Crohn's disease over 20 years after diagnosis in a referral population.

OBJECTIVES: Patients frequently ask questions about the lifetime prognosis of Crohn's disease. The aim of this study was to describe the outcomes of Crohn's disease more than 20 years after diagnosis. METHODS: Data from all patients with Crohn's disease whose diagnosis had been performed before 1st January 1978 were analyzed. All referred patients filled in a medical and health-related quality-of-life questionnaire. RESULTS: Among 273 patients with Crohn's disease diagnosed more than 20 years ago, 141 (52%) patients answered our questionnaire, 45 (16%) patients were alive but did not wish to answer our questionnaire, 51 (19%) could not be traced and 36 (13%) died before July 1998. At the end of follow-up, 25.7 (20.0-59.3) years after diagnosis, 24% had a relapse in the previous 12 months, and 48% and 28% had quiescent disease with and without treatment, respectively. These ratios were not different from those observed three years after Crohn's disease diagnosis. Sixteen patients died within 20 years after CD diagnosis, including 11 from CD-related causes. The risk of death estimated by Kaplan-Meier life-tables analysis was non-significantly higher if death was related to CD. An ileal or colic adenocarcinoma was noted in 6 (3.4%) patients. CONCLUSIONS: Crohn's disease activity does not burn out with time, and roughly one-quarter of the patients had active disease 20 years after diagnosis.

Colonoscopy accurately predicts the anatomical severity of colonic Crohn's disease attacks: correlation with findings from colectomy specimens.

OBJECTIVE: For the assessment of colonic Crohn's disease (CCD) attacks, no clinicobiological and/or morphological (endoscopic, radiological) criteria of severity have been validated in relation to anatomical criteria of severity (ACS) as a gold standard obtained from colectomy specimen examination. Our objective was to assess the accuracy of colonoscopy in predicting the anatomical severity grading of CCD. METHODS: Colectomy specimens from 78 consecutive patients operated between 1982 and 1996 for CCD resistant to medical treatment were analyzed and classified into two groups according to the presence (ACS+) or absence (ACS-) of ACS. These were defined as either deep ulcerations eroding the muscle layer, or mucosal detachments or ulcerations limited to the submucosa but extending to more than one third of one defined colonic segment (right, transverse, left colon). Three endoscopic criteria of severity (ECS) were then defined: 1) deep ulcerations eroding the muscle layer (ECS1), 2) deep ulcerations not eroding the muscle layer but involving more than one third of the mucosal area (ECS2), and 3) mucosal detachment on the edge of ulcerations (ECS3). RESULTS: According to colectomy specimen examination, 68 and 10 patients belonged to ACS+ and ACS- groups, respectively. ECS1, ECS2, and/or ECS3 were found in 70 patients. Positive predictive values of ECS1, ECS2, and ECS3 for the presence of ACS were 90%, 98%, and 92%, respectively. Negative predictive values were 43%, 72%, and 23% respectively. However, at least one ECS (ECS1, ECS2, or ECS3) was found in 95% of patients with ACS. The extent of ulcerations at colonoscopy was correlated to the results of colectomy specimen examination (p < 0.001). Taking into account only patients with ACS, 88% of those with at least one ECS were diagnosed through left side colonoscopy. Usual clinical and biological severity criteria were not different in ACS + and ACS- groups. Two cases of toxic megacolon and toxic shocks were observed after the colonoscopy. CONCLUSIONS: In experienced hands, colonoscopy can be useful in severe CCD attacks. When at least one ECS is found, colonoscopy predicts the anatomical severity of the colitis with a high probability. Conversely, when none of the three ECSs is found, colonoscopy can reasonably exclude the diagnosis of severe anatomical CCD.

Sugar intolerance: origin and mechanisms of symptoms?

The origin and mechanisms of symptoms in sugar intolerance were studied in 8 healthy volunteers. For two test periods, volunteers swallowed a probe with perfused catheters and an infusion catheter which migrated into the colon. A meal containing 40 g lactulose or 40 g sucrose was ingested; the sucrose meal was followed by colonic infusion of 40 g lactulose in order to bypass the small intestine. Recordings of small intestinal and colonic motility were performed. Abdominal pain, bloating, borborygmi, and flatulence were similar during both periods. Both meals increased small intestinal and colonic motility. Only 37% of the symptoms coincided in time with colonic motor events. Symptoms were not related to a specific motor event and were not correlated with breath hydrogen excretion. In conclusion, symptoms of sugar intolerance originate from the colon. They are not related to specific phasic motor events or to breath hydrogen excretion.