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PubMed2005

Infliximab for induction and maintenance therapy for ulcerative colitis.

BACKGROUND: Infliximab, a chimeric monoclonal antibody directed against tumor necrosis factor alpha, is an established treatment for Crohn's disease but not ulcerative colitis. METHODS: Two randomized, double-blind, placebo-controlled studies--the Active Ulcerative Colitis Trials 1 and 2 (ACT 1 and ACT 2, respectively)--evaluated the efficacy of infliximab for induction and maintenance therapy in adults with ulcerative colitis. In each study, 364 patients with moderate-to-severe active ulcerative colitis despite treatment with concurrent medications received placebo or infliximab (5 mg or 10 mg per kilogram of body weight) intravenously at weeks 0, 2, and 6 and then every eight weeks through week 46 (in ACT 1) or week 22 (in ACT 2). Patients were followed for 54 weeks in ACT 1 and 30 weeks in ACT 2. RESULTS: In ACT 1, 69 percent of patients who received 5 mg of infliximab and 61 percent of those who received 10 mg had a clinical response at week 8, as compared with 37 percent of those who received placebo (P<0.001 for both comparisons with placebo). A response was defined as a decrease in the Mayo score of at least 3 points and at least 30 percent, with an accompanying decrease in the subscore for rectal bleeding of at least 1 point or an absolute rectal-bleeding subscore of 0 or 1. In ACT 2, 64 percent of patients who received 5 mg of infliximab and 69 percent of those who received 10 mg had a clinical response at week 8, as compared with 29 percent of those who received placebo (P<0.001 for both comparisons with placebo). In both studies, patients who received infliximab were more likely to have a clinical response at week 30 (P< or =0.002 for all comparisons). In ACT 1, more patients who received 5 mg or 10 mg of infliximab had a clinical response at week 54 (45 percent and 44 percent, respectively) than did those who received placebo (20 percent, P<0.001 for both comparisons). CONCLUSIONS: Patients with moderate-to-severe active ulcerative colitis treated with infliximab at weeks 0, 2, and 6 and every eight weeks thereafter were more likely to have a clinical response at weeks 8, 30, and 54 than were those receiving placebo. (ClinicalTrials.gov numbers, NCT00036439 and NCT00096655.)

Adult↗

PubMed1985

T-antigen expression by peanut agglutinin staining relates to mucosal dysplasia in ulcerative colitis.

Staining of 326 rectal mucosal biopsies from ulcerative colitis patients with peanut agglutinin (PNA), which binds to the T-blood group antigen and has been claimed to reflect a cancer-associated mucin alteration, showed highly significant direct associations with mucosal dysplasia (P less than 0.001), disease activity (P less than 0.001), and subsequent development of rectal cancer in a smaller series of patients (P = 0.005). Staining for normal colonic mucin by the Dolichos biflorus (DBA) lectin related significantly and inversely to dysplasia. Intense normal colon mucin staining by DBA related significantly (P less than 0.025) to long disease duration and to subsequent development of cancer (P = 0.02). The latter association is based on a small number of patients only and is not considered conclusive evidence, but may provide a link with goblet-cell hyperplasia. The authors conclude that although T-antigen expression relates to dysplasia, the findings of "false" positive and negative rates of 22 and 33 percent respectively, make it unlikely that staining of biopsy sections for the T-antigen by peanut agglutinin will contribute materially to routine assessment for dysplasia and cancer risk prediction in patients with ulcerative colitis.

Adult↗

PubMed2006

Do patient preferences influence decisions on treatment for patients with steroid-refractory ulcerative colitis?

BACKGROUND & AIMS: Patients with steroid-refractory ulcerative colitis face a difficult treatment decision between colectomy and therapy with infliximab or cyclosporine. The aim of this study was to understand how individual patient preferences for the various treatment outcomes influence the optimal treatment decision for a given patient. METHODS: A Markov model was used to simulate treatment with total colectomy with an ileo pouch-anal anastomosis (TC/IPAA), cyclosporine (CSA), infliximab (INFLX), and infliximab followed by cyclosporine for treatment failures (INFLX-->CSA). Utility weights for treatment outcomes were elicited from 48 patients using both time trade-off and visual rating scale methods. Preference sets were applied to the model to identify the therapy that maximized quality-adjusted life years (QALYs) for each patient. Sensitivity analyses were performed to assess model robustness. RESULTS: Optimal treatment was highly variable among patients (INFLX-->CSA = 42%, 20/48; TC/IPAA = 37%, 18/48; CSA = 21%, 10/48; INFLX = 0%, 0/48). However, when average preference weights from our sample were applied to the model, medical treatments were superior to TC (CSA = .26 QALYs gained vs TC/IPAA; INFLX-->CSA = .25 QALYs gained vs TC/IPAA). CONCLUSIONS: Patient preferences have a clear impact on the optimal treatment for steroid-refractory ulcerative colitis. Although averaged preferences support the use of medical interventions, a third of individual patients may benefit most from proceeding directly to colectomy. Failure to fully assess individual preferences may result in suboptimal treatment for these patients.

