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Results for “Colitis, Ulcerative”

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At least 1,189 records · Page 66Linked to original sources

PubMed1994

Cigarette smoking and ulcerative colitis: a case-control study.

OBJECTIVE: To determine whether the previously reported decreased risk of ulcerative colitis in current smokers and increased risk in former smokers are explained by age, sex, race, ethnicity, or socioeconomic status. DESIGN: We conducted a case-control study at a university hospital gastroenterology clinic. MATERIAL AND METHODS: One hundred patients with ulcerative colitis and 100 age- and sex-matched community control subjects were randomly selected for a telephone interview to collect information on smoking habits, race, religion, income, education, and occupation. Smoking habits at the onset of symptoms were analyzed with use of conditional logistic regression for matched data to obtain adjusted odds ratios and 95% confidence intervals for current or former smokers. RESULTS: In comparison with those who had never smoked, current smokers were less likely to have ulcerative colitis: odds ratio = 0.13; 95% confidence interval = 0.05 to 0.38. Former smokers had no increased risk for ulcerative colitis: odds ratio = 1.24; 95% confidence interval = 0.52 to 2.95. No dose-response effect was noted on the basis of pack-years of cigarette smoking, and among former smokers, the interval since quitting smoking was not significantly associated with the relative risk of ulcerative colitis. No confounding effect was detected from race, religion, income, education, or occupation. CONCLUSION: An association seems to exist between ulcerative colitis and nonsmoking; perhaps patients with ulcerative colitis who smoke are less likely to experience symptoms than are nonsmokers because of the effects of nicotine.

Adult↗

PubMed2006

What is the origin of ulcerative colitis? Still more questions than answers.

Despite more than a century of existence as a clinical entity, the true origin of ulcerative colitis still remains elusive. Several factors probably contribute to the development of this condition. Recently discovered technologies have clarified the role of bacterial species, which may account for intestinal dysbiosis, as a factor triggering ulcerative colitis. Genetic susceptibility together with abnormal innate immunoreactivity probably comprise the essential prerequisites for the initiation and perpetuation of ulcerative colitis. Although the genetic background has been more clearly recognised in patients with Crohn's disease than in those with ulcerative colitis, some candidate loci associated with ulcerative colitis have also been intensively studied. Additionally, environmental factors may interfere with inherent predispositions to ulcerative colitis, and either suppress or reinforce them. Whatever the origin, the search for the aetiology of ulcerative colitis must have the same goal: the improvement of treatment and the quality of life in patients with ulcerative colitis.

Appendicitis↗

PubMed1987

Clostridium difficile, sulphasalazine, and ulcerative colitis.

Clostridium difficile has been implicated in the relapse of ulcerative colitis. Controversy exists over this role and its relationship to sulphasalazine exposure. Sixty two of 77 patients with a documented relapse of ulcerative colitis were investigated for the presence of Clostridium difficile, or its toxin, prior to hospitalization. There was a low incidence of detection which was related to antibiotic exposure (2/62). Sampling during the treatment period showed that the occurrence of Clostridium difficile in the stool was related to antibiotic treatment (2/66). Fifty six percent of patients were taking sulphasalazine, none of whom became culture or toxin positive. This study demonstrates that Clostridium difficile is not related to relapse of ulcerative colitis and is not secondarily acquired during relapse unless the patient is exposed to antibiotics. Sulphasalazine does not predispose to acquisition of Clostridium difficile. There is no role for routine screening or treatment of Clostridium difficile in ulcerative colitis.

Adult↗

PubMed1999

Acute pancreatitis secondary to 5-aminosalicylic acid therapy in a patient with ulcerative colitis.

Therapy with oral 5-aminosalicylic acid (5-ASA) for ulcerative colitis has been reported to be effective and safe. We describe a case of biochemically proven mild acute pancreatitis occurring after 9 d of oral 5-ASA therapy for ulcerative colitis. A hypersensitivity mechanism seemed to be involved in the development of pancreatitis probably owing to erratic systemic absorption of the drug. We suggest clinical and biochemical monitoring for early diagnosis of pancreatitis in patients with ulcerative colitis receiving 5-ASA administration. This is the first report of acute pancreatitis developed by oral 5-ASA therapy for the treatment of ulcerative colitis in the literature of Japan.

Acute Disease↗

PubMed1964