pleurisy, pericarditis, and myalgia. Serologic studies revealed a low complement level and anti-DNA antibodies. He was started on 40 mg of prednisone, and his.
LUPUS PANCREATITIS Uchenna R. Nwaneri, MD, Clive 0. Callender, MD, and Joel E. Stevens, MD Washington, DC
Among the many systemic manifestations of lupus is pancreatitis. It may be a part of the multiorgan lupus involvement or it may result as a complication of steroid therapy used in its management. A case of lupus pancreatitis following renal transplantation is presented. The difficulty in differentiating the diagnosis of lupus pancreatitis is illustrated. Emphasis is placed on rapid diagnosis to help decrease the high mortality associated with this disease process. (J Nati Med Assoc. 1995;87:575-576.) Key words * lupus * pancreatitis Lupus is a connective tissue disease characterized by the involvement of many organs.' It is associated with marked and varied immunologic abnormalities. Among the many systemic manifestations of lupus is pancreatitis. Pancreatitis may be an initial presentation of lupus or may result as a complication of steroid therapy used in the management of lupus.2-4 The mechanisms involved in the development of lupus pancreatitis include vasculitis, autoimmune phenomena, and steroid or toxic drug effects.3'4 Pancreatitis may be associated with ascites. Massive ascites complicating lupus pancreatitis following renal transplantation has not been previously reported in the literature. This article describes such a case.
CASE REPORT A 26-year-old African-American male was diagnosed as having systemic lupus erythematosus in 1982. His symptoms included polyarthralgia, malar rash, From the Division of Transplant Surgery, Howard University Medical Center, Washington, DC. Requests for reprints should be addressed to Dr Clive 0. Callender, Division of Transplant Surgery, Howard University Medical Ctr, 2041 Georgia Ave, NW, Washington, DC 20060. JOURNAL OF THE NATIONAL MEDICAL ASSOCIATION, VOL. 87, NO. 8
pleurisy, pericarditis, and myalgia. Serologic studies revealed a low complement level and anti-DNA antibodies. He was started on 40 mg of prednisone, and his symptoms resolved 2 years later. His clinical and serologic disease activity remained quiescent until February 1988 when he developed alopecia, photophobia, and proteinuria. He developed diffuse lupus glomerulonephritis, which was confirmed by a renal biopsy performed in June 1988. This rapidly progressed to end-stage renal failure. The patient was started on hemodialysis. His hemodialysis course was unremarkable. Although his serologic test values remained abnormal, there were no reported episodes of disease flare-ups until July 1989 when he developed alopecia and arthralgia. His rheumatologist attributed this flare-up of disease activity to change in weather-related arthralgia, and his prednisone dosage was increased from 15 mg to 40 mg per day. These symptoms resolved. Hence, pretransplantation workup proceeded, including appropriate pretransplantation crossmatch studies. A living related maternal renal transplantation was performed successfully in August 1989. Despite immunosuppressive treatment, his posttransplantation course was complicated by disease flare-up manifested as photophobia, episcleritis, alopecia, arthralgia, and lupus pancreatitis with massive ascites. The daily ascitic fluid output was as high as 7000 cc/24 hours. Both serum and ascitic fluid amylase levels were markedly elevated (Table). The ascitic fluid lupus erythematosus preparation was positive. The serum complement levels were decreased, and the anti-DNA antibody was positive (Table). His postoperative course was further complicated by the development of diffuse cytomegalovirus, pneumonitis, and serratia sepsis. Despite aggressive treatment
575
WPUS PANCREATITIS
TABLE. SERUM, ASCITIC FLUID, AND ANTI-DNA LEVELS Laboratory Tests Ascitic Anti-DNA Date Serum Fluid 1/88 65 12.6 1:640 47 7.7 11/88 1:160 67 4/89 15.8 1:320 71 6/89 15.5 1:320 52 8/1/89 10.0 1:320 64 8/7/89* 11.0 1:320 9.4 66.9 1:320 8/14/89 44.6 2.8 1:320 8/28/89 *Date of renal transplant was 8/2/89.
with appropriate antibiotics and pulmonary ventilatory support, he died on the 34th day posttransplantation.