Adult↗

PubMed1985

Large bowel mucosal dysplasia and carcinoma in ulcerative colitis.

The clinicopathological details of eight cases of ulcerative colitis complicated by carcinoma of the colon are described. There was a total of 14 primary colonic cancers, six of which were not detected before pathological examination of the resection specimens. The reason for this may be related to atypical tumour growth patterns. Three occurred in flat mucosa, one in a mucosal plaque lesion, and another in polypoidal mucosa. The occurrence, distribution, and morphology of mucosal dysplasia were noted in both resection specimens and biopsies taken at varying stages before resection. Tumour was associated with normal and adjacent dysplastic mucosa of varying grades. The extent and grade of dysplasia were not reliable indicators of tumour differentiation or subsequent clinical outcome. Only two cancers were poorly differentiated. In five cases a total of 23 mucosal biopsies were taken, all less than 12 months before resection. Three rectal biopsies were graded positive for dysplasia and three colonic biopsies indefinite for dysplasia. The subsequent resection specimens showed both dysplastic and carcinomatous changes. Three rectal and 14 colonic biopsies were graded negative for dysplasia despite positive findings in the subsequent resection specimens. This anomaly is partly attributed to the patchy nature of dysplasia in colitic mucosa. Two cases illustrate the possibility of dysplasia pursuing a rapidly progressive course. The mucosal changes of ulcerative colitis were assessed using a recently introduced and standardised international classification.

Adolescent↗

PubMed1996

Concentrations of platelet activating factor in rectal mucosa in patients with ulcerative colitis.

OBJECTIVE: To find out if concentrations of platelet activating factor (PAF), which has been proposed as a mediator in the pathogenesis of ulcerative colitis and Crohn's disease, are increased in the rectal mucosa of patients with ulcerative colitis. DESIGN: Open study. SETTING: University hospital, Sweden. SUBJECTS: 45 Patients with ulcerative colitis (19 with active disease and 26 in remission), and 6 control patients and 11 healthy volunteers who acted as controls. INTERVENTIONS: Rectal biopsy. MAIN OUTCOME MEASURE: PAF content of rectal biopsy specimens. RESULTS: There were no differences between the PAF content of rectal mucosa in patients with active disease (median 47 pmol/g wet weight), patients in remission (47 pmol/g), and controls (51 pmol/g). There was no correlation between PAF content and inflammation seen endoscopically or histologically. 13 Patients who had active disease were investigated on a second occasion 9 weeks later (range 7-17), when in remission having received steroids but steroid-free at that time. There was a slight but not significant trend towards lower concentrations of PAF (median 33 pmol/g) compared with their previous results, possibly as a result of treatment. PAF concentrations were significantly lower than those of a group of patients in clinically stable remission of longer duration (p < 0.05). CONCLUSIONS: We did not find high concentrations of PAF in the rectal mucosa of patients with active ulcerative colitis compared with patients in remission or controls. We therefore have no evidence that PAF has an important role as a mediator in the inflammation of ulcerative colitis.

Adult↗

PubMed1988

Altered lectin binding by colonic epithelial glycoconjugates in ulcerative colitis and Crohn's disease.

Evidence is accumulating that colonic mucin glycoconjugates are altered in ulcerative colitis. In order to investigate this further, the lectin-binding properties of rectal glycoconjugates have been studied in ulcerative colitis, Crohn's disease, and controls using lectin-peroxidase histochemistry. Ten lectins were used including peanut agglutinin (PNA) which is known to bind to malignant and adenomatous but not normal colonic mucins. Eight of 21 ulcerative colitis rectal biopsies and 10 of 17 Crohn's disease rectal biopsies showed PNA positivity, particularly in the supranuclear region of surface epithelial cells. There was no correlation between PNA positivity and duration of disease or inflammation, and none of the biopsies showed evidence of dysplasia. This abnormality in epithelial cell glycoconjugates seems to be commonly present in nondysplastic mucosa and occurs in both ulcerative colitis and Crohn's disease. It may reflect a fundamental abnormality in mucus glycoprotein synthesis in inflammatory bowel disease.

