Abstract

Dear Editor: The patient was a 51-year-old man, a heavy smoker, with a 24-year history of Crohn’s Disease (CD). He was initially diagnosed as having Crohn’s proctosigmoiditis with stenosis of the anal canal treated with several endoscopic dilatations. Barium enteroclysis was performed, giving negative results. The patient was administered mesalazine and oral steroids for 17 years, achieving symptomatic improvement. In 2000, he had experienced a peri-anal fistula and relapse of the anal stricture, together with abdominal pain and diarrhoea, and was subjected to fistulectomy and anal dilatation. Consequent to the worsening of the abdominal pain refractory to medical therapy and the occurrence of rectal tenesmus, the patient was clinically re-assessed. At anorectal exploration, apart from the scar of the fistulectomy, severe strictures both in the upper part of the anal canal and in the distal rectum were noted. There was no evidence of damage from the fistulectomy to the anal sphincter. In March 2002, left colectomy, proctectomy and mucosectomy of the anal canal, with colo-anal anastomosis and transient ileostomy, were performed. The post-operative outcome was regular and, in July 2002, the patient was readmitted for closure of the protective ileostomy. On account of post-prandial vomiting and weight loss (10 kg in 2 months), the patient was readmitted to hospital in September 2002. An abdominal computerised tomography (CT) scan showed a stenosis of the third duodenal portion measuring 1 cm in length, with marked gastroduodenal dilatation. No duodenal compression by the superior mesenteric artery was evident. After 10 days of total parenteral nutrition, the patient was operated. The duodenum was entirely mobilised by cutting the Treitz’s ligament, and the short, fibrous stricture of the third portion of the duodenum was confirmed. A Heineke–Mikulicz (HM) strictureplasty was carried out and the patient’s clinical condition improved. In May 2003, he presented again with post-prandial vomiting, and endoscopy showed segmental narrowing of the second portion of the duodenum. Endoscopic dilatation was successfully performed and the biopsies concurrently taken demonstrated inflammatory alteration without signs of dysplasia or cancer. Four months later, due to deterioration of the obstructive symptoms, the patient was submitted to intestinal transit with hydrosoluble contrast medium, displaying exacerbation of the stenosis previously treated endoscopically. Further dilatation was then carried out, but to little benefit, and, in December 2004, surgery was scheduled. At laparotomy, the duodenum appeared dilated up to the second portion, where a stenosis consisting of a thickened, whitish, fibrous tissue involved the posterior wall for 2–3 cm, adherent to the vena cava. Frozen sections of the stenotic tissue showed fibroblasts and inflammatory cells with no signs of malignant transformation. As further strictureplasty was not feasible, a Roux-en-Y jejunal loop was implanted on the second part of the duodenum. Definitive histological examination of the duodenal specimen revealed a poorly differentiated adenocarcinoma and, in January 2005, the patient underwent duodeno-pancreatectomy according to Whipple. Int J Colorectal Dis (2009) 24:475–477 DOI 10.1007/s00384-008-0582-1

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