Unusual Case of Sweet Syndrome Triggered by New Inhaler Therapy in Primary Care
A 42-year-old patient presented to their primary care clinic with a painful, raised, erythematous lesion on the forearm (see image) approximately one week after beginning a new combination inhaler containing a long-acting beta-agonist and corticosteroid for moderate asthma control.
The lesion began as a small erythematous papule, rapidly enlarging into a tender, well-demarcated, edematous plaque. The patient also reported low-grade fever, malaise, and joint stiffness, but denied respiratory infection, insect bites, or recent trauma.
Laboratory tests revealed:
Mild leukocytosis with neutrophilia
Elevated ESR and C-reactive protein
Negative autoimmune panel and infectious serology
A punch biopsy confirmed dense dermal neutrophilic infiltration consistent with Sweet syndrome. No evidence of vasculitis or infection was noted.
Given the timing of symptom onset and exclusion of other triggers, the new inhaler was suspected as the precipitating factor.
Management and Outcome
The inhaler therapy was discontinued immediately. The patient was started on systemic corticosteroids (prednisone 0.5 mg/kg/day), leading to rapid improvement in pain and reduction of lesion size within 72 hours.
Over the following week, systemic symptoms resolved completely, and the lesion healed without scarring. The patient was switched to an alternative inhaler without recurrence of symptoms over six months of follow-up.
Discussion
This case represents a rare medication-induced Sweet syndrome possibly linked to inhaler therapy. While systemic medications are known triggers, topically or locally delivered drugs—such as inhaled corticosteroids—are less commonly associated with systemic immune reactions.
The underlying mechanism may involve immune dysregulation or hypersensitivity, where the inhaler’s active component or excipient triggers neutrophilic activation and cytokine release.
Recognizing the condition early is crucial, as misdiagnosis can lead to unnecessary antibiotic use or delayed corticosteroid therapy. Primary care providers should maintain a high index of suspicion for drug-induced Sweet syndrome in patients developing unusual skin lesions following new medications, even those considered locally acting.
Conclusion
This case underscores the need for clinicians to be vigilant for rare dermatologic reactions to inhaler medications. Timely identification and cessation of the triggering agent, combined with short-course corticosteroid therapy, result in excellent outcomes.
While Sweet syndrome remains an uncommon diagnosis, this case broadens the spectrum of potential triggers and reinforces the vital role of primary care clinicians in early recognition and management of atypical drug reactions.
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