Adult↗

PubMed1999

The effects of migration on ulcerative colitis: a three-year prospective study among Europeans and first- and second- generation South Asians in Leicester (1991-1994).

OBJECTIVE: Our aim was to measure prospectively the incidence of ulcerative colitis in Leicester City and to compare this with a previous retrospective study in the same area. We also sought to compare the incidence and disease extent in the European community with that of the South Asian community and to compare the disease extent between first- and second-generation South Asian migrants. METHODS: A 3-yr prospective study of ulcerative colitis in the city of Leicester took place from October 1, 1991 to September 30, 1994 and included all cases resident in Leicester City and diagnosed as having ulcerative colitis, regardless of the extent and severity of the disease. RESULTS: Extensive colitis was commoner in second-generation migrants than in the first generation (chi2 = 4.3, p = 0.04) and was comparable to the European community. The annual average incidence of ulcerative colitis was 9.1/10(5) population/yr (95% confidence interval [CI] 7.1-11.3), which is similar to the previous retrospective study. However, the annual average incidence of ulcerative colitis in the European population was 7.0/10(5) population/yr (95% CI 5-9.5), whereas that of the South Asian population was 17.2/10(5) population/yr (95% CI 11.8-24.3), confirming that the risk of ulcerative colitis in this particular community is exceptionally high. CONCLUSIONS: These early results suggest that the disease pattern follows that of the indigenous population after only one generation and requires monitoring over the next decade. The incidence of ulcerative colitis in the South Asian population is high and continuing to rise.

Adult↗

PubMed1992

Childhood exposure to environmental tobacco smoke and the risk of ulcerative colitis.

Previous reports have suggested that there may be a protective effect of active cigarette smoking on the risk of ulcerative colitis. Because passive smoking may also have other health consequences, the authors examined the effect of exposure to environmental tobacco smoke during childhood on adult risk of ulcerative colitis in a case-control study of 172 cases drawn in 1986-1987 from the rosters of North Carolina chapters of the Crohn's & Colitis Foundation of America and 131 peer-nominated neighborhood controls. Active smokers were less likely to develop ulcerative colitis than were nonexposed nonsmokers (odds ratio = 0.53, 95% confidence interval 0.24-1.14). The risk was also decreased in passive smokers, i.e., those whose parents had smoked (odds ratio = 0.50, 95% confidence interval 0.25-1.00). Risk estimates were not related to sex, education, age at onset of symptoms, or year of onset of symptoms. Both active smoking in adulthood and passive childhood exposure to environmental tobacco smoke appear to decrease the risk of ulcerative colitis. The results indicate that childhood passive smoke exposures can influence adult susceptibility to ulcerative colitis.

Adult↗

PubMed2001

Flow cytometric and histologic evaluation in a large cohort of patients with ulcerative colitis: correlation with clinical characteristics and impact on surveillance.

PURPOSE: To examine the prevalence of DNA aneuploidy as a function of the extent of ulcerative colitis and to study the correlation of aneuploidy with clinical characteristics. Furthermore, the occurrence of aneuploidy and dysplasia during colonoscopic surveillance was studied in a subset of these patients. METHODS: By analyzing 5404 biopsy samples of 368 patients with ulcerative colitis, we have evaluated the importance of DNA ploidy measured by flow cytometry. We have also investigated the influence of extent (219 patients with extensive or total colitis vs. 149 patients with localized colitis) and duration of colitis on the development of dysplasia (patients with biopsy specimens that showed inflammation alone were compared with those with biopsy specimens that were equivocal or positive for dysplasia) and aneuploidy. Included was a subgroup of patients with ulcerative colitis and primary sclerosing cholangitis (n = 16). RESULTS: Aneuploidy was found in 8.7 percent (32/368) of all patients. The prevalence of aneuploidy increased by the extent of ulcerative colitis (2 percent localized, 6.8 percent extensive colitis, 14.9 percent total colitis). The frequency of aneuploidy was higher in patients with disease duration longer than 10 years (P = 0.007). Patients with ulcerative colitis and primary sclerosing cholangitis were more likely to develop aneuploidy (9/16, 56.3 percent vs. 14/120, 11.7 percent; P < 0.001) and dysplasia (4/16, 25 percent vs. 10/120, 8.3 percent; P = 0.06) than patients without primary sclerosing cholangitis. CONCLUSION: Because DNA aneuploidy represents an early alteration during neoplastic transformation in ulcerative colitis, flow cytometry is a valuable tool in the surveillance of those patients. Primary sclerosing cholangitis represents an additional risk factor for the development of DNA aneuploidy and dysplasia.

