PATCH TESTING TO GUIDE ALTERNATIVE AGENTS IN A PATIENT WITH DELAYED CUTANEOUS REACTION TO ANTIEPILEPTICS

• Published in: Annals of allergy, asthma, & immunology Vol. 131; no. 5; pp. S122 - S123
• Main Authors: Mirmelli, B., Estrada-Mendizabal, R., Gonzalez-Estrada, A., Paredes, A. Canel
• Format: Journal Article
• Language: English
• Published: Elsevier Inc 01.11.2023
• ISSN: 1081-1206; 1534-4436
• DOI: 10.1016/j.anai.2023.08.366

Diagnosis of delayed hypersensitivity reactions (HSRs) is based on clinical history alone; however, patch testing (PT) may guide clinicians when an alternative medication is needed. There is currently no international consensus on PT to antiepileptics. A 38-year-old female with a known history of epilepsy was evaluated for a maculopapular exanthem (MPE) to antiepileptics. As a teen, she developed a MPE from carbamazepine and was switched to valproic acid without further adverse reactions. Then at age 32, she was switched from valproic acid to levetiracetam while seeking a pregnancy but developed anxiety, dizziness, and palpitations. At age 37, the patient was started on lamotrigine, and after 7 days, she developed a MPE. No facial edema, fever, blisters, lymphadenopathies, pustules, or purpuric lesions were reported, and her laboratory tests were unremarkable. PTs to lamotrigine (aromatic anticonvulsant) and levetiracetam (non-aromatic anticonvulsant) were performed at 10%, 20%, and 30% diluted in petrolatum, 30% diluted in water, undiluted, and a negative control (petrolatum). Lamotrigine was positive (1+) with erythema and papules at 48 hours, and levetiracetam was negative (both in all concentrations). The patient tolerated an open challenge to levetiracetam without adverse reactions. Antiepileptic PT sensitivity varies between 20-80%. This variability is attributed to variable drug concentrations and vehicles, commercially available PT preparations, intrinsic drug factors such as lipophilicity, variable molecular weights, whether the drug or a metabolite is the immunogenic trigger, or secondary to transient potentiating factors that cannot be replicated such as viral infections or autoimmune conditions.