Abstract
To the Editor:
A 67-year-old man, who had previously been on bisoprolol without issue for ischemic heart disease, was admitted for a generalized pruritic pustular eruption, which began 8 days after initiation of oral propranolol. Prior to admission, he had seen his general practitioner for a rash on his back and was given cefuroxime and prednisolone 10 mg daily without improvement, requiring admission 2 weeks after rash onset.
Examination revealed generalized blanchable erythematous patches, with overlying non-follicular pustules coalescing into lakes of pus, and areas of desquamation (Fig. 1a). The body surface area affected was 75%. He was afebrile and systemically well. Initial laboratory evaluation was significant for marked neutrophilia of 21.39 × 109/L and acute renal impairment with creatinine of 148 μmol/L. The initial diagnostic considerations included generalized pustular psoriasis or acute generalized exanthematous pustulosis (AGEP).
Propranolol, cefuroxime, and prednisolone were discontinued, and topical corticosteroids were prescribed. His rash rapidly improved with resolution of all pustules and reduction of body surface area involvement to 30% in 5 days, and he was discharged.
On review 7 weeks after rash onset, his rash had completely resolved, and he had been restarted on oral bisoprolol, which he continued to tolerate without event. His skin biopsy demonstrated confluent parakeratosis and spongiosis with an absent granular layer, but no suprapapillary plate thinning or papillary dermal vessel dilation.
As the onset date of pustules was unclear, patch tests were done with both pulverized propranolol (30% pet) and cefuroxime tablets (30% pet) with occlusion for 48 hours, with reading at 48 and 96 hours, according to recommendations of the International Contact Dermatitis Research Group. 1 Patch testing to the pure drugs and preservatives was considered but not performed, as these were unavailable. Readings at 48 hours were negative, but readings at 96 hours were positive (+) to propranolol (30% pet) and negative (−) to cefuroxime (30% pet) (Fig. 1b). The final diagnosis was AGEP to propranolol.
AGEP presents as an acute diffuse erythematous eruption studded with numerous non-follicular sterile pustules, usually beginning on the face or intertriginous areas, and spontaneously resolves within 15 days. Many drugs, most commonly antimicrobials, have been implicated in AGEP. The EuroSCAR study group has established an AGEP validation score to determine the likelihood of AGEP, based on morphology, course, and histological features. 2 This patient’s score was 9, indicating a definite case. AGEP attributed to beta-blocker usage is exceedingly rare, with only 1 report. Cross-reactivity between beta-blockers is not well-established—isolated cases have demonstrated cross-reactivity to atenolol in labetalol-induced AGEP, cross-reactivity to levobunolol in timolol-associated allergic contact dermatitis, and tolerance of bisoprolol in propranolol-induced urticaria.3-5 In our case, even though drug patch testing to bisoprolol and other beta-blockers was not performed, the patient had already inadvertently restarted and tolerated bisoprolol prior to our outpatient review. This case illustrates the utility of patch testing in propranolol-induced AGEP, as well as tolerance of bisoprolol in a case of propranolol-induced AGEP, and may provide guidance for similarly afflicted patients who would otherwise derive therapeutic benefit from beta-blockers.