Aneuploidy↗

PubMed2001

Delivery of glucocorticoid conjugate in rat gastrointestinal tract and its treatment for ulcerative colitis.

AIM: To evaluate colonic delivery and therapeutic effect of the newly synthesized dexamethasone (DX)-dextran (500 000) conjugate (DXD50) in the rat. METHODS: The amount of dexamethasone was measured in the contents from different parts of rat gastrointestinal tract and in plasma after ig conjugate. Therapeutic effect of conjugate and DX was tested in trinitrobenzenesulfonic acid-induced colitis in rat. Repair of colitis was assessed by measuring colonic ulceration area, colon weight, and colonic myeloperoxidase (MPO) activity. Systemic immunosuppression of DX was evaluated with weight of thymus and spleen and lymphocyte count in peripheral blood from rat with ulcerative colitis. RESULTS: Dexamethasone released from conjugate was mainly distributed in contents of cecum and colon. When DXD50 and DX 0.25 micromol . kg-1 . d-1 were used ig to treat ulcerative colitis in rat, the ulcerative area of colon was reduced by 55.6 % and 33.3 %, respectively whereas colon weight was reduced by 17.9 % and 2.6 %, respectively. The conjugate had no effect on lymphocyte count in peripheral blood, spleen weight, and thymus weight of rat which could be reduced markedly by the same dose of DX (P < 0.05 vs control). CONCLUSION: DXD50, which could specifically deliver DX to large intestine, is a promising agent in the treatment of human inflammatory bowel disease.

Animals↗

PubMed2006

NK2 receptor-mediated spontaneous phasic contractions in normal and ulcerative colitis human sigmoid colon.

Human colonic circular muscle produces spontaneous phasic contractions that are reduced in ulcerative colitis. How the spontaneous phasic contractions develop and why they decrease in ulcerative colitis are not known. We found that spontaneous phasic contractions of normal sigmoid circular muscle strips were significantly reduced by 90-min incubation with tetrodotoxin (10(-5) M), which blocked neurokinin A release in basal conditions and in response to electrical stimulation. In addition, spontaneous contraction of human sigmoid colon was significantly decreased by the NK2 receptor antagonists MEN10376 (Asp-Tyr-D-Trp-Val-D-Trp-D-Trp-Lys-NH2) and NK2ra (Bz-Ala-Ala-D-Trp-Phe-D-pro-Pro-Nle-NH2) but not by atropine or by the NK1 antagonist FK888 (N2-[(4R)-4-hydroxyl-1-(1-methyl-1H-indol-3-yl)carbonyl-l-prolyl]-N-methyl-N-phenylmethyl-3-(2-naphthyl)-l-alaninamide), suggesting that NK2 receptors are involved in their development. The spontaneous phasic contractions were abolished by thapsigargin and cyclopiazonic acid and significantly decreased by the protein kinase C inhibitor chelerythrine and by the calmodulin inhibitor CGS9343B (1,3-dihydro-1-[1-[(4-methyl-4H,6H-pyrrolo[1,2-a]-[4,1]-benzoxazepin-4-yl)methyl]-4-piperidinyl]-2H-benzimidazol-2-one (1:1) maleate), suggesting that spontaneous phasic contractions may be mediated by Ca2+ release from intracellular stores and by a protein kinase C- and calmodulin-dependent pathway. In strips from patients with ulcerative colitis, spontaneous contractions were significantly reduced, and this reduction was partially restored by the hydrogen peroxide scavenger catalase. Neurokinin A release, however, was not affected. We conclude that spontaneous phasic contractions of human sigmoid circular smooth muscle may be mediated by activation of NK2 receptors, calcium release from intracellular stores, and activation of calmodulin and protein kinase C. In ulcerative colitis patients, spontaneous phasic contractions are decreased, and this decrease may be in part due to overproduction of hydrogen peroxide affecting sigmoid circular muscle.

