Carbamazepine induced anticonvulsant hypersensitivity syndrome.

Anticonvulsant hypersensitivity syndrome (AHS) is a potentially fatal drug-induced, multi-organ syndrome. The syndrome has been reported with anticonvulsants such as carbamazepine, phenytoin, phenobarbitone, and lamotrigine. A 17-year-old female who presented with papules and desquamation all over was diagnosed with AHS. She gave a history of fever, earache, peripheral edema, and erythematous papular eruptions 3 days prior. She gave a history of carbamazepine treatment since 15 days for generalized tonic-clonic seizures. On examination, there was cervical lymph node enlargement without tenderness. Investigations revealed elevated absolute eosinophil count at 550/mm3 and positive C-reactive protein tests. Carbamazepine was immediately withdrawn. Symptomatic treatment was administered, and resolution of the symptoms was observed. In this case, causalty assessment using Naranjo adverse drug reaction probability scale showed that carbamazepine was a probable cause for the AHS (Score - 7).

Lamotrigine-induced Anticonvulsant Hypersensitivity Syndrome: Treatment with Steroid and Intravenous Immunoglobulin / 대한소아신경학회지

Lamotrgine is an antiepileptic drug that is effective for multiple types of seizure and has side-effects such as headache, nausea, dizziness, diplopia, ataxia, cutaneous lesions, and anticonvulsant hypersensitivity syndrome. Anticonvulsant hypersensitivity syndrome consists of the hallmark features of fever, rash, lymphadenopathy and internal organ involvement, induced by aromatic anticonvulsants, for example phenytoin, phenobarbital, carbamazepine, and lamotrigine. We report a case of 13-year-old girl who had a fever, generalized erythematous skin eruption, facial edema, eosinophilia, and elevated liver enzyme induced by lamotrigine and resolved with discontinuation of medication and intravenous steroid and immunoglobulin.

A Case of Anticonvulsant Hypersensitivity Syndrome thought to be Caused by Lamotrigine / 대한피부과학회지

Anticonvulsant hypersensitivity syndrome (AHS) is a rare and potentially life-threatening drug reaction, which has been associated with aromatic anticonvulsants such as phenytoin, carbamazepine, and phenobarbital. It is characterized by the triad of fever, rash and internal organ involvement, which mostly includes hepatitis. Histopathological findings usually show characteristic erythema multiforme. Lamotrigine is a new antiepileptic drug, chemically distinct from other anticonvulsant medication, however, AHS has recently been documented in patients treated with lamotrigine. We report a case of AHS in a 29-year-old man, thought to have been caused by the use of lamotrigine.

Hypersensitivity Reaction in a Patient Treated with Lamotrigine and Aripiprazole: a Case Report / 신경정신의학

We described a case of a 30-year-old female patient with bipolar disorder who experienced the anticonvulsant hypersensitivity syndrome (AHS) during treatment with lamotrigine and aripiprazole. She developed fever (38.4 degrees C), leukopenia, skin rash, and elevated serum transaminase levels on the 11th day of lamotrigine treatment (20th day of aripiprazole). Hypersensitivity to lamotrigine was suspected; lamotrigine was discontinued and prednisolone (30 mg/day) was administered to the patient. The clinical manifestations and laboratory findings showed improvement. However, on the 11th day of lamotrigine discontinuation (7th day of prednisolone treatment), she developed maculopapular skin rash over the entire body except the mucosa. There were no other symptoms and the laboratory findings were within normal limits. Skin biopsy showed erythema multiforme. After prescribing 55 mg/day of predisolone for additional 8 days, the recovery was uneventful, and it took 4 weeks from the onset of the second skin rash. Lamotrigine induced AHS showed broad spectrum of presentation and some manifestations can be flared up several days after discontinuation as did in this case. If unexplained systemic symptoms or a skin rash of unknown cause develop during the use of lamotrigine, clinicians should discontinue lamotrigine promptly and monitor the patient carefully at least for several weeks.

