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PubMed1990

Return to normal body composition after ileoanal J-pouch anastomosis for ulcerative colitis.

In 16 patients with ulcerative colitis, total body fat, total body protein, and total body water were measured before and two weeks, three months, and twelve months after the establishment of an ileoanal J-pouch anastomosis. The 16 patients underwent elective surgery for their inflammatory bowel disease but were significantly protein depleted before surgery when their body composition was first measured. Twelve months later, all patients were in good health, back to work, and had normally functioning pouches (average stool frequency 4.3 +/- 1.4 per day). As a group, their stores of body protein and hydration state had returned to normal limits although their body fat stores were increased. Over the postoperative period there were significant losses of weight, protein, fat, fat-free mass, and total body water. These levels had returned to preoperative values (but not to normal) three months later. It is concluded that protein depleted patients with ulcerative colitis presenting for major surgery continue to have distorted body composition for several months after surgery but after approximately 12 months, when they have returned to work and feel well, body composition has returned to normal.

Adult↗

PubMedDate not supplied

Non-Hodgkin's lymphoma of the colon and ulcerative colitis. Case report.

The association between ulcerative colitis and lymphoma is rare. The authors report the case of a 54-year old white man who presented a clinical picture and radiological and colonoscopic findings suggesting the diagnosis of idiopathic ulcerative colitis. Histopathological and immunohistochemical studies of tissue specimens obtained at autopsy led to the diagnosis of non-Hodgkin's B-cell T-cell-rich lymphoma throughout the colon. Possible relations between ulcerative colitis and gastrointestinal lymphoma are discussed.

Colitis, Ulcerative↗

PubMed2000

Tacrolimus in corticosteroid-resistant ulcerative colitis.

We report a case of refractory ulcerative colitis treated with tacrolimus. The patient was a 73-year-old woman with a 45-year history of ulcerative colitis. An attack unresponsive to intravenous corticosteroid therapy occurred when she was age 73. Leukocytapheresis therapy was attempted, but was discontinued because of the patient's poor general condition. Cyclosporine A therapy brought about fair control of the disease. A liver injury that was suspected to be associated with this agent, however, occurred within 5 weeks of its initiation. At that time, the cyclosporine A was discontinued and azathioprine treatment was started. Within 6 weeks, signs of exacerbation of the ulcerative colitis became apparent. Tacrolimus administered at that time brought about remission of the disease, and the corticosteroid dose was then reduced. Tacrolimus, like cyclosporine A, appears to be effective for the treatment of attacks of ulcerative colitis.

Aged↗

PubMed1998

Sulfides impair short chain fatty acid beta-oxidation at acyl-CoA dehydrogenase level in colonocytes: implications for ulcerative colitis.

The disease process of ulcerative colitis (UC) is associated with a block in beta-oxidation of short chain fatty acid in colonic epithelial cells which can be reproduced by exposure of cells to sulfides. The aim of the current work was to assess the level in the beta-oxidation pathway at which sulfides might be inhibitory in human colonocytes. Isolated human colonocytes from cases without colitis (n = 12) were exposed to sulfide (1.5 mM) in the presence or absence of exogenous CoA and ATP. Short chain acyl-CoA esters were measured by a high performance liquid chromatographic assay. 14CO2 generation was measured from [1-14C]butyrate and [6-14C]glucose. 14CO2 from butyrate was significantly reduced (p < 0.001) by sulfide. When colonocytes were incubated with hydrogen sulfide in the presence of CoA and ATP, butyryl-CoA concentration was increased (p < 0.01), while crotonyl-CoA (p < 0.01) and acetyl-CoA (p < 0.01) concentrations were decreased. These results show that sulfides inhibit short chain acyl-CoA dehydrogenase. As oxidation of n-butyrate governs the epithelial barrier function of colonocytes the functional activity of short chain acyl-CoA dehydrogenase may be critical in maintaining colonic mucosal integrity. Maintaining the functional activity of dehydrogenases could be an important determinant in the expression of ulcerative colitis.

Acyl Coenzyme A↗

PubMed2004

A high degree of aneuploidy, loss of p53 gene, and low soluble p53 protein serum levels are detected in ulcerative colitis patients.

