Lamotrigine-associated anticonvulsant hypersensitivity syndrome in bipolar disorder

Chang, Chia-Wei; Shiah, I‐Shin; Yeh, Chin‐Bin; Wang, Tzong-Shi; Chang, Hsin‐An

doi:10.1016/j.pnpbp.2005.11.033

Cited by 20 publications

(22 citation statements)

References 13 publications

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“…In three of the 18 cases reviewed, the use of antibiotics either delayed the discontinuation of the offending anticonvulsant drug 31,37 or delayed specific treatment for AHS. 30 The onset of signs and symptoms of AHS in these 18 cases was as early as 6 days in two cases 23,25 and as late as 12 weeks in another case 21 and started with either rash or fever.…”

Section: Clinical Manifestationmentioning

confidence: 96%

“…2 We reviewed 18 cases that were published in English and readily obtainable, including four cases published before 2004. [21][22][23][24][25][26][27][28][29][30][31][32][33][34][35][36][37] Among these cases, fever and rash occurred in 100% of patients. Maculopapular rashes as a specific type of rash, elevated transaminase levels, and eosinophilia were the next most common findings (Table 1).…”

Section: Clinical Manifestationmentioning

confidence: 99%

“…Reports of AHS from lamotrigine have been published, and this drug certainly should be avoided in patients with previous AHS. 25,29,35 Despite the lack of case reports of AHS with felbamate, oxcarbazepine, and zonisamide, it would be prudent to avoid these aromatic anticonvulsant drugs as well. Fortunately, numerous other nonaromatic anticonvulsant drugs are available commercially (Figure 2), and valproic acid or a benzodiazepine was safely tolerated in 38 of the patients who had rashes to carbamazepine, phenytoin, or phenobarbital in the above-mentioned study.…”

Section: Cross-sensitivitymentioning

confidence: 99%

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Anticonvulsant Hypersensitivity Syndrome: Implications for Pharmaceutical Care

2007

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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.

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Section: Clinical Manifestationmentioning

confidence: 96%

Section: Clinical Manifestationmentioning

confidence: 99%

Section: Cross-sensitivitymentioning

confidence: 99%

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Anticonvulsant Hypersensitivity Syndrome: Implications for Pharmaceutical Care

2007

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“…A systemic allergic reaction to anticonvulsant therapy was first described in 1950 and was named anticonvulsant hypersensitivity syndrome when associated with phenytoin therapy. [1] Since then it has been known as drug hypersensitivity syndrome and is now more often referred to as DRESS syndrome, when it involves a case of “drug rash with eosinophilia and systemic symptoms.”[12] DRESS syndrome is a specific, severe, idiosyncratic drug reaction characterized by a skin rash with fever, facial edema, lymphadenopathy, and visceral involvement (hepatitis, pneumonitis, myocarditis, nephritis, and colitis). The diagnosis can be difficult because many of the clinical features can be nonspecific, and the syndrome often mimics infectious, neoplastic, or rheumatologic conditions.…”

Section: Discussionmentioning

confidence: 99%

Drug rash with eosinophilia and systemic symptoms syndrome due to anti-TB medication

Kaswala

2013

J Family Med Prim Care

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Drug rash with eosinophilia and systemic symptoms (DRESS) syndrome is a severe, idiosyncratic, multi-system reaction characterized by the clinical triad of fever, rash, and internal organ involvement. The mortality rate is estimated to be 8%, especially among patients with liver involvement, so early recognition is imperative. Drugs commonly associated with the development of DRESS syndrome include anticonvulsants, long-acting sulfonamides, and anti-inflammatory medications; however, there are no reported cases implicating anti-tuberculosis (anti-TB) medications. We report a case of DRESS syndrome from anti-TB therapy. A 68-year-old male with pulmonary TB presented with pruritic skin eruption and sore throat, 8 weeks after starting Rifampin, Isoniazid, Pyrazinamide, and Ethambutol (RIPE) therapy. He takes metformin and glyburide for diabetes. Physical exam was significant for diffuse, exfoliative erythematous macules with target lesions involving the entire skin surface, without mucosal involvement. Laboratory data was significant for mild transaminitis and new onset eosinophilia. Given suspicion of drug eruption, RIPE therapy was discontinued. Skin biopsy confirmed erythema multiforme. Despite discontinuation of the implicated medications, eosinophilia and transaminitis continued to worsen, and so systemic corticosteroids were started. After 4 weeks of discontinuation of RIPE therapy, the cutaneous eruption resolved and laboratory data returned to normal. The patient is finishing course of anti-TB with cycloserine and moxifloxacin. Upon follow up as outpatient, the rash was resolving and disappeared in 1 month. DRESS syndrome is always considered when there is high eosinophil counts and multisystem involvement with skin eruptions. It can be potentially life threatening with certain drugs and infectious agents in predisposed individuals. It is imperative to discontinue the causative medication and avoid re-exposure.

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“…In another case report, 17 two patients, one treated with carbamazepine alone and another treated with a combination of lamotrigine and VPA, developed AHS, which subsided immediately after the interruption of the causative agents and supportive treatment was begun. In a unique report, Chang et al 18 described the case of a woman, age 48 years, with bipolar disorder who was treated with lamotrigine and VPA and then developed AHS because of the lamotrigine. The patient recovered after discontinuation of the anticonvulsant medication and initiation of supportive treatment.…”

Section: Introductionmentioning

confidence: 99%