Prevalence rates and an evaluation of reported risk factors: METHODS AND CASE PRESENTATIONS part 2

26 Dec
2011

Case 2: A 29-year-old man first developed diarrhea, up to 10 watery movements daily, in 1983. Colonoscopic evaluation in a community hospital showed colitis with deep ulcera- tions, thought to be consistent with Crohn’s colitis. He was treated with sulphasalazine 2 g daily and corticosteroid ene­mas. His symptoms improved, but he had occasional epi­sodes of bloody diarrhea. In 1986, his bloody diarrhea became more severe, up to 20 times per day. Progressive weight loss, estimated to be about 15 kg, developed. He was admitted to hospital and treated with 5-aminosalicylic acid 1600 mg (Asacol) and intravenous hydrocortisone 400 mg daily. Colonoscopic changes were extensive with cecal and rectal sparing. Biopsies showed inflammatory changes only, with no granulomas. He was transferred to another hospital for parenteral nutrition (including lipid emulsion). His weight increased by 10 kg, and his diarrhea improved with a frequency of about 10 movements/day. Surgical treatment was declined.

In April 1987, he was referred for further management to the University of British Columbia Hospital. Physical ex­amination showed steroid-related ‘Cushingoid’ features. His weight was now identical to his documented preillness weight. Laboratory studies were normal, except for a serum albumin level of 32 g/L (normal range 35 to 50 g/L). Colono­scopy confirmed previous findings; inflammatory pseudopolyps were also present. Biopsies showed only inflammatory changes; no granuloma was present. Parenteral nutrition was discontinued, and he was discharged from hospital having two nonbloody soft bowel motions daily. His prednisone dose was progressively reduced over the next six weeks to 10 mg daily. By August 1987, results of his laboratory studies, including serum albumin levels, were normal and the prednisone dose was further tapered to 5 mg daily. One week later, he noted discomfort in both hips. Because it was believed that osteonecrosis might be present, the prednisone was ter­minated.
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Results of radiographic studies of his hips in September and October 1987 were normal; no changes were present to suggest osteonecrosis. In November 1987, MRI of both hips showed bilateral subarticular low signal changes on both T1 and T2 weighted images consistent with osteonecrosis. Over the next three months, there were no intestinal symptoms, but hip pain was present. In March 1988, MRI showed pro­gression of the osteonecrosis, particularly in the right femo­ral head. In February 1989, he complained of pain in both shoulders, and radiographic studies demonstrated osteone- crosis, particularly in the right humeral head. In December 1990, he presented emergently to another teaching hospital with an acute abdomen. Laparotomy revealed a perforated rectosigmoid carcinoma with generalized peritonitis. Exten­sive bilateral bronchopneumonia developed in the postop­erative period followed by death.

 

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