PURPOSE: The causes for the increased risk of colorectal cancer associated with ulcerative colitis have not been fully defined. Colonic tissue of ulcerative colitis patients was examined for changes in chromosome-17-centromere copy number, loss of the p53 gene, and alterations in serum levels of the 53-kDa protein. This study was performed under the assumption that these molecular events correlate with ulcerative colitis status and duration. METHODS: Ulcerative colitis patients (n = 42) and healthy controls (n = 37) participated in the study. All participants were histopathologically and medically diagnosed. The stage of ulcerative colitis patients was stratified according to increasing risk factors for the development of colorectal cancer: left-sided colitis, pancolitis, sclerosing cholangitis, and dysplasia-associated lesions or masses. Changes in centromere number of chromosome 17 alone or in association with changes in copy number of the p53 gene were analyzed in colon tissue biopsies by fluorescence in situ hybridization. Serum p53 level was determined in blood samples by immunoprecipitation followed by separation using high-pressure liquid chromatography. RESULTS: Changes in chromosome 17 and p53 copy number and lower levels of serum p53 protein in ulcerative colitis patients directly correlated with colorectal cancer risk factors. All values significantly differed from controls. Significant direct correlations were obtained for ulcerative colitis disease duration, levels of p53 in the serum, and extent of aneuploidy. CONCLUSIONS: We demonstrate that in the colonic mucosa of ulcerative colitis patients, high levels of genomic instability, changes in p53 gene copy number, and lower levels of p53 in the serum directly correlate with the extent of disease duration and increased risk factors for colorectal cancer. Any of the measurements described herein can provide an acceptable prognostic tool in the assessment of colorectal cancer risk in ulcerative colitis patients.

Adult↗

PubMed2000

Intravenous azathioprine in severe ulcerative colitis: a pilot study.

OBJECTIVE: Azathioprine use in acute ulcerative colitis has been limited by its perceived long onset of action. The aim of this study was to determine the safety and clinical effect of an i.v. loading dose of azathioprine in the setting of severe steroid refractory ulcerative colitis. METHODS: Nine hospitalized patients with severe steroid refractory ulcerative colitis were enrolled. Patients 1-3 received 20 mg/kg i.v. azathioprine over 36 h. Patients 4-6 received 40 mg/kg i.v. azathioprine over 36 h. Patients 7-9 received 40 mg/kg i.v. azathioprine as three 8-h infusions over 3 days. Clinical remission was defined as steroid withdrawal and an Ulcerative Colitis Disease Activity Index score of 0. The Inflammatory Bowel Disease Questionnaire was obtained at each visit. White blood cell concentrations and erythrocyte concentrations of 6-thioguanine were obtained. RESULTS: Five of nine patients (56%) had a response and avoided colectomy. Three of nine patients (33%) met the definition for clinical remission. Response was seen within 4 wk. The mean 6-thioguanine concentration for those five patients at 12 wk after infusion was 148.2 pmol/8 x 10(8). Two patients had transient leukopenia and one had transient hepatotoxicity. CONCLUSIONS: Intravenous azathioprine appears to be safe and of clinical benefit in inducing response and avoiding colectomy in severe steroid refractory ulcerative colitis. Data from an i.v. azathioprine trial in Crohn's disease suggests oral dosing alone may obtain the same results. The role of oral dosing alone in severe ulcerative colitis and the role of azathioprine metabolite levels in monitoring efficacy should be investigated further.

Adult↗

PubMed2005

Differential expression of multiple transglutaminases in human colon: impaired keratinocyte transglutaminase expression in ulcerative colitis.

BACKGROUND AND AIMS: Ulcerative colitis (UC) is characterised by refractory inflammatory ulceration and damage to the colon. The mechanisms underlying impaired healing have yet to be defined. As transglutaminase expression resulting in matrix protein cross linking is associated with increased wound healing in a rat model of colitis, we hypothesised that different types of transglutaminase might also play a role in UC. PATIENTS AND METHODS: Endoscopic and histological indices were studied in 26 patients with UC (10 active and 16 inactive) and in 20 normal controls undergoing colonoscopy. Transglutaminase activity was evaluated in plasma (factor XIIIa) by a radioenzymatic method. Factor XIIIa, tissue and keratinocyte transglutaminase protein content, and mRNA expression in the colon were evaluated by western blot analysis and semiquantitative reverse transcription-polymerase chain reaction (RT-PCR), respectively. Colonic location of transglutaminases and their reaction products, the epsilon-(gamma-glutamyl)lysine bonds, was evaluated by immunohistochemistry using specific monoclonal antibodies. RESULTS: Transglutaminase activity was significantly lower in the plasma of patients with active UC (4.2 (2.4) mU/ml; p<0.05 v controls) than in those with inactive UC and controls (10.6 (2.2) and 12.1 (1.7) mU/ml). As shown by western blot, protein levels of tissue transglutaminase and factor XIIIa were unchanged in active UC compared with inactive disease and controls, while the keratinocyte form was reduced in active UC. Tissue transglutaminase and factor XIIIa immunostaining was strongly present in damaged areas colocalising with isopeptide bonds. In contrast, the keratinocyte form was almost absent in active UC and localised in the upper part of the crypts in normal subjects. RT-PCR showed upregulation of tissue transglutaminase mRNA in active UC (320% compared with controls) while keratinocyte transglutaminase gene expression was downregulated in active UC. CONCLUSIONS: The results of the present study support the concept that, in the damaged colon, transglutaminases are needed in response to chronic injury and underline the key role of these enzymes in mucosal healing.

