[CLINICO-ROENTGENOLOGICAL AND ROENTGENO-MORPHOLOGICAL COMPARISONS IN NONSPECIFIC ULCERATIVE COLITIS].
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Prior studies confirm the increased incidence of carcinoma of the colon in chronic ulcerative colitis. The authors reviewed clinical and histologic data retrospectively in 23 patients with colon carcinoma and chronic ulcerative colitis. Twenty-two of these patients had dysplasia of colonic epithelium remote from the cancer. The authors prospectively reviewed clinical data and rectal and colonoscopic biopsy specimens on 36 patients with chronic ulcerative colitis, 12 with Crohn's colitis, and 12 with miscellaneous disorders. Eight patients with chronic ulcerative colitis had dysplasia; 6 have had colectomy, and 2 of these had carcinoma. No patient without chronic ulcerative colitis had dysplasia. Patients with chronic ulcerative colitis should have periodic rectal and colonoscopic biopsies, and those with moderate to marked dysplasia require colectomy because of the increased risk of colon carcinoma.
The aim of the study was to estimate the usefulness of measuring the circulating concentration of serum aminoterminal propeptide of type III collagen (S-PIIINP) in screening for hepatobiliary diseases in patients with ulcerative colitis. S-PIIINP was measured in 69 patients with ulcerative colitis and normal liver biochemistry, in 14 patients with ulcerative colitis and elevated catalytic concentration of alkaline phosphatases in serum (S-ALP, EC 3.1.3.1) but without primary sclerosing cholangitis (PSC), and in 20 patients with ulcerative colitis and PSC. The median S-PIIINP was 3.1 micrograms l-1 in patients with ulcerative colitis and normal liver biochemistry, 4.3 micrograms l-1 in patients with ulcerative colitis and hepatobiliary disorder other than PSC and 8.9 micrograms l-1 in those with ulcerative colitis and PSC. When the S-PIIINP cut-off level was set at 5.0 micrograms l-1, 1% of the patients with ulcerative colitis and normal liver biochemistry, 21% of those with hepatobiliary disorder, not PSC, and 90% of the patients with PSC had S-PIIINP values above that concentration. In conclusion, S-PIIINP above 5.0 micrograms l-1 in a patient with ulcerative colitis strongly suggests concomitant PSC.
OBJECTIVE: To determine whether azathioprine can prevent relapse in ulcerative colitis. DESIGN: One year placebo controlled double blind trial of withdrawal or continuation of azathioprine. SETTING: Outpatient clinics of five hospitals. SUBJECTS: 79 patients with ulcerative colitis who had been taking azathioprine for six months or more. Patients in full remission for two months or more (67), and patients with chronic low grade or corticosteroid dependent disease (12) were randomised separately. 33 patients in remission received azathioprine and 34 placebo; five patients with chronic stable disease received azathioprine and seven placebo. MAIN OUTCOME MEASURE: Rate of relapse. Relapse was defined as worsening of symptoms or sigmoidoscopic appearance. RESULTS: For the remission group the one year rate of relapse was 36% (12/33) for patients continuing azathioprine and 59% (20/34) for those taking placebo (hazard rate ratio 0.5, 95% confidence interval 0.25 to 1.0). For the subgroup of 54 patients in long term remission (greater than six months before entry to trial) benefit was still evident, with a 31% (8/26) rate of relapse with azathioprine and 61% (17/28) with placebo (p less than 0.01). For the small group of patients with chronic stable colitis (six were corticosteroid dependent and six had low grade symptoms) no benefit was found from continued azathioprine therapy. Adverse events were minimal. CONCLUSIONS: Azathioprine maintenance treatment in ulcerative colitis is beneficial for at least two years if patients have achieved remission while taking the drug. Demonstration of the relapse preventing properties of azathioprine has implications for a large number of patients with troublesome ulcerative colitis, who may benefit from treatment with azathioprine.
Corticosteroids are effective in bringing about clinical remission for ulcerative colitis. However, relapsed cases are frequently refractory to corticosteroids. In addition, the long-term use of corticosteroids often causes serious side effects. We have already reported that leukocyte apheresis using a centrifugal procedure was effective for patients with corticosteroid-resistant ulcerative colitis after conducting a pilot study in 14 patients. In the present paper, the clinical efficacy of leukocyte apheresis using a centrifugal procedure was evaluated again for corticosteroid-resistant ulcerative colitis. Twenty-three patients with corticosteroid-resistant severely active ulcerative colitis were treated by centrifugal leukocyte apheresis. Eighteen patients (78.3%) achieved clinical remission which was evaluated by the clinical activity index within 4 weeks after apheresis. Both colonoscopic and histological examinations confirmed the beneficial effect of this procedure. No significant side effects were noticed throughout the therapy.
A case of ulcerative colitis complicated with gastric and duodenal lesions is reported. The patient was a 17-year-old male who was admitted with bloody diarrhea and abdominal pain. Based on the endoscopic and histological findings of the colon, a diagnosis of ulcerative colitis was made. Upper gastrointestinal endoscopy showed multiple erosions and granular changes in the antral greater curvature of the stomach and descending portion of the duodenum. Histological examination of the stomach and duodenum revealed marked inflammatory cell infiltration and crypt abscesses. Clinically, the gastric and duodenal lesions did not respond to antiulcer drugs, but were alleviated by steroid. It was concluded that the pathogenesis of the gastric and duodenal lesions in this patient was similar to that of the colonic lesions of ulcerative colitis.
Two patients who had undergone proctocolectomy for ulcerative colitis developed lesions in their ileal stoma that appeared to be inflammatory polyps morphologically similar to those encountered in the large intestine of ulcerative colitis patients. One of these patients eventually developed mucinous adenocarcinoma in the ileal stoma. The ileal mucosa adjacent to the neoplasm had morphologic features of large-bowel mucosa and was richly populated by sulfomucin-containing goblet cells, which are characteristic of large-bowel mucosa. Sulfomucin-containing goblet cells were also found in the inflammatory lesions biopsied from the ileal stomas of both patients, as well as from the adenocarcinoma found in one patient. These findings support the hypothesis that colonic metaplasia can occur in ileal stomas of ulcerative colitis patients. Furthermore, the metaplastic colonic tissue is the site of origin of lesions typically found in ulcerative colitis. Colonic metaplasia occurring in ileal stoma should be recognized by pathologists as a clinical entity. When colonic metaplasia is identified in the ileal stoma of an ulcerative colitis patient, biopsy surveillance of stomal mucosa is recommended.
This report describes a young woman with ulcerative colitis who developed rapidly fatal pneumococcal septicaemia. Necropsy revealed splenic atrophy. This case supports the hypothesis that splenic atrophy might contribute to the morbidity of ulcerative colitis. The occurrence of splenic atrophy in ulcerative colitis is now well established. Splenic atrophy from other causes has been associated with severe bacterial infections, often pneumococcal. It has been suggested that splenic atrophy is most severe when ulcerative colitis is active and may contribute to postoperative morbidity. This case documents overwhelming septicaemia in a patient with splenic atrophy whose colitis was in remission.