[A case of ulcerative colitis following smoking cessation].

A 59-year-old man was admitted to our hospital because of watery diarrhea and bloody stool lasting for a month. The patient had been a habitual smoker, smoking 25 cigarettes/day for 35 years. However, he had recently stopped smoking since a giant bulla in the left lung had been found. One month after discontinuing smoking, the patient's symptoms appeared. Colonoscopic examination demonstrated granulated mucosa, edema, and diminished vascular pattern were over the entire colon. Endoscopic and histological findings were compatible with the diagnosis of ulcerative colitis. We reported a case of ulcerative colitis that developed after smoking cessation and discussed the relationship between smoking and ulcerative colitis. Smoking may be associated with ulcerative colitis developed in middle aged person.

Oral administration of mesalazine protects against mucosal injury and permeation in dextran sulfate sodium-induced colitis in rats.

OBJECTIVE. Mesalazine, from which 5-aminosalicylic acid is released, is a therapeutic drug for inflammatory bowel disease. There has been no study concerning the effect of orally administered mesalazine on dextran sodium sulfate (DSS)-induced colitis in the rat model of ulcerative colitis. MATERIAL AND METHODS. Colitis was evaluated by means of the length of the colon, white blood cell count (WBC), tissue myeloperoxidase (MPO) activity, and histological inflammation scores. Colonic mucosal permeation was evaluated using Evans blue. The localization of a tight junction protein, occludin, was evaluated immunohistochemically and examined using confocal laser scanning microscopy. RESULTS. Mesalazine significantly improved changes in the length of the colon, tissue MPO activity, WBC, and the histological inflammation score as compared with DSS-induced colitis. Furthermore, the drug completely inhibited the increased permeation in DSS-induced colitis in rats. The immunofluorescence signals of occludin were disrupted and irregularly distributed in DSS-induced colitis, while the signals appeared as a typical reticular pattern but with reduced intensity by the administration of mesalazine, without any reduction in the protein content. In addition, the oral administration of mesalazine significantly improved mucosal permeation, thereby protecting the intestinal mucosa against injury in DSS-induced colitis in rats. CONCLUSIONS. These findings suggest that the recovery of mucosal impairment due to treatment with mesalazine may be associated with the protection of the tight junction protein occludin in DSS-induced colitis.