Adult↗

PubMed1977

HLA antigens and ulcerative colitis in Japan.

The HLA antigens in 44 cases of ulcerative colitis and 271 control individuals in Japan were studied. The NIH tissue typing method was used according to the new leukocyte nomenclature adapted by the WHO Committee. In normal Japanese populations, the HLA antigens, which were of high frequency, were HLA A2(37.3%), A9(60.9%) and B5 (40.6%). On the contrary, the significantly high frequency of HLA B5 was demonstrated in ulcerative colitis, compared with that in control. Moreover, HLA B5 in cases with ulcerative colitis excluding those with proctitis only, was found with higher frequency than that in total cases. Although the most frequent haplotype was HLA A9-B5 in control, so frequent haplotype was not found in ulcerative colitis. A family study revealed no significant diathesis on the hapolytpe of HLA in ulcerative colitis. The relationship between MLC locus and ulcerative colitis was not yet clarified from the study of one family whose two members suffered from ulcerative colitis.

Adult↗

PubMed1995

Low incidence of significant dysplasia in a successful endoscopic surveillance program of patients with ulcerative colitis.

BACKGROUND/AIMS: Colorectal cancer associated with ulcerative colitis may be preceded by dysplastic changes potentially detectable by repeated endoscopic examinations. The aim of this study was to evaluate the incidence, course, and risk factors for dysplasia in a prospective endoscopic study. METHODS: One hundred fifty-four patients with ulcerative colitis for 7 or more years' duration were followed from 1976 to 1994 in an endoscopic surveillance program. RESULTS: Five patients had 10 adenomatous polyps managed by polypectomy. Indefinite dysplasia was found in 16 patients, and none showed progressive dysplasia on follow-up. Low-grade dysplasia was detected in 10 patients; 2 had and 2 progressed to high-grade dysplasia. High-grade dysplasia was found in 7 patients; 4 were concurrent with or just preceded cancer. All 4 cases of cancer were first detected by surveillance, and 3 were successfully treated. Significant risk factors for dysplasia (all grades) and cancer included the extent of disease (P < 0.01), older age at onset of colitis (P = 0.01), and the duration of disease (P < 0.05). The adjusted risk for cancer was significantly increased (P = 0.04). CONCLUSIONS: Indefinite dysplasia did not predict developing cancer. Low- or high-grade dysplasia was not frequent (8.5%) but was associated with progression to cancer. These can be detected and successfully treated by systematic endoscopic surveillance of patients with chronic (> or = 7 years), extensive (more than the rectosigmoid colon) ulcerative colitis.

Adenomatous Polyps↗

PubMed1995

[Local production of eicosanoids in patients with ulcerative colitis].

BACKGROUND: Eicosanoids act obviously as mediators of inflammation in ulcerative colitis. The objective of the submitted paper was to assess relations between intraluminal concentrations of prostaglandin E and leukotriene B4 and the activity of ulcerative colitis evaluated according to clinical, endoscopic and histological criteria. METHODS AND RESULTS: In 56 patients with ulcerative colitis the PGE concentration was assessed in the rectal dialysate (3H Prostaglandin E Radioimmunoassay Kit Ca-501, Clinical Assay Cambridge USA). In 35 patients with ulcerative colitis the authors assessed the LTB4 concentration in the rectal dialysate (Leukotriene B4 3H Assay RPN 70, Amersham, G. Britain). The authors proved a statistically significant correlation between the intraluminal PGE concentration and the activity of ulcerative colitis according to clinical criteria (p < 0.1), endoscopic criteria (p < 0.05) and histological criteria (p < 0.01). The intraluminal LTB4 concentration correlated significantly with the activity of ulcerative colitis according to clinical criteria (p < 0.05). When comparing LTB4 values with the activity of the disease according to endoscopic and histological criteria, a tendency of rising LTB4 values with increasing activity of the disease is apparent. However, a significant relationship was not found; this can be explained by the fact that relatively small groups of patients were investigated with a relatively great scatter of LTB4 concentrations. CONCLUSIONS: During the period of active ulcerative colitis the intraluminal PGE concentration rises and correlates with the clinical, endoscopic and histological activity. There is also a rise of the intraluminal LTB4 concentration which correlates with the clinical activity of the disease. A high eicosanoid concentration is found in cases with a severe course and complications.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed2004

