Reprint requests and correspondence:James S. Scolapio, M.D.,4500 San Pablo Road, Jacksonville, FL 32224.

Received June 19, 1998; accepted Aug. 19, 1998.

REFERENCES

1. Callen JP. Skin manifestations of digestive disease. In:Haubrich WS, Schaffner F, Berk JE, eds. Bockus gastroenter-ology, Vol. 4. Philadelphia: WB Saunders, 1995:3324–44.

2. Sherertz EF, Jorizzo JL. Skin lesions associated with gastro-intestinal diseases. In: Yamada T, ed. Textbook of gastroen-terology, Vol. 1. Philadelphia: JB Lippincott, 1995:953–68.

3. Mirowski GW, Berger TG. Oral and cutaneous manifestationsof gastrointestinal disease. In: Feldman M, Scharschmidt BF,Sleisinger MH, eds. Sleisinger & Fordtran’s gastrointestinaland liver disease: Pathophysiology/diagnosis/management.Philadelphia: WB Saunders, 1998:439–53.

4. Kohlmeier W. Multiple Hautnekrosen bei Thrombangiitis ob-literans. Arch Dermatol 1941;181:783–92.

5. Degos R, Delort J, Tricot R. Dermatite papulo-squameuseatrophiante. Bull Soc Fr Dermatol Syphiligr 1942;49:148–50.

6. Snow JL, Muller SA. Degos syndrome: Malignant atrophicpapulosis. Semin Dermatol 1995;14:99–105.

7. Atchabahian A, Laisne´ MJ, Riche F, et al. Small bowel fistulaein Degos’ disease: A case report and literature review. Am JGastroenterol 1996;91:2208–11.

8. Burg G, Vieluf D, Stolz W, et al. Maligne atrophische Papu-lose (Morbus Ko¨hlmeier-Degos). Hautarzt 1989;40:480–5.

9. Magrinat G, Kerwin KS, Gabriel DA. The clinical manifesta-tions of Degos’ syndrome. Arch Pathol Lab Med 1989;113:354–62.

10. Su WPD, Schroeter AL, Lee DA, et al. Clinical and histologicfindings in Degos’ syndrome (malignant atrophic papulosis).Cutis 1985;35:131–8.

11. Subbiah P, Wijdicks E, Muenter M, et al. Skin lesion with afatal neurologic outcome (Degos’ disease). Neurology 1996;46:636–40.

12. Degos R. Malignant atrophic papulosis. Br J Dermatol 1979;100:21–35.

Pericarditis AssociatedWith Inflammatory BowelDisease: Case ReportTamas Molnar, M.D., Marta Hogye, Ph.D., Ferenc Nagy, Ph.D.,and Ja´nos Lonovics, Ph.D.First and Second Departments of Medicine, Albert Szent-Gyorgyi Medical University, Szeged, Hungary

INTRODUCTION

Extraintestinal manifestations are common complications ofinflammatory bowel disease (IBD), whereas the associationof cardiac disease with IBD is rarely reported. Up to 1997102 IBD patients had been reported with associated cardiacdiseases as extraintestinal manifestations of IBD or theconsequence of drug-induced side effects (Medline Express,SilverPlatter International N.V.). Pericarditis was found tobe the most frequent symptom (70% of the cases), followedby myocarditis (10%). The majority of these cases wereinterpreted as true extraintestinal manifestations of IBD;only nine patients were considered to develop cardiac com-plications as a side effect of treatment (sulfasalazine inthree, mesalamine in five, and azathioprine in one case) (1).

We present here a case from our group of 500 IBDpatients, in whom severe cardiac complication was ob-served.

CASE REPORT

A 29-yr-old woman was referred to our clinic in 1996because of a severe relapse of IBD, with 6-month history ofbloody diarrhea. She was observed in another hospital 3months before her present admission. At that time, herdisease was diagnosed on the basis of endoscopic and his-tological findings as ulcerative colitis (UC), and sulfasala-zine was started at a daily dose of 3 g. Five weeks latersulfasalazine administration was discontinued because ofupper gastrointestinal symptoms and was replaced by me-salamine (500 mgb.i.d.). On admission, the woman had fourto seven episodes of bloody diarrhea daily, fever, nausea, acough, dyspnea, and chest pain. Auscultation of the heartand the lungs was normal (no pericardial rub was audible)and examination of the abdomen was also negative. Hertemperature was 38.6°C, the blood pressure 120/80 mm/Hgand the pulse rate was 105/min. The laboratory data with theexception of erythrocyte sedimentation rate (ESR: 72 mm/h), hemoglobin (11.9 g/dl), white cell count (12.23 109/L),platelets (5333 109/L) and fibrinogen (6.34 g/L) werewithin the normal ranges. Viral serology showed no evi-dence of recent viral infection, repeated blood cultures werenegative, and the pANCA was positive. Results of otherimmunoserology (antinuclear antibody, anti-DNA, latextest, lupus erythematosus preparation, and complementmeasurement) were normal. The chest x-ray and electrocar-

Figure 1. Degos’ disease. Multiple porcelain papules with eryth-romatous borders. Normal postoperative surgical staples.

