A man with a leg-vein clot and colonic ulcers

Abstract

A 48-year-old man was admitted to hospital on May 28, 1995, with spasms of lower abdominal pain of variable intensity for 5 weeks, associated with weight loss. He had had a pulmonary embolism after a deep-vein thrombosis 15 years previously. 2 years before admission, he had had pancreatitis of unknown cause. 1 year before admission, colonoscopy had shown a segmental ulcer in the midtransverse colon. He had a segment of colon removed. Histological examination did not establish a cause for the ulcer. He continued to complain of recurrent lower abdominal pain and weight loss. Angiography of his mesenteric arteries was normal. Barium enema radiography of the colon showed a cicatricial stenosis in the mid-transverse colon at the site of the previous resection. This was removed at operation. Histological examination showed a segmental ulcer of unclear cause. After discharge from hospital he still had lower abdominal pain, especially after food. At our institution, physical examination showed he was 180 cm in height and weighed 60 kg. There was paraumbilical tenderness, but no other abnormalities. Repeated stool cultures were negative. Colonoscopy showed a segmental ulcer in the right side of the transverse colon. The ulcer was shallow and 10 cm in diameter. Colonic mucosa at the borders of the ulcer was friable and had petechial haemorrhages. The remainder of the colonic mucosa appeared normal (figure). Ten biopsy specimens were taken. The crypts were of normal height in three specimens and hyperplastic in one. The lamina propria contained normal numbers of lymphocytes and plasma cells and no granulocytes. Six specimens showed granulation tissue and inflammatory cells at the base of an ulcer. The lesion was consistent with an ischaemic ulcer. Histological slides from the second resection of his colon at another hospital showed similar findings. The diagnostic feature was thrombosis of small submucosal and mesenteric vessels, consistent with mesenteric thrombosis. An examination of the clotting system showed resistance to activated protein C, 1 caused