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)

Infectious episodes in 90 patients with hematological disorders were treated with sulbactam/cefoperazone (SBT/CPZ), a new combination drug of a potent beta-lactamase inhibitor, sodium sulbactam, and a third generation cephalosporin, sodium cefoperazone. Clinical responses to the SBT/CPZ regimen were excellent in 23 cases, good in 30 cases, fair in 11 cases, and poor in 26 cases. The overall efficacy rate (percentage of cases showing excellent or good responses) was 58.9%. Efficacy rates classified according to different infections were: 80% in documented sepsis, 57.6% in suspected sepsis, 61.1% in pneumonia and 50% in other infections. One episode of side effect was encountered with redness and itching of skin. Hepatic disorders were observed in 3 cases. These adverse reactions, however, were not serious. These results indicate that SBT/CPZ has a high therapeutic efficacy to severe infections in patients with hematological disorders.
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PMID:[Treatment with sulbactam/cefoperazone of severe infections in patients with hematological disorders]. 281 Jul 34

Proposed mechanisms, clinical features, prevalence, and treatment of phenothiazine-induced cholestatic jaundice are reviewed, and interactions between phenothiazines and other drugs that could theoretically alter the risk of cholestasis are described. Phenothiazine-induced jaundice is classified as a form of cholestatic hepatocanalicular hepatotoxicity and as an acute liver disease. Occasionally cholestatic jaundice may progress to chronic liver disease. The mechanism of hepatotoxicity is not completely understood but may involve a combination of physiochemical, immune, and direct toxic effects. Based on proposed mechanisms, concomitant use of drugs that alter microsomal hepatic enzyme function or have metabolic pathways that interfere with or overlap with those of the phenothiazines could be expected to potentiate or reduce the risk of cholestasis. The estimated prevalence of jaundice with chlorpromazine is 1-2%. The prevalence of jaundice with other phenothiazines is probably similar. The onset of jaundice usually occurs during the first one to four weeks of therapy. In most cases, discontinuation of the offending drug is the only treatment required. Jaundice usually resolves without sequelae two to eight weeks later. Pruritus can be relieved by topical corticosteroid or analgesic therapies or by oral antihistamines or bile acid sequestrants if topical therapy is ineffective. Whenever possible, reinstitution of neuroleptic therapy should be delayed until the reaction has resolved. Selection of a nonphenothiazine neuroleptic agent may be preferred. Phenothiazine-induced cholestatic jaundice occurs relatively infrequently and is usually self-limited; topical agents and oral antihistamines can alleviate the discomfort associated with the reaction.
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PMID:Phenothiazine-induced cholestatic jaundice. 290 41

In contrast to the well known chlorpromazine-induced cholestatic hepatitis, we report the case of a schizophrenic patient who presents a cytolytic hepatitis, without any prior hepatic disease. Mr G. was first hospitalized for depressive symptomatology. A pseudo-nevrotic schizophrenia was diagnosed. Pretherapeutic clinical and biological data were normal. A treatment with chlorpromazine 400 mg/day was given. At day 8, the patient was still anxious and began to be agitated. An increase to 500 mg/day of chlorpromazine posology and an addition of haloperidol 200 mg/day was implemented. At day 10, the following clinical symptoms appeared: 38.6 degrees C fever; headache; myalgia; epigastralgia and hypocondrium pain. Biological hepatitis disturbances (ALAT, 984 U/L; ASAT, 414 U/L) and hypereosinophilia with normal white cell count were found. Clinical and biological investigations were normal. Blood-culture, A, B, C hepatitis, HIV and CMV serologies were negative. Neuroleptic treatment was discontinued. Evolution to normality of the disturbances and biological data suggested a cytolytic hepatitis. Mr G... remained treated with flupentixol without side-effects. Phenothiazine-induced cholestatis is frequent, mild, and recovers spontaneously. The biological mechanism is supposed to be immunologic. Prevalence of biological hepatic disturbances is 10 to 20% with chlorpromazine in long-term treatment. More often, symptomatology is the same; jaundice, pruritus, abdominal pain, fever. Although pharmacological data suggest for a cytotoxic activity of phenothiazines, cytolytic hepatitis is poorly described. Maximum range of transaminase blood level reported in previous studies is about 400 U/l. This level is not clearly correlated with hepatic cell lysis. Few cases of hepatic necrosis have been reported. In all cases, preexistent hepatic injuries were observed. Chlorpromazine-induced cytolytic hepatitis is uncommon and cholestatic hepatitis mild. Biological hepatic parameters investigations remain necessary during neuroleptic treatment.
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PMID:[Cytolytic hepatitis during treatment with phenothiazines: apropos of a case]. 903 96