Pustular panniculitis in a patient with rheumatoid arthritis

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Abstract
A 51‐year‐old woman presented with a 10‐day history of painful red swelling of the right lower leg. She had been treated with prednisolone for classic (seven criteria according to the American Rheumatism Association), seropositive, rheumatoid arthritis of 5 year's duration. She had received prednisolone at an initial dose of 60 mg/day, with gradual tapering over 16 weeks to a final dose of 7.5 mg/day. In addition, mizoribine (immunosuppressive agent) 100 mg/day was administered for 2 months. Examination of the skin revealed erythematous lesions with shiny surfaces that were markedly swollen and involved the entire right lower leg, with partial violaceous, eroded areas, and bullous formation (Fig. 1). Extensive fat necrosis was accompanied by necrosis of the overlying skin, and a large amount of an oily, yellow serous liquid, approximately 200 mL, was discharged from the lesions. There were no sign or symptom of arteritis or venous insufficiency. A skin biopsy showed prominent edematous change in the reticular dermis, and perivascular inflammatory cell infiltrate. In addition, lobular and septal panniculitis with fat necrosis accompanied by a massive cellular infiltrate consisting of numerous neutrophils, neutrophilic dust, and occasional eosinophils, was observed mainly in the subcutaneous lobules and partially in the septa (Fig. 2). Leukocytoclastic vasculitis of the whole dermis, involving small and medium‐sized arteries and venules, with fibrlnoid necrosis of the vessel walls, was present. However, no deposition of immunoglobulins and complements was demonstrated on immunohistopathologic examinations. The overall thickness of the subcutaneous space had collapsed, leaving extensive microcysts lined by membranous fat necrosis and filled with massive neutrophilic and eosinophilic infiltrate. Stains for organisms, including acid‐fast bacteria, were negative. Laboratory studies showed anemia (hemoglobin, 10.3 g/L), elevated erythrocyte sedimentation rate;.,. (98 mm/h), white blood cell count (8000/μL), increased levels of aspartate aminotransferase (44 U/L), alanine aminotransferase (41 U/L), alkaline phosphatase (29.1 King‐Arnnstrong Unit), Leucine amino peptidase (567 lU/L), gamma‐glutamyl transferase (483 IU/L), hepatitis B antigen (5361 U/mL), hepatitis B antibody (13.3 mU/mL), circulating immune complexes (9.8 (xg/mL), and positive rheumatoid factor (40 IU/mL), positive antinuclear antibody test (1: 640) in a speckled pattern, without anti‐DNA, and a decreased complement level of C4 (11.5 mg/dL). Serum protein electrophoresis showed hypergamma‐globulinemia (40.7%). Hepatitis C antibody, C‐reactive protein, cryogiobulin, complement level (CH50, C3), extractable nuclear antigen (Sm, RNP), amylase, alpha‐1 antitrypsin inhibitor, chest roentgenogram, and electrocardiogram were within normal limits or revealed negative findings. No organisms were cultured from repeated swabs. Treatment with prednisolone 60 mg (2 mg/kg)/day along with methotrexate 10 mg/week was started. Shortly after, the erythematous swelling of the affected leg regressed moderately and within 4 weeks the ulcers became clean and were totally healed. The dose of prednisolone was decreased to 25 mg/day along with methotrexate 10 mg/week, but no relapse has occured during the 8 months’follow‐up.

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