NODULAR FAT NECROSIS ASSOCIATED WITH LUPUS-INDUCED PANCREATITIS

A 29-year-old black woman presented with a B-year history of lupus nep hritis, cerebritis, arthritis, and recurrent facial erythema. She was admitted to the National Naval Medical Center following an acute lupus flare manifested by the onset of acute tubular necrosis requiring the initiation of hemodialysis. The patient had also developed a Staphylo coccus aureus septicemia secondary to an infected IV site. During the first and second weeks in hospital, the patient responded well to aggr essive antibiotic therapy and oral prednisone. As the oral prednisone was decreased from 60 mg to 40 mg per day on day 19 in hospital, the p atient developed several tender, erythematous, subcutaneous nodules ov er the lower extremities (Fig. 1). There was no cutaneous ulceration o r drainage. Although the initial clinical diagnosis was erythema nodos um, a deep incisional biopsy was performed to rule out infectious, vas culitic, or lupus panniculitis, Histologic findings of a representativ e leg nodule included lobular panniculitis with extensive fat necrosis , 'ghost cell' formation, acute suppurative inflammation, and focal ca lcification (Fig, 2). Stains and cultures for organisms were negative. These findings were felt to be pathognomonic for nodular fat necrosis associated with pancreatic disease. Laboratory data revealed serum am ylase and lipase to be markedly elevated at 1342 U/L (N=28-110 U/L) an d 4160 U/L (N=7-60 U/L), respectively; white blood cell count and diff erential were within normal limits. Other significant laboratory data included an anti-DNA of 692 IU/mL (N=<100 IU/mL) and positive anti-Sjo gren's syndrome-A. Simultaneous punch biopsy of an erythematous facial macule revealed epidermal atrophy, vacuolar interface change, and a m ild perivascular and periadnexal lymphohistiocytic infiltrate, consist ent with lupus erythematosus. Computed tomography (CT) scan and ultras ound examination of the abdominal cavity failed to provide further evi dence of pancreatitis. Although the patient was initially asymptomatic , 1 week following the onset of her leg nodules she developed severe a nkle and knee arthralgias, abdominal pain, nausea, and vomiting which were attributed to her pancreatitis. She was treated with high-dose pr ednisone and Cytoxan for control of her lupus flare, which brought abo ut the resolution of her leg nodules and associated symptoms over the following 6 weeks, Only postinflammatory hyperpigmentation remained in the skin overlying the sites of nodular fat necrosis.