Presentation:
A 44 year old woman presented with a two week history of myalgias and fevers. Three weeks prior to admission the patient received a 10 day course of trimethoprim‐sulfamethoxazole (T‐S) for sinusitis. Her symptoms improved. One week after treatment, she developed myalgias, fevers, and an erythematous patch on her left flank. Continued fevers and an enlarging skin lesion prompted her to seek medical attention. She was admitted for presumed cellulitis.
Physical examination revealed a healthy appearing woman. Temperature was 101 (F), B.P 118/70 mmHg, and pulse was 110/min. Skin examination revealed a 10cm erythematous plaque with a 2 cm central necrosis on her left flank (picture). She had no lymphadenopathy or splenomegaly. The remainder of her physical exam was unremarkable. Laboratory studies revealed a WBC count of 1.3, with an ANC of 0. Bone marrow aspirate showed that all three cell lines were present with a granulocytic predominance and left shift with maturation arrest of the neutrophils, consistent with marrow recovery after drug toxicity from T‐S. Flow cytometry and cytogenetics showed no leukemia. Skin biopsy revealed a Sweet's‐like reaction with mixed cellular infiltrate, but predominantly neutrophils in maturation arrest. An infectious work‐up including blood, urine, marrow and wound cultures was negative. The patient's WBC count and lesion slowly improved over the next week without any directed therapy and she remained well at one month follow‐up.
Discussion:
Sweet's syndrome is the classic neutrophilic dermatosis, first described in 1964 by Dr. Robert Sweet. Sweet's syndrome is characterized by a typical rash with a neutrophilic infiltrate, lack of vasculitis on pathologic examination, peripheral leukocytosis, fever, and response to treatment with glucocorticoids. Sweet's syndrome can be idiopathic or secondary to a systemic process such as pregnancy, infection, drugs, or malignancy. Myelodysplastic syndromes and myeloid leukemias represent 25% of cases. Drug induced Sweet's syndrome can be caused by G‐CSF and antibiotics such as T‐S. Sweet's syndrome in the setting of a peripheral neutropenia is usually limited to patients receiving G‐CSF, but in our case, concomitant T‐S‐induced marrow toxicity resulted in a very atypical presentation of Sweet's.
Conclusion:
Sweet's syndrome is a condition known to mimic cellulitis and should be included in every hospitalist's differential diagnosis for atypical or antibiotic unresponsive cellulitis. Sweet's in the setting of neutropenia is rare, and almost always associated with use of G‐CSF for a known malignancy. Our case describes another such example. Trimethoprim‐sulfamethoxazole is known to cause both bone marrow toxicity and Sweet's syndrome, but when they occur simultaneously, it can result in a very atypical Sweet's ‐like syndrome.
Author Disclosure Block:
J. Piersma, None; B. Garvin, None; S.A. Flanders, None.