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There is increasing evidence that ulcerative colitis is associated with an abnormality of the immune system. Although the aetiology remains unknown, it has been suggested that the immune system of these patients is implicated in the pathogenesis of their disease. T cell function was investigated in ulcerative colitis patients and defective phytohaemagglutinin induced T cell mitogenesis was found. The DNA synthesis induced by stimulation with phorbol esters plus ionophore (ionomycin), however, was normal. These changes cannot be ascribed to either decreased interleukin 2 synthesis or to a defective interleukin 2 receptor expression after cellular activation. Moreover, this defective proliferative response of the T lymphocytes was observed even in the presence of saturated concentrations of exogenous interleukin 2. These results emphasise that the interleukin 2 dependent proliferation pathway is deficient in T lymphocytes from ulcerative colitis patients.
OBJECTIVE: The incidence of ulcerative colitis ranges from 3 to 15 cases per 100,000 persons per year with a prevalence of 50-80 cases per 100,000, and the disease is 3-5 times more common among Jews. In Israel, Ashkenazi Jews have a higher incidence than Sephardi Jews, but a lower incidence than Ashkenazi Jews in the United States or Northern Europe. The aim of this study was to examine the prevalence, mean annual incidence, and clinical patterns of ulcerative colitis in a stable population of communal settlements (kibbutz). METHODS: We repeated a community-based survey in 124,400 kibbutz residents, 10 yr after our first study. This population represents 2.5% of the Jewish population of Israel. All ulcerative colitis patients were located by contacting the kibbutz clinics of the 269 kibbutz settlements (100% compliance). Data were updated to December 31st, 1997, which was designated the point prevalence date, and included information on gender, age, origin, education, profession, extent of the inflammatory process, clinical spectrum of the disease, therapy, complications of the disease, and treatment. The mean annual incidence for the 10 yr was calculated from the prevalence data. Only cases with a definite diagnosis of ulcerative colitis made in a recognized gastroenterology unit were accepted into the study. RESULTS: There were 208 confirmed cases of ulcerative colitis disease, 113 women and 95 men (female:male ratio = 1.19). The prevalence rate rose from 121.0/100,000 in 1987 to 167.2/100,000 in 1997 (p < 0.001). The prevalence rates were higher in women than men. Prevalence was highest in Israeli-born members in 1987 but in European/American-born members in 1997. The average annual incidence rate for the 10-yr period was 5.04/100,000/yr. In 1987, 146 cases of ulcerative colitis were collected. During 10 yr of surveillance 17 patients left the kibbutz, 12 died, and 62 new cases were added. The mean age at presentation of the disease was lower in 1987 than in 1997, 46.14 +/- 11.10 and 51.43 +/- 16.67 yr, respectively. Prevalence was highest in men with >16 yr and in women with 9-10 yr of education, 259.3 and 242.9/100,000, respectively. CONCLUSIONS: The prevalence of ulcerative colitis in this Israeli population increased and has reached the upper range for European and American populations. The mean annual incidence rate of ulcerative colitis is in the lower range of that reported for the Western countries.
BACKGROUND: Published data on the risk of colorectal neoplasia in patients with ulcerative colitis with and without primary sclerosing cholangitis are conflicting. A meta-analysis was performed to synthesize available publications and to compare the risk of colorectal neoplasia in patients with ulcerative colitis with and without primary sclerosing cholangitis. METHODS: By using MEDLINE and manual search methods, studies were identified that compared the risk of colorectal neoplasia (dysplasia and carcinoma) in patients with ulcerative colitis with and without primary sclerosing cholangitis. In addition, citations were reviewed in relevant articles and proceedings from gastroenterology meetings, and investigators were contacted when data were incomplete. The summary odds ratio (OR) was then calculated for the risk for patients with ulcerative colitis and primary sclerosing cholangitis of having colorectal neoplasia develop compared with that of patients with ulcerative colitis without primary sclerosing cholangitis. RESULTS: Eleven studies met all eligibility criteria for the meta-analysis. Patients with ulcerative colitis and primary sclerosing cholangitis are at increased risk of colorectal dysplasia and carcinoma compared with patients with ulcerative colitis alone; OR 4.79: 95% CI [3.58, 6.41] with the Mantel-Haenszel method, and OR 5.11: 95% CI [3.15, 8.29] with the Der Simonian and Laird method. This increased risk is present even when the risk of colorectal carcinoma alone is considered; OR 4.09: 95% CI [2.89, 5.76] and OR 4.26: 95% CI [2.80, 6.48] by using, respectively, the Mantel-Haenszel and the Der Simonian and Laird methods. CONCLUSIONS: Patients with ulcerative colitis and primary sclerosing cholangitis have a significantly higher risk for the development of colorectal neoplasia than patients with ulcerative colitis but not primary sclerosing cholangitis. More intensive colonoscopic surveillance should be considered for patients with ulcerative colitis and primary sclerosing cholangitis.