1099AJG – April, 1999 Brief Case Reports

diogram were both negative. Endoscopy, histology, andtechnetium-99m HMPAO–labeled leukocyte scintigraphydemonstrated active left-sided (indeterminate) colitis, with-out a clear distinction between UC and Crohn’s disease(CD). The echocardiogram revealed pericarditis with mod-erate-sized circumferential and 1.5 cm of posterior pericar-dial fluid. Methylprednisolone, 125 mg, was started, andmesalamine therapy was continued without a break. Atdischarge, the patient’s fever and bloody diarrhea had dis-appeared. The steroid was tapered off and 1 yr later sheremains completely well. The last echocardiogram con-firmed the disappearance of the pericardial effusion. She iscurrently on a maintenance dose of 3 g of mesalamine daily,with 4 mg of methylprednisolonep.o. on alternate days.Repeated coloscopy revealed a typical cobble stone appear-ance of the mucosa, suggesting CD with narrowing of theproximal sigmoid colon. The histology did not differentiatebetween the two types of IBD.

DISCUSSION

Pericarditis has been described as the most frequently ob-served cardiac association with IBD. This extraintestinalmanifestation usually starts together with a relapse of thebowel symptoms (2), or may be the initial manifestation ofIBD (3). Most cases of pericarditis are associated withcolonic involvement in both common types of IBD (4),nevertheless the incidence of pericarditis is slightly higherin UC. However, pericarditis, as well as myocarditis orpleuritis, may also be caused by the drugs used to treat IBD.The sulfapyridine moiety of sulfasalazine can induce a lu-pus-like syndrome, which can also present with pleural orpericardial effusion (5). Similar reactions have rarely beenreported in connection with mesalamine products (6, 7) andazathioprine (8). The pathogenesis of drug-induced cardiacdamage (like the etiology of IBD) remains unknown. In ourcase, the pericardial effusion and the relapse of IBD pre-sented together.1 month after the mesalamine therapy hadbeen started without any complication. Possible infectionswere excluded, the immunoserological findings were nega-tive. Treatment with 5-aminosalicylic acid (5-ASA) wasnever stopped and pericarditis has not relapsed.

This case shows that serious cardiac complications maybe associated with IBD as an unusual extraintestinal mani-festation. During the follow-up of patients with IBD, caremust be taken concerning extraintestinal cardiac manifesta-tions.

Reprint requests and correspondence:Tamas Molnar, M.D.,First Department of Medicine, Albert Szent-Gyo¨rgyi Medical Uni-versity, Szeged, P.O. Box 469, Hungary, H-6701.

Received May 15, 1998; accepted Sep. 18, 1998.

REFERENCES

1. Gujral N, Friedenberg F, Friedenberg J, et al. Pleuropericarditisrelated to the use of mesalamine. Dig Dis Sci 1996;41:624–6.

2. Farley JD, Thomson AR, Dasgupta MK. Pericarditis and ulcer-ative colitis. J Clin Gastroenterol 1986;8:567–8.

3. Sarrouj B, Zampino DJ, Cilursu AM. Pericarditis as the initialmanifestation of the inflammatory bowel disease. Chest 1994;106:1911–2.

4. Patwrdhan RV, Heilpern J, Brewster AD, et al.Pleuropericarditis: An extraintestinal complication of inflam-matory bowel disease. Arch Intern Med 1983;143:94–6.

5. Griffiths ID, Kane SP. Sulphasalazine-induced lupus syndromein ulcerative colitis. Br Med J 1977;2:188–9.

6. Jenss H, Becker EW, Weber W. Pericardial effusion duringtreatment with 5-aminosalicylic acid in a patient with Crohn’sdisease. Am J Gastroenterol 1990;85:332–3.

7. Agnholt J, So¨rensen HT, Rasmussen SN, et al. Cardiac hyper-sensitivity to 5-aminosalicylic acid. Lancet 1990;I:1135.

8. Simpson CD. Azathioprine-induced pericarditis in a patientwith ulcerative colitis. Can J Gastroenterol 1997;11:217–9.

A Double Stomach in an AdultGeorge Blinder, M.D., Nurith Hiller, M.D., andSamuel N. Adler, M.D., F.A.C.G.MAR Institute for Diagnostic Radiology; Department ofRadiology, Shaare Zedek Medical Center; and Department ofGastroenterology Bikur Holim Hospital, Jerusalem, Israel

ABSTRACTGastric duplication cysts are uncommon congenital anom-alies and are rarely diagnosed in adults. We present a uniquecase of a communicating type gastric duplication in a youngwoman with the multimodality imaging findings includingbarium examination, CT, and endoscopy. The morphologi-cal criteria for diagnosis of duplication cyst suggestedpathogenetic mechanisms for its formation as well as clin-ical presentation. Associated pathologies are reviewed. (AmJ Gastroenterol 1999;94:1100–1102. © 1999 by Am. Coll.of Gastroenterology)

INTRODUCTION

Gastric duplications are relatively rare, comprising about4% of all alimentary duplications (1). Communication withthe gastric lumen is extremely rare. Review of the literaturerevealed only one report of complete duplication of thestomach diagnosed on barium examination (1). We presenta case of a complete gastric duplication in a young woman,and describe the endoscopic appearance as well as thefindings on barium examination and CT.

CASE REPORT

A 26-yr-old, usually healthy woman was refered by herfamily physician for gastroscopy because of recurrent epi-gastric pain. The endoscopic examination revealed an areawith erosions and mucosal hemorrhages in the pylorus and

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