Pancreatitis has been previously described in association with systemic lupus erythematosus (SLE) (1-16). We report here a lupus patient who developed severe hemorrhagic pancreatitis within 48 hours of initiation of corticosteroid therapy; we also discuss the relation between pancreatitis and SLE.
CASE REPORTA 50-year-old black woman was admitted to the hospital on March 23, 1981, after she had a generalized seizure at home. She was known to have discoid lupus since 1963 but first became systemically ill in November 1980 when she developed new skin lesions, fever, and malaise. There was no history of photosensitivity, pleuritic chest pain, Raynaud's phenomenon, or arthritis. Previous illnesses included pulmonary tuberculosis in 1969, which was treated with isoniazid, ethambutol, and streptomycin. The patient was a nondrinker with no history of jaundice or intravenous drug abuse. Medications were methyprylon (300 mg nightly) and propanolol (40 mg twice daily).During examination the patient was agitated and disoriented. Temperature was 39.5"C. Skin lesions consistent with discoid lupus were present. Cotton wool spots were observed in each fundus, and oral mucosal ulcerations were noted. The liver was moderately enlarged, and there was synovitis of both knees; the abdomen was not tender.Results of laboratory investigations included: hemoglobin 9.0 g d d l ; white blood cell count (WBC) 5 ,000/mm3; platelet count 1 1 0,000/mm3; erythrocyte sedimentation rate (Wintrobe) 57 mm/hour; partial thromboplastin time 57.6 seconds; urinalysis 3+ protein, 10-20 red blood celldhigh power field, and several granular casts; blood urea nitrogen and creatinine normal; total bilirubin 1.6 mg/dl; alkaline phosphatase 350 mUlml (30-1 10 mUlml); lactate dehydrogenase 600 mU/ml ( Intravenous therapy with hydrocortisone sodium succinate (100 mg every 8 hours) was started on the evening of March 23, 1981. By the night of March 25, 1981, she had become afebrile and well-oriented but had begun to experience diffuse abdominal pain. On the next morning her serum amylase was 1,400 DYE units and, by the evening of March 26, 1981, her blood pressure and urine output had dropped, the abdomen was distended, and ascites was detectable. Despite management with nasal gastric suction, intravenous fluids, and ventilatory support, the patient experienced a rapidly downhill course consistent with severe pancreatitis. There was persistent elevation of serum amylase, a marked drop in serum calcium, the development of the adult respiratory distress syndrome, and disseminated intravascular coagulation.