Ulcerative colitis (UC) represents a risk factor for colorectal cancer, but the association between UC and appendix cancer is uncommon. A 60-year-old woman with a 5-year history of UC initially received medical treatment with mesalazine and prednisone with no satisfactory response; therefore surgery was indicated. The procedure was a total intersphincteric proctocolectomy with ileostomy. Histopathological analysis indicated adenocarcinoma from the cecal appendix, and chronic-active ulcerative colitis of the colon. In conclusion, surgeons and pathologists should examine every surgical specimen from patients with UC because of the possibility, although remote, of a neoplasic pathology. The appendix adenocarcinoma and ulcerative colitis may or may not be associated, same as colon cancer in patients with UC.
The presence of hepatic changes in ulcerative colitis ranges from 4.7% to 90% and the mechanisms are not clear. This study had the purpose to verify their frequency, observe the relation between clinical forms and hepatic lesions and identify the possible histological changes in the liver. We studied 21 patients with ulcerative colitis (Group 1, subdivided in Group 1A non-alcoholic and 1B alcoholic) and compared with 10 patients with irritable bowel syndrome (Group 2). The study involved clinical evaluation, ultrasonography liver function tests and needle biopsy of the liver, performed by laparoscopy, when necessary. Clinical alterations were present in three patients. The ultra-sonographic study was altered in 14.3% in Group 1A and in 57.1% in Group 1B. The albumin and cholinesterase levels were the most frequent abnormality in ulcerative colitis. In irritable bowel syndrome (Group 2), these exams were normal. Liver biopsy was performed in 15 patients and variable degrees of histologic changes were present in all.
BACKGROUND: Steroid resistance represents a major clinical problem in the treatment of ulcerative colitis. In vitro, interleukin-2 renders lymphocytes steroid resistant. AIM: To explore the therapeutic potential of interleukin-2 receptor blockade in steroid-resistant ulcerative colitis with both in vitro measures and a pilot in vivo study. METHODS: Ten patients with steroid-resistant ulcerative colitis received a single bolus of 40 mg of intravenous basiliximab plus steroid treatment in an open-label, uncontrolled, 24-week study. The outcome was assessed using the Ulcerative Colitis Symptom Score, rectal biopsy and Inflammatory Bowel Disease Questionnaire. Lymphocyte steroid sensitivity was measured in vitro in 39 subjects in the presence or absence of basiliximab. RESULTS: Nine of the 10 patients achieved clinical remission within 8 weeks. At 24 weeks, seven patients were in clinical remission. Marked improvement in the Ulcerative Colitis Symptom Score was seen by 1 week (P = 0.004) and on rectal biopsy and Inflammatory Bowel Disease Questionnaire by 2 weeks (both P < 0.05). Improvements persisted to 24 weeks (Ulcerative Colitis Symptom Score, Inflammatory Bowel Disease Questionnaire, both P < 0.005). Eight of the nine responders relapsed (median, 9 weeks), but remission was re-achieved with further corticosteroids and the addition of azathioprine. At 24 weeks, seven patients were in full clinical remission, five off all steroid therapy. In vitro measurement of lymphocyte steroid sensitivity demonstrated steroid resistance in 22% of subjects. All were rendered steroid sensitive in the presence of basiliximab. CONCLUSIONS: Basiliximab appears to be effective at inducing remission in steroid-resistant ulcerative colitis. In vitro, basiliximab also produced a dramatic increase in lymphocyte steroid sensitivity in healthy subjects. Confirmation in randomized controlled studies is required.
OBJECTIVE: Haemostatic changes may be involved in the pathogenesis and progression of ulcerative colitis. We studied longitudinally inflammatory and haemostatic parameters in patients treated for severe ulcerative colitis. DESIGN AND SETTING: We carried out a descriptive study of longitudinal blood measurements in patients with severe ulcerative colitis from one large regional hospital. METHODS: Nineteen patients with severe ulcerative colitis were assessed by an endoscopic score and a patient score at baseline. Patients were assessed by patient scores during treatment at scheduled intervals. At each visit, inflammatory and haemostatic parameters were determined. RESULTS: At baseline, the erythrocyte sedimentation rate, C-reactive protein, leucocyte and granulocyte count, thrombin-antithrombin complexes, prothrombin fragment 1+2, fibrinogen and degradation products of fibrinogen and fibrin were increased in patients when compared with controls, whereas albumin concentration and factor XIII activity were significantly lower. Antithrombin activity was normal. During treatment, the median patient score diminished significantly from 12 to 4.5 points after 2 weeks, decreased further to 4 points after 4 weeks and remained below 4 points throughout the remaining study period. Inflammation parameters returned to within the reference range in two patients after 4 weeks, whereas the coagulation markers prothrombin fragment 1+2 and thrombin-antithrombin complexes returned to normal values after 8 weeks and 24 weeks, respectively. In contrast with markers of inflammation, slightly increased concentrations of the degradation products of both fibrinogen and fibrin were found for almost 1 year, which indicated low-grade activation of coagulation and fibrinolysis. CONCLUSIONS: These results are compatible with a condition of persistent hypercoagulation in patients with ulcerative colitis who are in clinical remission. Persistent hypercoagulation may contribute to the clinical course of ulcerative colitis.