Colitis, Ulcerative↗

PubMed1994

Appendiceal involvement as a skip lesion in ulcerative colitis.

Despite the frequency of ulcerative colitis (UC), and numerous studies related to this disease, controversy remains regarding its distribution patterns. It is generally believed that UC starts in the rectum and progresses proximally in continuity to involve cecum along with appendix in 50% of all cases. However, recent endoscopic and histological studies suggest that UC can occur as a discontinuous process. Furthermore, the few existing studies specifically addressing appendiceal histology in UC are divided over whether ulcerative appendicitis (UA) may be seen without cecal involvement (i.e., as a "skip lesion"). To study the appendiceal pathology in UC, and in particular the frequency of UA as a "skip lesion," we retrospectively evaluated 39 proctocolectomy specimens containing appendices removed for UC. Six cases (17%) had obliterated appendices; appendiceal and cecal histologies of the remaining 33 cases were divided into (a) active disease, (b) quiescent disease, or (c) nonspecific or normal histology. Twenty of 39 appendices (51%) showed active disease, four (10%) had quiescent disease, and nine (23%) were either normal or nonspecifically inflamed. After exclusion of one case for inadequate cecal sampling, comparison of cecal and appendiceal histologies showed concordance in 16 cases and discordance in the remaining 16. Of these discordant cases, six had greater disease activity in the cecum and 10 had greater activity in the appendix. Of these latter 10 cases, six showed normal or nonspecific cecal histology associated with active UA. Thus, "skip lesions" of the appendix were detected in 15% of the UC specimens examined.

Adolescent↗

PubMed1993

p53 point mutations in dysplastic and cancerous ulcerative colitis lesions.

BACKGROUND: The molecular basis of colorectal dysplasia and carcinoma arising in ulcerative colitis is poorly understood. Loss of heterozygosity involving the tumor suppressor gene p53 occurs frequently in neoplastic ulcerative colitis lesions. Point mutation affecting p53 is associated with loss of heterozygosity in other cancers. Therefore, it was determined whether p53 point mutation occurs in ulcerative colitis-associated neoplasia. METHODS: Single-strand conformation polymorphism analysis, DNA sequencing, and loss of heterozygosity studies were performed on 45 patients with ulcerative colitis-associated dysplasia and carcinoma. RESULTS: Point mutations were detected in 26 lesions from 20 patients, including 18 carcinomas, 6 dysplasia-associated masses, 1 flat dysplasia, and 1 lymph node metastasis. In two cases, identical p53 mutations were observed in both carcinoma and adjacent dysplasia. Missense mutations causing amino acid substitutions as well as nonsense mutations resulting in premature stop codons were seen. Tandem mutations, in which more than 1 sequence alteration occurred on the same allele of p53, were also detected. Point mutation was accompanied by loss of the other p53 allele in 8 of 10 patients informative for both loss of heterozygosity and mutation assays. CONCLUSIONS: These findings suggest that inactivation of p53 by mutation and loss of heterozygosity is a common mechanism of malignant transformation in ulcerative colitis. They also imply that in contrast to sporadic colorectal carcinoma, ulcerative colitis-associated neoplastic progression may involve p53 inactivation at relatively early, noninvasive stages.

Chromosome Deletion↗

PubMedDate not supplied

Bacterial invasion into the colonic mucosa in ulcerative colitis.

This study investigated interactions between mucosal lesions and bacterial invasion in ulcerative colitis using the acridine-orange staining method. In all 16 cases of ulcerative colitis, the mucosa was found to be invaded by small rods and cocci. In five of 10 controls, bacteria were seen only adhering to the mucosa and no bacteria were detected in the five remaining cases. It is suggested that the presence of bacteria in the colonic mucosa may be a factor responsible for the persistence or aggravation of ulcerative colitis.

Acridine Orange↗

PubMed1997

Ulcerative colitis: a genetic disease?

