indicant frequency. The results of probabilistic diagnosis were poor. Only 49% of the cases were correctly classified into twelve diagnostic groups. In particular the computer model was poor at separating different causes of malignant bile duct obstruction and at differentiating between malignant and benign bile duct obstruction. However, all cases of acute viral hepatitis were correctly classified and the computer model was 87% accurate in differentiating between medical and surgical jaundice. Reclassification of the 144 patients on their own data showed the computer system to be well calibrated and 97% of the cases were correctly classified according to this procedure. In conclusion, the computer system could not be directly transferred for use in a Swedish hospital but the results of reclassification were sufficiently encouraging to warrant prospective studies.
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PMID:Computer aided diagnosis of jaundice. A comparison of two data bases. 330 98

We report the case of a patient in whom amitriptyline administration for 5 wk was followed by prolonged cholestasis. Jaundice and pruritus lasted 19 and 20 mo, respectively. Three liver biopsies were performed at different stages of the disease showing the course of liver lesions. Cholestasis initially located in the region of the hepatic venule came to be associated with the progressive development of portal tract lesions consisting of inflammatory infiltration, fibrosis, and disappearance of interlobular bile ducts. Amitriptyline hydroxylation and dextromethorphan O-demethylation are deficient in subjects with the poor metabolizer phenotype of debrisoquine. Drug oxidation phenotyping with dextromethorphan showed that this patient had the extensive metabolizer phenotype. This observation demonstrates that amitriptyline can induce prolonged cholestasis and suggests that the susceptibility to develop liver injury while taking this drug may not be related to a genetic deficiency of its hydroxylation.
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PMID:Amitriptyline-induced prolonged cholestasis. 333 90

The authors report the cases of 3 women who developed hepatic injury during administration of metapramine, a tricyclic antidepressant introduced in France in 1984. One patient had jaundice and pruritus; the 2 others had loss of weight. Serum alkaline phosphatase and serum transaminase activities were increased in 3 and 2 patients, respectively. Blood hypereosinophilia was found in one patient; erythrocyte sedimentation rate was elevated in 2 patients. The outcome was favorable after drug withdrawal in the 3 patients. Liver biopsy showed centrolobular cholestasis in the 3 patients. There was no rechallenge; in 2 patients, other drugs than metapramine might be implicated in hepatic injury; however, the similarity of these 3 cases suggests that metapramine, like other tricyclic antidepressants, may be responsible for hepatic injury.
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PMID:[Hepatic involvement associated with ingestion of metapramine]. 335 Feb 53

Partial diversion of bile flow to an external stoma was performed in 6 patients with chronic intrahepatic cholestasis with severe pruritus that had been refractory to medical measures. Four patients with progressive intrahepatic cholestasis and 2 with arteriohepatic dysplasia were treated. Follow-up has been 3-8 yr. Patients with progressive intrahepatic cholestasis have been free of itching since surgery. Serum bile salt concentrations fell from 218-275 microM (normal less than 10) before to less than 10 microM after surgery. Biochemical tests of liver function and histology returned to normal or near normal. Patients with arteriohepatic dysplasia had persistent mild pruritus after surgery. Serum bile salt concentrations fell from 153-317 to 25-37 microM. There was little or no improvement in biochemical tests or histology. Bile volume and bile salt diverted were higher in patients with progressive intrahepatic cholestasis (7.3-13.0 ml/kg.day and 83-137 mumol/kg.day, respectively) than those with arteriohepatic dysplasia (3.2-4.5 ml/kg.day and 21-36 mumol/kg.day). The quality of life since surgery has been excellent in patients with progressive intrahepatic cholestasis, but not as optimal in those with arteriohepatic dysplasia. These findings suggest that partial external biliary diversion can provide effective relief from pruritus and perhaps reversal of liver disease in patients with progressive intrahepatic cholestasis. It should be used in patients with arteriohepatic dysplasia only in those with disabling pruritus.
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PMID:Partial external diversion of bile for the treatment of intractable pruritus associated with intrahepatic cholestasis. 337 8

Serum 3 beta-hydroxy-5-cholenoic acid (3 beta-OH-delta 5) was analyzed in 100 cases (90 patients with hepatobiliary diseases, 10 normal subjects) and its clinical significance investigated. The measurement of 3 beta-OH-delta 5 was performed by high performance liquid chromatography (HPLC) with immobilized 3 beta-hydroxysteroid dehydrogenase (3 beta-HSD) as the enzyme column. Esterified 3 beta-OH-delta 5 was measured after enzymatic hydrolysis with sulfatase and beta-glucuronidase. 3 beta-OH-delta 5 was hardly detected in normal cases. On the other hand, serum 3 beta-OH-delta 5 levels were remarkably high in cholestatic cases and also high in other cases with high bilirubin levels. The ratio of glycine- to taurine-conjugates (G/T ratio) was effective in discriminating cholestasis from hepatocellular damage such as in cases of acute hepatitis or fulminant hepatitis. More than 90% of the 3 beta-OH-delta 5, which is toxic, was sulfated or glucuronidated, suggesting detoxification by esterified bile acids. Significant increases of taurine-conjugated 3 beta-OH-delta 5 were observed in cases with pruritus, and a relationship between taurine-conjugated and pruritus was presumed. Therefore, analysis of 3 beta-OH-delta 5 is considered to be effective in clarifying the pathogenesis of hepatobiliary diseases.
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PMID:Clinical evaluation of serum 3 beta-hydroxy-5-cholenoic acid in hepatobiliary diseases. 347 20

