Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0021345 (infectious mononucleosis)
 3,358 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Data deriving from comprehensive hospital monitoring systems suggest that drug-induced skin effects occur in 2-5% of patients receiving any drug medication. Exanthematous (maculopapular) reaction (75%) and urticaria with/without angioedema (30%) are the most frequent of all cutaneous reactions to drugs. The incidence of cutaneous reactions relates to the quantity of the drugs which is prescribed and consumed worldwide. Thus penicillin, sulfonamides and nonsteroidal antiinflammatory drugs show the highest rate of cutaneous side effects. Drug reactions may be classified as either predictable (e.g. chemotherapy-induced alopecia) or unpredictable. Unpredictable side effects of drugs may be the result of allergic (type I to IV) or non-allergic reactions. Hereditary and acquired enzyme deficiency and variations in metabolic pathway may delay drug metabolism and cause nonallergic, toxic side effects. Such a mechanism is known to occur in patients with a low acetylation rate under hydralazine, INH or sulfonamide treatment. Some immunologic although nonallergic factors may facilitate eruptions in patients with infectious mononucleosis under ampicillin medication and in AIDS patients on co-trimoxazole therapy. When a cutaneous drug reaction is diagnosed, withdrawal of the drug is recommended. In instances in which patients display mild drug eruptions and no alternative therapy is available, the drug may be continued. However, it should be kept in mind that mild morbiliform eruption is often the initial presentation of toxic epidermal necrolysis. In AIDS patients sulfonamides most frequently have been implicated as a risk factor for the development of toxic epidermal necrolysis. In other than type 1 hypersensitivity reactions, skin testing and in vitro tests have low sensitivity and specificity.
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PMID:[Skin and hair]. 866 68

To assess epidemiological and clinical significance of drug hepatotoxicity in the setting of liver diseases consultation, ten thousand and three hundred forty two prospectively designed clinical records from patient cared for in our Liver Unit in the period 1988-1998 were incorporated into the study; 58 out of 10,342 (prevalence = 5.6%) fulfilled at least the first three of the following causality requirements: 1.--Liver injury associated in time to drug exposition; 2.--Negative evaluation of more common other etiologies; (alcohol, viruses, immunologic, metabolic, etc) 3.--Favourable response to drug withdrawal (ALT < 50% of baseline in 8 to 30 days in acute hepatitis type, and alkaline phosphatase and/or total bilirubin < 50% of baseline up to 6 months, in acute cholestasis) 4.--Inadverted or rarely prescribed positive challenge. Acute hepatitis type of injury were considered when serum ALT rise 8 times or more above normal superior level with alkaline phosphatase (APh) below 3 times; "pure" cholestasis when APh rise 3 times or more above normal with ALT below 8 times; mixed acute injury or cholestatic hepatitis when both ALT and APh were elevated above 8 and 3 times respectively, and indeterminate type when both enzymes were below the referred levels. Chronic injury were considered when six or more month of evolution and compatible liver histology happens. Clinical severity were expressed as mild (absence of major clinical complications, serum bilirubin < 5 mg/dl and prothrombin concentration > 75%), moderate (presence of clinical complications, bilirubin > 5 mg/dl and prothrombin concentration between 50-75%), and severe (major clinical complications with bilirubin > 5 mg/dl and prothrombin concentration < 50%). Female/male ratio was 1.4:1, with age average 39 years (R = 15-77) and major concentration of cases above 40. More than 50% of cases received 2 or more drugs. Jaundice was present in 60.4%, and systemic manifestations of hypersensibility (fever, adenomegalies, rush, mononucleosis like syndrome, eosinophilia) in 29.3%. Acute injury represented 91.4% of the cases: 41.4% acute hepatitis, 15.5% "pure" cholestasis, 24.1% cholestatic hepatitis, and 10.3% indeterminate type. Four patients (4.5% of acute injury cases) were presented as severe acute liver failure, leading to liver transplant in one of them, drug association (INH-rifampicin and carbamazepine-phenobarbital) and inadverted challenge (sulphonamides and pemoline) were associated to clinical severity. Chronic injury were found in five patient (8.6%), four of them associated to chronic hepatitis and the other one to a ductopenic syndrome. Six drugs represented 53.4% of our cases; oral contraceptives (7 cases), INH alone or combined with rifampicin (6 cases), sulfonamides and clorpropamida (5 cases each), carbamazepine and amiodarone (4 cases each). Normalization of liver enzymes after drug suppression took 2 to 8 weeks in acute hepatitis type (X = 4 weeks), 4 to 20 in "pure" cholestasis (X = 12 weeks) and 8 to 24 weeks in cholestatic hepatitis or mixed type (X = 16 weeks). Two cases of chronic hepatitis normalize the histological activity index in 20 and 18 month respectively, one case remains as chronic hepatitis at 10 month and the other one progress to cirrhosis; the ductopenic syndrome normalize histology in 19 months receiving urso-deoxicolic acid, 10 mg/k/day.
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PMID:[Clinic-epidemiological significance of drug hepatotoxicity in liver disease consultation]. 1092 31