A 46-year-old woman visited our clinic with a 7 day history of painful, multiple plaques with superimposed 2 day old vesicles on her extremities, trunk and face. She also complained of fever, headache, myalgia, arthralgia, a cough and sputum. She was diagnosed with atypical pneumonia at the local internal medicine clinic within 5 days, namely 2 days after the outbreak of skin lesions, but her respiratory symptoms were none-responsive to the empirical use of antibiotics and the vesicles and pustules suddenly became superimposed on the plaques. She was in good health before this present illness. There was no history of medication and prior systemic disease, including infection and malignancy. She also denied any recent history of an upper respiratory infection.
On physical examination, skin lesions were tender and red-to-purple. Some plaques had multiple superimposed vesicles (Fig. 1). Her breathing sounds were coarse. Initial laboratory investigations showed WBC 10,400/mm3 (seg: 87%), ESR 36mm/hr, CRP 147 mg/L, Hb 10.9 gm/dL, AST/ALT 70/76 U/L. Other CBC panel, blood chemistry and urinalysis were allwithin normal limits. EKG showed non-specific findings. Plain X-ray and CT of the chest showed bilateral pleural effusions and mild lower lobar infiltrations (Fig. 2). Investigations for infectious causes of pulmonary symptoms included sputum culture and special staining for bacteria, fungi, and mycobacteria, all of which yielded negative results. A skin biopsy specimen from the vesicle of the right leg revealed epidermal spongiosis and exocytosis, severe dermal edema and dermal infiltration of neutrophils and nuclear dust without evidence of vasculitis (Fig. 3). Viagra Professional
Fig. 1. Tender, multiple, red-to-purple plaques and superimposed vesicles and pustules on the upper (A) and lower (B) extremities.
The clinical basis of painful erythematous plaques, fever, leukocytosis, elevated ESR, CRP, and histologic findings of the skin biopsy were suitable for the diagnostic criteria of the Sweet syndrome. To exclude infectious complications, broad-spectrum empiric antibiotics and antiviral agents were given. But pulmonary manifestations were non-responsive to the empirical use of antibiotics, and an extensive search for microbial (bacterial, fungal and mycobacterial) pathogens was negative. There fore, we thought that this patient had Sweet syndrome involving the skin and lungs. Antibiotics and antiviral therapy were stopped after 6 days of admission, and systemic corticosteroidal therapy (lmg/kg) was started. Clinical, and then radiologic features improved dramatically after 5 days and her symptoms almost cleared.
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Fig. 2. Bilateral pleural effusions and mild lower lobar infiltrations upon chest X-ray (A) and improved radiologic features after the systemic corticosteroidal therapy for 5 days (B). An arrow marks the pleural effusion and an asterisk marks lobar infiltrates on the chest CT (C).
For the purpose of detecting an underlying malignancy, we performed a bone marrow biopsy and investigated tumor markers such as AFP, CA72.4, CA19-9, SCC-Ag, CEA, and CA125. All were negative except CA125. As CA125 was high, gastrointestinal and gynecologic studies were recommended, but she refused them. The patients was discharged after her 12 days admission period and did not have a relapse for the 1 year follow-up period.
Fig. 3. A skin biopsy specimen of the lesion revealed epidermal spongosis and exocytosis, severe dermal edema and dermal infiltration of neutrophils and nuclear dust without evidence of vasculitis.