DISCUSSION Ascites has been seen in 8% to 11% of lupus patients.' Although systemic lupus erythematosus has been called a form of polyserositis, true primary abdominal ascitic serositis is rare.5 The development of ascites has been related to widespread vasculitis or a form of serositis involving the peritoneal membrane.6 The clinical diagnosis of lupus pancreatitis following renal transplantation in the patient described in this article was based on the development of abdominal pain, nausea, vomiting, and laboratory values of low complement level and high amylase in both serum and ascitic fluid. The ascitic fluid complements were decreased, the anti-DNA antibody was positive, and the lupus erythematosus preparation was positive. Previous studies have documented these findings and suggested the association of ascites with other features of illness as seen in this patient.5'6 It is critical to make the diagnosis of lupus pancreatitis given the above clinical setting. The diagnosis may be aided with its association with multiorgan involvement.3 Lupus pancreatitis must be differentiated from pancreatitis resulting from steroid therapy because the management of each is different. While the steroid dose needs to be decreased in steroid-induced pancreatitis, the dosage will need to be increased in lupus pancreatitis. The severe consequence associated with failure to make this differentiation is highlighted by the work of Goldberg,7 who ascribed pancreatitis in a patient with active lupus to the steroid therapy begun the previous
576
day. This steroid therapy then was reduced, and the patient died 3 days later of widespread vasculitis and interstitial pneumonitis. Increasing the steroid dosage in cases of lupus pancreatitis usually leads to the resolution of symptoms.4-8 The prior cases of massive ascites in lupus patients reported in the literature responded neither to steroid nor immunosuppressive regimens.5'6 None of the prior cases reported was in a renal transplant patient who routinely received this combination therapy as part of the postoperative protocol. However, Olek9 reported a case of lupus serositis with ascites. This patient subsequently developed rapidly progressive glomerulonephritis, and as was the case described here, the patient died.
CONCLUSION Renal transplantation in systemic lupus erythematosus should be avoided during periods of disease flare-up. The differentiation of lupus pancreatitis from drug-induced pancreatitis must be made rapidly. Delay in diagnosis may result in a fatal outcome. Institution of appropriate treatment must be made rapidly. However, as demonstrated in this case, despite institution of appropriate treatment with steroids and immunosuppressive drugs, lupus pancreatitis may still prove to be fatal. Literature Cited 1. Dubois EL, ed. Lupus Erythematosus. Los Angeles, Calif: University of Southern California Press; 1974. 2. Mallory A, Kern F Drug-induced pancreatitis: a critical review. Gastroenterology. 1980;78:813-820. 3. Reynolds JC, Inman MD, Kimberly RP, et al. Acute pancreatitis in systemic lupus erythematosus: report of 20 cases and a review of the literature. Medicine (Baltimore). 1982;61 :25-31. 4. Sparberg M. Recurrent acute pancreatitis associated with systemic lupus erythematosus: report of a case. American Journal of Digestive Diseases. 1 967;1 2:522-525. 5. Bitran J, McShane D, Ellman M. Ascites as the major manifestation of systemic lupus erythematosus. Arthritis Rheum. 1976;1 9:782-785. 6. Schocket AL, Lain D, Kohler PF, Steigerwald J. Immune complex vasculitis as a cause of ascites and pleural effusions in systemic lupus erythematosus. J Rheumatol. 1978;5:33-38. 7. Goldberg BH, Bergstein JM. Acute respiratory distress in a child after steroid-induced pancreatitis. Pediatrics. 1978;61 :317. 8. Hossain J, Davies M, Williams JD. Acute abdomen in systemic lupus erythematosus. 1984:31-34. 9. Olek S. Przypadek Tocznia Rumieniowatego UlkIadowego Wodobr Zuszem Jako Objawein Wiodacym. Wiad Lek. 1 972;25:997-1 001.
JOURNAL OF THE NATIONAL MEDICAL ASSOCIATION, VOL. 87, NO. 8