A number of lines of evidence support the hypothesis that ulcerative colitis is an inherited disorder in a proportion of cases. First, there is a pattern of familial aggregation. Second, there are differences in the prevalence of the disease in different ethnic groups. Finally, the concordance rate in monozygotic twin pairs is higher than that of dizygotic twin pairs, although not as high as the concordance rates observed in Crohn's disease. Genetic models of the inheritance patterns suggest that ulcerative colitis is probably caused by one major gene, although that gene (or genes) remains to be identified. While at least one localization for susceptibility to Crohn's disease now seems certain, efforts to localize and characterize the susceptibility genes involved in the inheritance of ulcerative colitis are still underway. While the genes of the major histocompatibility complex have been imputed as causal in susceptibility to ulcerative colitis, a consensus of proof continues to elude us.

Chromosomes, Human, Pair 6↗

PubMed2003

Topical butyrate improves efficacy of 5-ASA in refractory distal ulcerative colitis: results of a multicentre trial.

BACKGROUND: The treatment of distal ulcerative colitis, refractory to conventional 5-ASA/steroid treatment, is still a matter of debate. The present study aimed at confirming, with adequate statistical power, previous data indicating the usefulness of topical butyrate and 5-ASA in the treatment of this condition. DESIGN: Double-blind, placebo-controlled, multicentre study. A total of 51 patients with distal (< 65 cm) ulcerative colitis, refractory to topical 5-ASA/cortisone, were randomly allocated to receive topical 5-ASA 2 g and 80 mM L-1 sodium-butyrate bid (Group A; 24 patients) or 5-ASA 2 g and 80 mL saline bid (Group B; 27 patients) for 6 weeks. Sigmoidoscopy with biopsies, as well as clinical and laboratory evaluations, were carried out at enrollment and at the end of the trial. Primary endpoints: remission or marked improvement in endoscopic, histologic and clinical findings. RESULTS: Most parameters showed a significant improvement vs. baseline in both groups. Remission in six patients and improvement in 12 patients in Group A vs. one remission and 13 with improvement in Group B (P < 0.05). A significant difference in favour of Group A was recorded regarding the number of bowel movements (P < 0.01), urgency (P < 0.05) and the patients' self evaluation (P < 0.01). DISCUSSION: The combined treatment with topical butyrate and 5-ASA is significantly more effective than 5-ASA alone in the management of refractory distal colitis. Further improvements in the treatment of refractory distal ulcerative colitis may be feasible based on the identification of patient subgroups and the association of two or more active drugs. Butyrate may well be one of them.

Adult↗

PubMedDate not supplied

HLA antigens in ulcerative colitis and primary sclerosing cholangitis.

The aims of this study were to find out whether the alleles of the HLA class I or II region are associated with susceptibility to ulcerative colitis, and to show whether there is a difference or similarity in HLA associations between primary sclerosing cholangitis and ulcerative colitis. HLA-A, B, C and DR antigens were studied using the standard lymphocyte microcytotoxicity test in 24 Finnish patients with primary sclerosing cholangitis, 77 patients with ulcerative colitis, and 106 controls. HLA-B8 (54%) and DR3 (60%) were associated with primary sclerosing cholangitis. HLA-DR1 (46%) and DR6 (20%) seemed more common in ulcerative colitis than in controls. A positive association with Cw7 was common to both ulcerative colitis (25%) and primary sclerosing cholangitis (33%). Our results indicate that ulcerative colitis is more heterogeneous than primary sclerosing cholangitis in its HLA-DR associations.

Adolescent↗

PubMed1986

Free colonic perforation without dilatation in ulcerative colitis.

Free perforation occurred in only 7 of 702 patients with ulcerative colitis (1 percent) without toxic dilatation seen at The Mount Sinai Hospital from 1960 to 1981; however, these seven patients represented 30 percent (7 of 23) of all colonic perforations seen in patients with ulcerative colitis in our institution during the same period. Classic physical signs of peritonitis (silent, rigid abdomen and rebound tenderness) were absent in six of the seven patients, but all had a marked deterioration in general condition after perforation. Other signs included a sudden increase in severity of abdominal pain (three patients), marked abdominal distention (four patients), and a sharp decrease in frequency of bowel movements (six patients). Mortality was high (four of seven patients, 57 percent) and characterized by comparatively longer patient histories of colitis, longer current attacks, slightly greater delays between presumed perforation and operation, much higher transfusion requirements, and a 100 percent incidence of coagulopathy (thrombocytopenia and increased prothrombin time in three of four patients, and increased partial thromboplastin time in all four patients). The possibility of free perforation in ulcerative colitis must be considered in fulminating cases, even in the absence of colonic dilatation. Careful clinical monitoring and early surgical intervention may be the keys to reducing mortality.

Adult↗

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