Fecal excretion of human deoxyribonucleic acid as an index of inflammatory activity in ulcerative colitis.

BACKGROUND & AIMS: Several indices evaluate disease activity in ulcerative colitis, but most have drawbacks to their application (invasiveness, complexity, or lack of specificity), and discrepancies between them are frequent. Assuming that desquamation of epithelial and inflammatory cells increases in damaged colonic mucosa, we hypothesized that fecal excretion of human DNA is an index of mucosal inflammation and damage. The aim of our study was to determine whether excretion of human DNA is useful in the evaluation of disease activity in ulcerative colitis. METHODS: Thirty-one controls and 36 ulcerative colitis patients were included. Ulcerative colitis patients and controls underwent colonoscopic examination after preparation by gut lavage with polyethylene-glycol electrolyte solution. In patients, disease activity was established using the clinical index of Rachmilewitz and an endoscopic score. Feces and gut lavage fluid were obtained and DNA levels were measured by quantitative polymerase chain reaction of the human beta-globin gene. RESULTS: Fecal DNA excretion correlated with the clinical index (r = 0.59, P < 0.05) and the endoscopic score (r = 0.76, P < 0.01). Gut lavage fluid DNA levels also correlated with clinical and endoscopic activity scores (r = 0.41 and 0.51, respectively, P < 0.05). Fecal DNA excretion was significantly higher in patients with endoscopically or clinically active disease than in controls or patients in remission. Fecal DNA excretion discriminates between endoscopically active disease and remission (sensitivity 0.67, specificity 1.00, P < 0.01). CONCLUSIONS: Excretion of human DNA in feces, as an expression of cellular desquamation, is a novel noninvasive technique to objectively assess disease activity in ulcerative colitis.

Adult↗

PubMed1999

The unsolved problem of surveillance for colorectal cancer in ulcerative colitis.

The association between long standing extensive ulcerative colitis and the increased risk for developing colorectal cancer suggests that surveillance by frequent and regular colonoscopies may provide a means for reducing cancer-related morbidity and mortality. A crude calculation suggests that such a surveillance program would also be cost effective. None of several clinical trials, however, has been able to provide unequivocal evidence in favour of surveillance. The major reason for this failure relates to the prohibitively large number of patients with ulcerative colitis who need to be followed over a prolonged time period before statistically sound results would be obtained. Because models of decision analyses themselves have to rely on medical evidence, they cannot provide a substitute for deficient clinical data. The issue of surveillance colonoscopy cannot be resolved by the available knowledge or analytical tools. Hopefully, new techniques of surveillance or even a cure for ulcerative colitis will render the question mute of whether or not to screen patients with ulcerative colitis by frequent colonoscopy.

Colitis, Ulcerative↗

PubMed1983

Increased colonic adenylate cyclase activity in active ulcerative colitis.

To investigate the pathogenesis of diarrhea in ulcerative colitis, colonic adenylate cyclase activity was determined in patients and normal subjects. Basal adenylate cyclase activity in 19 patients with active disease [61.5 +/- 9.6 (mean +/- SE) pmol cyclic adenosine monophosphate/mg protein . 10 min] was two times higher (p less than 0.01) than its activity in colonic mucosa of 30 normal subjects or 10 ulcerative colitis patients in remission [31.4 +/- 2.0 and 23.6 +/- 1.9 pmol cyclic adenosine monophosphate/mg protein . 10 min, respectively]. The enzyme activity was stimulated to the same extent in all groups by sodium fluoride, vasoactive intestinal polypeptide, or by substitution in the assay mixture of guanosine triphosphate by its hydrolysis-resistant analogue--GTP gamma S. Prostaglandin E2 significantly stimulated the enzyme activity in tissue obtained from normal subjects, patients with shigellosis, and ulcerative colitis patients in remission while it had no effect on adenylate cyclase activity in colonic mucosa of patients with active ulcerative colitis. These results suggest that stimulation of colonic adenylate cyclase activity, possibly secondary to the reported enhanced colonic prostanoid synthesis, may contribute to the diarrhea in ulcerative colitis.

