Familial occurrence of hypersensitivity to phenytoin
Article Abstract:
Delayed hypersensitivity adverse drug reactions (ADRs) can occur days or even weeks after patients begin using aromatic anticonvulsants (phenytoin, phenobarbital, carbamazepine), but can be difficult to diagnose because their symptoms mimic those of disease or infection. (These three anticonvulsants are also known as Dilantin, Phenobarbital and Tegretol, respectively.) It is possible that patients who experience this kind of ADR have a biochemical abnormality that is inherited; specifically, an inability to detoxify arene oxide metabolites of the drugs. In this study, the first to confirm a familial predisposition to hypersensitivity ADRs, three siblings were studied who had experienced hypersensitivity ADRs to phenytoin. After treatment with phenytoin, the subjects developed fever, rash, facial edema (swelling) swollen lymph nodes, eosinophilia (high levels of eosinophils, a type of white blood cell), and a type of hepatitis (liver inflammation). When drug treatment was discontinued, the symptoms disappeared with the exception of those related to liver function, which continued for several months. Blood samples were analyzed from the patients, 5 other siblings with no previous exposure to anticonvulsants, and 59 control subjects. Results showed that the blood cells from the three affected patients were much more vulnerable to metabolites of phenytoin than were cells from the controls. Increased toxicity was also seen for metabolites of carbamazepine. No differences were seen between patients and controls for phenobarbital metabolites. These results differ from those of previous studies, which have reported toxicity to the metabolites of all three drugs. Four of the five siblings also had increased toxicity to phenytoin. The findings of the current study demonstrate that a predisposition to hypersensitivity ADRs is familial. Siblings of patients who have experienced an ADR to an anticonvulsant should be carefully evaluated if they are to receive such a drug for seizure control. (Consumer Summary produced by Reliance Medical Information, Inc.)
Publication Name: American Journal of Medicine
Subject: Health care industry
ISSN: 0002-9343
Year: 1991
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Eosinophilic myocarditis associated with high-dose interleukin-2 therapy
Article Abstract:
Treatment of certain resistant cancers with interleukin-2 (IL-2) and lymphokine-activated killer (LAK) has recently been reported. Some of the well-known side effects of this treatment include fever, lethargy, blood and liver malfunction, and leakage of blood from the capillaries causing low blood pressure, excessive urine production, and weight gain. The authors describe a patient with metastatic kidney cancer treated with IL-2 therapy, who developed inflammation of the myocardial muscle of the heart. Prior to treatment, the patient had normal results for an electrocardiogram (EKG) and exercise stress test. On the sixth day of treatment, the patient developed abnormal lung sounds (rales), but still had a relatively normal EKG. By day seven, there were changes in the cardiac enzymes, as well as evidence of a small pericardial effusion (fluid in the sac which surrounds the heart). A biopsy of the myocardium performed on day ll showed infiltration consistent with eosinophilic endocarditis. The symptoms of congestive heart failure disappeared, and the patient was discharged on the 14th day. The patient's cancer responded partially to this therapy, and eight weeks later the patient was again treated with IL-2 with no evidence of heart toxicity. Although heart toxicity occurs in about five percent of patients treated with IL-2, in this case, the injury was directly to the heart muscle and did not involve the heart vessels. The authors conclude that myocarditis may result from high doses of IL-2, and should be added to the list of possible complications of IL-2 treatment. (Consumer Summary produced by Reliance Medical Information, Inc.)
Publication Name: American Journal of Medicine
Subject: Health care industry
ISSN: 0002-9343
Year: 1990
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