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/////////////////////Anticonvulsant Hypersensitivity Syndrome: Implications for Pharmaceutical Care
Posted 11/02/2007
KarenBeth H. Bohan, Pharm.D.; Tarannum F. Mansuri, Pharm.D.; Natalie M. Wilson, Pharm.D.Author Information
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Clinical Insights In The Treatment of ADHD Learn more about ADHD prevalence and treatment, recent data on ADHD and SUD comorbidity, important conventions in 2007, and more. Read expert interviews from key opinion leaders in ADHD.
Abstract and Introduction
Abstract
Anticonvulsant hypersensitivity syndrome (AHS) is a delayed adverse drug reaction associated with the use of aromatic anticonvulsant drugs. It has been most commonly reported with the use of phenytoin, carbamazepine, and phenobarbital. Although its occurrence is rare, 1 in every 1000–10,000 exposures, AHS is a serious adverse event often resulting in hospitalization and even death. The clinical manifestations of AHS include a triad of symptoms consisting of dermatologic rashes, fever, and evidence of systemic organ involvement. Diagnosis is most frequently based on the recognition of this triad of symptoms and clinical judgment. The exact mechanism of AHS remains to be determined but is thought to have at least three components: deficiency or abnormality of the epoxide hydroxylase enzyme that detoxifies the metabolites of aromatic amine anticonvulsants, associated reactivation of herpes-type viruses, and ethnic predisposition with certain human leukocyte antigen subtypes. Arene oxides, the toxic intermediaries in the metabolism of anticonvulsant drugs, can accumulate and directly bind to macromolecules, causing cell death, as well as act as prohaptens that bind to T cells, initiating an immune response and systemic reactions. Management of AHS primarily includes discontinuation of the associated anticonvulsant drug. Systemic corticosteroids are usually required for full recovery. An important issue regarding AHS is the cross-sensitivity among aromatic anticonvulsant drugs, which has been reported to be 40–80%. This means that patients with a history of AHS should avoid further use of any aromatic anticonvulsant drug. In addition, a familial association with AHS exists, and family members of the patient with AHS should be educated that they may be at increased risk for developing AHS if they use aromatic anticonvulsant drugs. Anticonvulsant drugs that are generally considered safe are valproic acid and benzodiazepines. Other nonaromatic anticonvulsant drugs should also be acceptable. Pharmacists as health care providers can play an important role in the diagnosis, treatment, and prevention of AHS.
Introduction
Anticonvulsant hypersensitivity syndrome (AHS) is an adverse effect of anticonvulsant drugs, with phenytoin, carbamazepine, and phenobarbital being the most commonly implicated. It includes a triad of symptoms that consists of dermatologic reactions, fever, and evidence of systemic organ involvement.[1] Severity ranges from mild with self-limiting symptoms to death. Numerous cases describing the same phenomenon have been reported in the literature, but several different names have been used. Anticonvulsant hypersensitivity syndrome has also been referred to as drug hypersensitivity syndrome, drug-related eosinophilia with systemic symptoms, Dilantin hypersensitivity reaction, phenytoin syndrome, Kawasaki-like syndrome, mononucleosis-like syndrome, and phenobarbital hypersensitivity syndrome.[1–3]
A major concern with AHS is that cross-sensitivity among anticonvulsants of different pharmacologic drug classes occurs, which is atypical for most allergic drug reactions. An occurrence of AHS in one of our patients led us to further investigate this syndrome. Our patient had a previous phenytoin allergy (rash) and was prescribed carbamazepine for continued seizure control. The pharmacist entered phenytoin as a drug allergy and carbamazepine as an active drug order in the patient's electronic drug profile; however, no drug-allergy interaction warning alert appeared. The patient subsequently developed a dermatologic allergic reaction to carbamazepine, and probable AHS was diagnosed.
Although AHS has been reported in the literature since 1950, many health care professionals are unaware of the potential for cross-sensitivity among anticonvulsant drugs.[1] If computerized pharmacy database checking systems also are unaware, the administration of cross-sensitive anticonvulsant drugs that may elicit AHS can occur.
The goal of this article is to describe the pathogenesis and clinical manifestation of AHS so that health care practitioners can recognize it and treat it appropriately. The most recent studies of AHS have focused on factors that influence the severity of AHS, like reactivation of human herpes viruses (HHVs).[4–14] Others have studied the propensity for people of certain ethnic backgrounds to be at a greater risk for this adverse drug effect.[15–17] In addition, a genetic predisposition to AHS exists. Family members of patients who develop AHS should be aware that they are at an increased risk of developing the same reaction if they use certain anticonvulsants.