Adenylyl Cyclases↗

PubMed1996

Diagnostic difficulty arising from rectal recovery in ulcerative colitis.

AIMS: To ascertain whether the dogma that a normal rectal biopsy precludes a diagnosis of ulcerative colitis is correct. METHODS: Rectal biopsy specimens from a prospective group of 24 asymptomatic patients, with an established diagnosis of ulcerative colitis, were examined in a blinded study alongside 10 normal rectal biopsy specimens from an age and sex matched patient cohort without ulcerative colitis. Each biopsy specimen was assessed by three pathologists and ascribed to one of four categories: normal; borderline abnormality (one or more minor nonspecific abnormalities which, when combined, did not fulfil the minimal acceptable criteria for a diagnosis of ulcerative colitis); minimal features of chronic ulcerative colitis; and unequivocal ulcerative colitis. RESULTS: Two patients with ulcerative colitis had normal biopsy specimens; nine specimens were categorised as borderline abnormality, one as showing the minimal changes of chronic ulcerative colitis, and 12 as having the typical changes of chronic ulcerative colitis. Thus, 11 (46%) of the 24 patients had a rectal biopsy specimen that was devoid of the acceptable attributes on which a diagnosis is established, despite a confident previous diagnosis. Ten of these 11 cases had disease limited to the rectum. Review of all previous histological biopsy specimens (n = 164) and clinical data, including drug treatment, failed to identify any attributes that might be prognostic markers for future rectal mucosal healing. CONCLUSIONS: A normal rectal biopsy specimen, though uncommon, may occur in longstanding colitis. Moreover, in 46% of these asymptomatic but established cases the degree of healing may preclude a diagnosis of ulcerative colitis without comprehensive clinical and radiological details. Pathologists need to be aware of this minimal end of the spectrum of disease.

Adult↗

PubMed2001

Appendectomy and protection against ulcerative colitis.

BACKGROUND: A history of appendectomy is rare in patients with ulcerative colitis. This suggests a protective effect of appendectomy or that appendicitis and ulcerative colitis are alternative inflammatory responses. We sought to characterize this inverse relation further. METHODS: We studied a cohort of 212,963 patients who underwent appendectomy before the age of 50 years between 1964 and 1993 and a cohort of matched controls who were identified from the Swedish Inpatient Register and the nationwide census. The cohort was followed until 1995 for any subsequent diagnosis of ulcerative colitis. RESULTS: Patients who underwent appendectomy for appendicitis and mesenteric lymphadenitis had a low risk of ulcerative colitis (for patients with perforated appendicitis, the adjusted hazard ratio was 0.58 [95 percent confidence interval, 0.38 to 0.87]; for those with nonperforated appendicitis it was 0.76 [95 percent confidence interval, 0.65 to 0.90]; and for those with mesenteric lymphadenitis it was 0.57 [95 percent confidence interval, 0.36 to 0.89]). In contrast, patients who underwent appendectomy for nonspecific abdominal pain had the same risk of ulcerative colitis as the controls (adjusted hazard ratio, 1.06; 95 percent confidence interval, 0.74 to 1.52). For the patients who had appendicitis, an inverse relation with the risk of ulcerative colitis was found only for those who underwent surgery before the age of 20 years (P<0.001). CONCLUSIONS: Appendectomy for an inflammatory condition (appendicitis or lymphadenitis) but not for nonspecific abdominal pain is associated with a low risk of subsequent ulcerative colitis. This inverse relation is limited to patients who undergo surgery before the age of 20 years.

Abdominal Pain↗

PubMed2006

Infiltration of CD19+ plasma cells with frequent labeling of Ki-67 in corticosteroid-resistant active ulcerative colitis.