A Case of Anticonvulsant Hypersensitivity Syndrome with Subcarinal Lymph node Enlargement and Eosinophilic Pneumonia Induced by Carbamazepine / 결핵및호흡기질환

Anticonvulsant hypersensitivity syndrome (AHS) is an uncommon, but potentially fatal and mutilsystemic disorder that occurs after exposure to the arene oxide-producing anticonvulsants-carbamzepine, phenobarbital and phenytoin. The multisystemic reactions include fever, skin eruptions, lymphadenopathy, hematologic abnormality and hepatitis. The diagnosis of AHS is made by history of drug exposure and clinical course. No specific treatments are proved as benefit except discontinuing the offending drug and trying the steroids in some severe cases. We report a case of carbamazepine induced anticonvulsant hypersensitivity syndrome characterized by skin rash, eosinophilia, subcarinal lymphadenopathy and eosinophilic pneumonia. The patient was resolved completely after only discontinuing carbamazepine.

A Case of Anticonvulsant Hypersensitivity Syndrome Induced by Carbamazepine / 대한피부과학회지

Anticonvulsant hypersensitivity syndrome is a life threatening immunologic reaction of anticonvulsants therapy such as phenytoin, phenobarbital, or carbamazepine, characterized by multiple abnormalities such as fever, rash, lymphadenopathy, acute hepatocellular injury, leukocytosis, and eosinophilia. We report a case of anticonvulsant hypersensitivity syndrome thought to be caused by the use of carbamazepine in a 65-year-old male. He developed erythematous skin eruption four weeks after beginning therapy with carbamazepine. The clinical, laboratory and histologic findings of this patient were compatible with anticonvulsant hypersensitivity syndrome.

Three Cases of Anticonvulsant Hypersensitivity Syndrome Associated with Lamotrigine

Among the various side effects of anticonvulsant medication, the anticonvulsant hypersensitivity syndrome (AHS) is underrecognized. This condition developed frequently with aromatic anticonvulsants, but with new antiepileptic drugs as well. We experienced three lamotrigine-induced AHS cases with symptoms such as fever, rash, leukopenia, eosinophilia and lymphadenopathy, which subsided after withdrawal of lamotrigine.

A case of carbamazepine-induced anticonvulsant hypersensitivity syndrome expressing eosinophilic pneumonia / 천식및알레르기

Anticonvulsant hypersensitivity syndrome is a potentially fatal drug reaction with cutaneous and systemic reactions to the arene oxide-producing anticonvulsants: phenytoin, carbamazepine, and phenobarbital. In most cases, the hallmark features of fever, rash, and lymphadenopathy are accompanied by multiorgan-system abnormalities. We experienced a 41-year-old man with a carbamazepine-induced reaction, presenting with fever, rash, eosinophilia, hepatitis, and eosinophilic pneumonia. Because symptoms persisted in spite of discontinuation of carbamazepine, we administered a systemic steroid. After use of the steroid, symptoms were relieved and liver and pulmonary functions improved gradually.

A case of anticonvulsant hypersensitivity syndrome with pseudolymphoma induced by carbamazepine / 천식및알레르기

Anticonvulsant hypersensitivity syndrome(AHS) is an uncommon, but potentially fatal, multi-systemic disorder that occurs after exposure to phenytoin, carbamazepine, phenobarbital. Clinical features and laboratory data are diverse and variable. The multi-systemic reaction presents as fever, skin eruptions, lymphadenopathy, hematologic abnormality, and hepatitis. It is postulated that this mechanism can cause deficient enzymatic reduction by epoxide hydrolase. The diagnosis of AHS is made by reviewing the history of drug exposure and clinical course. It is important to discontinue use of the offending drug suspected for AHS and to closely observe patients with anticonvulsant therapy. We experienced a case of anticonvulsant hypersensitivity syndrome developed by carbama-zepine, presented with pseudolymphoma in lymph node biopsy and improved by discontinuing the drug and implementing steroid treatment. We report this case with pathologic findings and a brief review.