We report the case of a patient in whom troleandomycin-induced hepatitis was followed by prolonged anicteric cholestasis. Jaundice occurred after administration of troleandomycin for 7 days and was associated with hypereosinophilia. Jaundice disappeared within 3 months but was followed by prolonged anicteric cholestasis marked by pruritus and high levels of alkaline phosphatase and gammaglutamyltransferase activities. Finally, pruritus disappeared within 19 months, and liver tests returned to normal 27 months after the onset of hepatitis. This observation demonstrates that prolonged cholestasis can follow troleandomycin-induced acute hepatitis.
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PMID:Prolonged cholestasis after troleandomycin-induced acute hepatitis. 349 78

Intrahepatic cholestasis, defined as arrested bile flow, mimics extrahepatic obstruction in its biochemical, clinical and morphological features. It may be due to hepatocyte lesions of which there are three types, termed canalicular, hepatocanalicular and hepatocellular, respectively; or it may be due to ductal lesions at the level of the cholangiole or portal or septal ducts. Defective bile flow due to hepatic lesions reflects abnormal modification of the ductular bile. Defective formation of canalicular bile may involve bile acid-dependent or independent flow. It appears to result most importantly from defective secretion of bile acid-dependent flow secondary to defective uptake from sinusoidal blood, defective transcellular transport and defective secretion; or from regurgitation of secreted bile via leaky tight junctions. An independent defect in bile acid-independent flow is less clear. Defective flow of bile along the canaliculus may reflect increased viscosity and impaired canalicular contractility secondary to injury of the pericanalicular microfibrillar network. Impaired flow beyond the canaliculus may result from ductal injury. Sites of lesions that contribute to cholestasis include the sinusoidal and canalicular plasma membrane, the pericanalicular network and the tight junction and, less certainly, microtubules and microfilaments and Golgi apparatus. A number of drugs that lead to cholestasis have been found to lead to injury at one or more of these sites. Other agents (alpha-naphthylisothiocyanate, methylenedianiline, contaminated rapeseed oil, paraquat) lead to ductal injury resulting in cholestasis. Reports of inspissated casts in ductules (benoxaprofen jaundice) and injury to the major excretory tree (5-fluorouridine after hepatic artery infusion) have led to other forms of ductal cholestasis. Most instances of drug-induced cholestasis present as acute, transient illness, although important chronic forms also occur. The clinical features include the reflection of the cholestasis (pruritus, jaundice), systemic manifestations and extrahepatic organ involvement. While nearly all classes of medicinal agents include some that can lead to cholestasis, there are differences among the various categories. Phenothiazines and related antipsychotic and 'tranquillizer' drugs characteristically lead to cholestatic hepatic injury. The tricyclic antidepressants may lead to cholestatic or hepatocellular injury.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Drug-induced cholestasis. 355 33

A syndrome of intrahepatic cholestasis leading to death in early childhood was studied in 16 Greenland Eskimo children. The pedigrees are compatible with autosomal recessive inheritance. Jaundice, bleeding, pruritus, malnutrition, steatorrhoea, osteodystrophy and dwarfism were typical clinical features. Eight had died between the ages of six weeks and three years due to bleeding or infections. Hyperbilirubinaemia, profound hypoprothrombinaemia, thrombocytosis and elevated alkaline phosphatase levels were evident. Serum calcium, phosphate and parathyroid hormone levels indicated a secondary hyperparathyroidism. Hepatic fibrosis developed with increasing age. Follow-up of the surviving patients was 4 to 30 months. The aetiology of the disease is unknown. The syndrome has some features in common with previously described patients with familial intrahepatic cholestasis. No specific treatment is available. Genetic counselling is essential.
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PMID:Fatal familial cholestatic syndrome in Greenland Eskimo children. 356 58

A case of intrahepatic cholestasis of pregnancy (ICP) in a black American is presented. This is the first case reported in a black. Marked elevation of transaminases with mild biochemical evidence of cholestasis was initially suggestive of viral hepatitis. A clinical course characterized by pruritus with minimal constitutional symptoms, rapid resolution of biochemical abnormalities after delivery, and negative hepatitis A and B serologies was consistent with the diagnosis of ICP. Review of the classic features of ICP with emphasis on some unusual aspects of the disorder is included.
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PMID:Intrahepatic cholestasis of pregnancy with marked elevation of transaminases in a black American. 356 54


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