Abnormalities in humoral immunity are implicated in the pathogenesis of ulcerative colitis. However, the detailed mechanisms of B-cell activation in the locale remain unaccounted for. We analyzed ulcerative colitis from the standpoint of lymphocytic expansion in the loco. Intestinal specimens obtained at surgery from 30 patients with ulcerative colitis treated with corticosteroids and 15 with Crohn's disease were analyzed by immunohistochemistry and flow cytometry. Ulcerative colitis was characterized by a diffuse distribution of Ki-67(+) small round cells particularly in the ulcer base (that were CD19(+) and CD20(-)), with a significant number of them also CD138(+). Immunoelectron microscopy for CD19 revealed an abundance of rough endoplasmic reticulum in the cytoplasm. These indicated that they are of immature plasma lineage cells. By contrast, plasma cells in Crohn's disease were negative for CD19, and the labeling for Ki-67 was infrequent, showing mature phenotype. Flow cytometry revealed an occurrence of CD19(+) and CD20(-) cells in ulcerative colitis but not in Crohn's disease. The labeling index of Ki-67 among CD19(+) plasma cells was positively correlated with the clinical activity of ulcerative colitis. High labeling of Ki-67 in CD19(+) plasma cells is specific for active ulcerative colitis that was resistant to medical treatment by corticosteroids.

Adolescent↗

PubMed1997

Calcium and colorectal epithelial cell proliferation in ulcerative colitis.

In persons at higher risk for colon cancer (e.g., those with sporadic adenoma or ulcerative colitis), compared to those at lower risk, colonic epithelial cell proliferation kinetics are altered. We have shown previously that calcium supplementation appears to normalize the distribution of proliferating cells without affecting the proliferation rate in the colorectal mucosa of sporadic adenoma patients. In a pilot randomized, double-blind, placebo-controlled, clinical trial conducted concurrently with our previously published sporadic adenoma trial, we tested whether calcium supplementation can also modulate cell proliferation kinetics in patients with ulcerative colitis. Ulcerative colitis patients (n = 31) were randomized to placebo or 2.0 g of supplemental calcium daily. Colorectal epithelial cell proliferation was determined by immunohistochemical detection of proliferating cell nuclear antigen labeling of cells in "nonprep" rectal biopsies taken at randomization and after 2 months treatment. All biopsies were scored by one reviewer. Differences in mean follow-up minus baseline labeling index (LI; the proportion of colon crypt epithelial cells that were labeled) and in the phi(h) (proportion of labeled cells that were in the upper 40% of the crypts) were compared with analysis of covariance. Pill-taking adherence was 97%. Biopsy-scoring reliability was high (r = 0.89). The pooled baseline LI and phi(h) were 6.3% and 5.6%, respectively. The LI in the calcium group decreased by 0.5% (proportionately, 3%) more than in the placebo group (P = 0.91). Similarly, the phi(h) in the calcium group decreased by 0.3% (proportionately, 10%) more than in the placebo group (P = 0.85). This pilot study does not suggest that 2.0 g of calcium as calcium carbonate daily can substantially normalize either the rate or distribution of proliferating cells over a 2-month period in the colon crypts of patients with ulcerative colitis; a more definitive answer to the question of whether calcium may be effective would require a study with a larger sample size and/or other study design modifications.

Adult↗

PubMed2004

Does appendectomy reduce the risk of ulcerative colitis?

BACKGROUND: Persons who have had an appendectomy are less prone to develop ulcerative colitis than those who have not. The underlying mechanism and the clinical use of this finding are unknown. METHODS: Two competing hypotheses were examined: (1) the inverse association between appendectomy and ulcerative colitis is conferred by a mutual determinant such as genes, and (2) the appendix itself has biologic effects that promote the development of ulcerative colitis. We performed a population-based cohort study of all 234,559 persons who had an appendectomy performed in Denmark 1977 through 1999. We used a bidirectional cohort design, calculating the standardized incidence rate of ulcerative colitis both before and after the appendectomy. If the hypothesis of a constant, confounding factor were true, incidence rates of ulcerative colitis would be equal before and after appendectomy. If the incidence of ulcerative colitis were lower after appendectomy than before, it would support the second hypothesis and a true protective effect of the appendectomy. We controlled confounding by age and sex using direct standardization. RESULTS: Of 234,559 persons who had an appendectomy, 559 developed ulcerative colitis during a mean follow up of 17.5 years. The standardized incidence rate of ulcerative colitis was lower in the postappendectomy period than in the preappendectomy period (incidence rate ratio = 0.74; 95% confidence interval = 0.62-0.88). CONCLUSIONS: The inverse association between appendectomy and ulcerative colitis is not explained by time-stable factors such as genes. Appendectomy might have a genuine protective effect toward development of ulcerative colitis.

Adolescent↗