Drug-Induced Sweet Syndrome: A Clinical Case and Review of Management Strategies

Abstract:
Sweet Syndrome (SS), also known as acute febrile neutrophilic dermatosis, is a rare inflammatory skin disorder characterized by the sudden onset of erythematous, painful skin lesions accompanied by systemic symptoms such as fever and elevated white blood cell count. While the condition can occur idiopathically or in association with malignancies, drug-induced SS is increasingly recognized. This article presents a clinical case of drug-induced SS following the initiation of a new inhaled medication and reviews current diagnostic and therapeutic approaches.Introduction:
Sweet Syndrome is a rare condition that presents with acute-onset, tender erythematous plaques or nodules, often accompanied by fever, leukocytosis, and elevated C-reactive protein levels. The pathogenesis involves neutrophilic infiltration of the dermis without evidence of vasculitis. While the exact etiology remains unclear, SS has been classified into three subtypes: classical (idiopathic), malignancy-associated, and drug-induced .

Clinical Case:
A 55-year-old female with a history of hypertension and chronic obstructive pulmonary disease (COPD) presented with erythematous, painful lesions on her face and neck, accompanied by low-grade fever. She had no known drug allergies and was a smoker. Her medication regimen included enalapril and inhaled formoterol. Due to worsening pulmonary function, her pulmonologist switched her to a combination inhaler containing indacaterol and glycopyrronium. Within 48 hours of initiating the new therapy, the patient developed the characteristic skin lesions.

Diagnostic Workup:
The patient was referred to dermatology, where a skin biopsy confirmed a dense neutrophilic infiltrate without vasculitis, consistent with SS. Laboratory tests revealed leukocytosis with neutrophilia and negative autoimmune serologies. The temporal relationship between the initiation of the new medication and the onset of symptoms suggested a drug-induced etiology

Management:
The offending medication was discontinued, and the patient was started on systemic corticosteroids. Within 48 hours, there was significant improvement in both the skin lesions and systemic symptoms. This rapid response to corticosteroid therapy is characteristic of SS and supports the diagnosis of drug-induced SS .

Discussion:
Drug-induced SS is a recognized entity, with several medications implicated, including granulocyte colony-stimulating factors, azathioprine, bortezomib, and antibiotics such as trimethoprim-sulfamethoxazole . The pathophysiology may involve drug-induced cytokine release leading to neutrophil recruitment and activation. Management primarily involves discontinuation of the offending agent and initiation of systemic corticosteroids. In refractory cases, alternative therapies such as potassium iodide or colchicine may be considered .

Conclusion:
Sweet Syndrome, particularly the drug-induced form, should be considered in patients presenting with acute-onset erythematous skin lesions and systemic symptoms following the initiation of a new medication. Early recognition and appropriate management, including discontinuation of the causative drug and initiation of corticosteroid therapy, are essential for favorable outcomes. Clinicians should maintain a high index of suspicion for SS in such clinical scenarios to ensure timely diagnosis and treatment.

Keywords: Sweet Syndrome, acute febrile neutrophilic dermatosis, drug-induced, corticosteroids, skin biopsy, neutrophilic infiltrate, medication-induced rash, dermatology, pharmacovigilance, systemic corticosteroids.