BACKGROUND: Chronic ulcerative colitis is a disease of unknown etiology. Its incidence is on the rise in various developing countries as has been reported in studies from South-East Asia and the Middle East. There seems to be significant differences in the pattern and the clinical course of this disease in our patient population. The aim of our study is to assess the incidence and the clinical course of the disease in Kuwait. METHODS: This is a retrospective study of cases identified over a period of 14 years (1985-1999). Three hundred forty-six patients were identified to have chronic ulcerative colitis. Ninety patients were interviewed for this study. RESULTS: Chronic ulcerative colitis is being identified with increasing frequency. Our local incidence was 2.8 per 100,000 persons per year. The disease was seen in both sexes with equal frequency. It peaks at the third decade of life, with no second peak observed in the sixth decade. The disease was of mild to moderate severity in 93% of the cases. The distribution of the disease in the colon showed pancolitis in 45%, left-sided colitis in 14%, proctosigmoiditis in 21% and proctitis in 20%. Arthritis and arthralgia were the most frequent extraintestinal manifestation seen in 31%. Perianal disease, although rare in ulcerative colitis, was seen in 8%. Of interest is the fact that over 14 years of follow-up, none of our patients developed high-grade dysplasia or colorectal cancer. Four patients required total colectomy mainly due to failure of medical therapy. CONCLUSIONS: Chronic ulcerative colitis is occurring with increasing frequency similar to that seen in Western countries. The disease observed in our patient population was of mild to moderate severity, with fewer complications than reported in Western countries. It peaks in the third decade with no second peak. None of our patients developed high-grade dysplasia or colorectal carcinoma.
Arachidonic acid metabolites formed by both the cyclooxygenase and lipoxygenase pathways may contribute to the clinical diarrhea and colitis of inflammatory bowel disease. Patients with active ulcerative colitis have increased levels of leukotriene B4 in their rectal mucosa, and these levels tend to correlate with severity of the disease. In this study, we evaluated the efficacy of ingestion of fish oil n-3-omega-fatty acids, inhibitors of leukotriene synthesis, in the treatment of ulcerative colitis. Eleven patients with ulcerative colitis of mild to moderate severity were studied in a 8-month, double-blind, placebo-controlled, crossover trial of dietary supplementation with fish oil, which provided about 4.2 g of omega-3- fatty acids per day. A disease activity index based on patient symptoms and sigmoidoscopic appearance was used to assess efficacy. Mucosal leukotriene B4 production was measured by radioimmunoassay. Mean disease activity index declined 56% for patients receiving fish oil and 4% for patients on placebo (p less than 0.05). There were no statistically significant differences in histopathologic scores or colonic mucosal leukotriene B4 levels. All patients tolerated fish oil ingestion and showed no alteration in routine blood studies. No patient worsened; anti-inflammatory drugs could be reduced or eliminated in eight patients (72%) while receiving fish oil. We conclude that fish oil dietary supplementation results in clinical improvement of active mild to moderate ulcerative colitis but is not associated with significant reduction in mucosal leukotriene B4 production, compared with placebo therapy. Further studies are needed to elucidate the mechanism of action and optimal dose and duration of fish oil supplementation in ulcerative colitis.
The monitoring of patients with ulcerative colitis is easier than in patients with Crohn's disease for several reasons: the severity of symptoms and activity of inflammation tend to run parallel in ulcerative colitis when involvement of the large bowel is more extensive. The easy accessibility of the colonic mucosa by endoscopic and histologic examination provides further information concerning the degree of inflammation. In severe attacks, the patient must be admitted to hospital and monitored carefully. Clinical and laboratory parameters (such as daily stools, CRP, fever, haemoglobin, albumin, etc.) and plain abdominal X-ray are useful in monitoring the activity of the disease and to predict the outcome. In mild to moderate attacks, endoscopic and histologic evaluation are the best methods for choosing the appropriate treatment and for assessing response.
It has been suggested that ulcerative colitis might be associated with excessive production of histamine released locally from mast cells. These cells also contain a proteolytic enzyme, leucine aminopeptidase, which might also be released at the same time if this hypothesis were correct. The studies reported do not invalidate this concept of aetiology in ulcerative colitis but provide no positive evidence in support of it.
Biopsy specimens from long-standing ulcerative colitis were frozen shortly after resection and homogenized before measurement of lactate dehydrogenase (LD) isoenzymes by agar electrophoresis. Results were related to histological changes in inflammation or dysplasia. The percentage of total LD M monomers was significantly higher in homogenates of specimens with dysplastic changes than in homogenates of specimens with only inflammatory changes. A positive correlation was found between total LD M monomers and LD5 monomers (isoenzyme) for the whole material, for each of the histological subgroups of ulcerative colitis, and for the control specimens of adenomas, carcinomas, and normal mucosa. A positive correlation between total LD activity and total percentage of LD5 monomers was only seen for dysplastic, adenomatous, and malignant tissues. The results support the use of dysplasia as a marker for premalignant changes in mucosal specimens and indicate a possible role for LD isoenzyme measurements in specimens from patients with long-standing ulcerative colitis.