Stevens-Johnson syndrome or toxic epidermal necrolysis from antihypertensive medications: A systematic review of cases.

BACKGROUND: Stevens-Johnson syndrome and toxic epidermal necrolysis represents a life-threatening disease spectrum that occurs primarily as a medication reaction. While antibiotics, allopurinol, and anticonvulsants are among the most commonly implicated medications, case reports exist showing antihypertensive medications as a less-recognized culprit. METHODS: A systematic review of literature identified cases of Stevens-Johnson syndrome and toxic epidermal necrolysis from antihypertensive medications, and we compiled a comprehensive description of offending medications and the subsequent clinical course. RESULTS: There were 34 studies that met inclusion criteria, with 1 study being a case series of 3 cases, for a total of 36 cases. Patients had a median age of 65-years-old, are predominantly females, and present to the hospital at a median of 11 days after initiation of the medication. Symptoms at presentation are primarily rash with fever/chills, oral/mucosal lesions, and malaise also being frequently seen. Diltiazem was the most frequently implicated medication, followed by minoxidil and captopril, while calcium channel blockers were the most frequently implicated antihypertensive class, followed by diuretics and vasodilators. Diagnosis was obtained primarily through biopsy or clinically. Treatment consisted of discontinuation of the offending drug in all cases, as well as systemic corticosteroids in over half of cases. Patients were hospitalized for a median of 10 days, with complications including sepsis, renal failure, and cardiopulmonary arrest. Ultimately, complete resolution and discharge occurred in 74% of cases, with death in 26%. CONCLUSION: Early recognition by clinicians is vital to achieving a favorable outcome, but identification of culprit medications can be difficult. Future studies should seek larger sample sizes and try to prove causation by further understanding the underlying pathophysiology.