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PubMed2006

Maternal and fetal outcome after colectomy for fulminant ulcerative colitis during pregnancy: case series and literature review.

PURPOSE: Previous studies have reported high morbidity and mortality in mothers and their offspring after colectomy for ulcerative colitis during pregnancy. This study was designed to assess the maternal and fetal outcomes of pregnant females undergoing colectomy for ulcerative colitis in the current era. METHODS: A retrospective analysis was performed at our institution of all pregnant females undergoing operation for ulcerative colitis between 1980 and 2004. To compare this data to that of past literature, a MEDLINE search from 1951 to 2004 reviewed all cases reported on this topic. RESULTS: Between 1980 and 2004, five females underwent an operation at our institution for fulminant ulcerative colitis while pregnant. All five patients underwent subtotal colectomy with Brooke ileostomy. Postoperative maternal morbidity included a superficial wound infection and a small asymptomatic intra-abdominal abscess. All females had successful pregnancies, and no maternal or fetal deaths occurred. Two patients went on to have an ileal pouch-anal anastomosis, one had a completion proctectomy and end ileostomy, one is scheduled for an ileal pouch-anal anastomosis, and one patient is lost to follow-up. The literature review revealed 37 cases. The overall fetal and maternal mortality was 49 and 22 percent respectively. Postoperative maternal morbidity was reported in 24 percent. CONCLUSIONS: In contrast to historic data, the maternal and fetal mortality from our series was zero and maternal morbidity was low. Subtotal colectomy and Brooke ileostomy for ulcerative colitis during pregnancy is safe. A multidisciplinary team that includes a gastroenterologist, high-risk obstetrician, and experienced surgeon is necessary for an optimal outcome.

Acute Disease↗
PubMed2005

Rebamipide enema is effective for treatment of experimental dextran sulfate sodium induced colitis in rats.

We investigated therapeutic efficacy of rebamipide using dextran sulfate sodium (DSS) induced colitis model in rats. Three percent DSS solution was given to rats for 9 days. After that, we evaluated the drug efficacy on colitis sustained with continuous drinking of 1% DSS. Twice-daily treatment with 0.3% or 1% rebamipide for 14 days significantly ameliorated the stool abnormality in the colitis model, preferentially suppressed hematochezia. The colonic mucosal lesion, determined by Alcian blue staining on day 24, was significantly reduced by rebamipide enema in a dose-dependent manner. Either rebamipide or 5-aminosalycilic acid (5-ASA) enema treated once daily significantly ameliorated colitis. The minimum effective dose of rebamipide was 0.3% in once-daily treatment, and that of 5-ASA was 10%. In a mechanistic study, the epithelial cell sheet formation of the T84 colon cancer cell was measured as an increase in generation of trans-epithelial electrical resistance in vitro. Rebamipide accelerated the increase, while 5-ASA conversely suppressed it. These results suggest that rebamipide enema is effective for treatment of experimental ulcerative colitis (UC).

Alanine↗
PubMed2006

Recommendations for improved use of the murine TNBS-induced colitis model in evaluating anti-inflammatory properties of lactic acid bacteria: technical and microbiological aspects.

Probiotic bacteria have been shown to exert promising beneficial effects in different types of intestinal disorders, including chronic inflammation. In this context, animal models of inflammatory bowel disease are useful in studying the possible prophylactic role of candidate probiotic strains. This study aimed at evaluating the critical technological and microbiological parameters as well as the robustness of the murine trinitrobenzene sulfonic acid (TNBS)-induced model of colitis, after intragastric administration of lactic acid bacteria (LAB) preparations. A standardized methodology was applied to assess the protective effect achieved by various bacterial concentrations and culture conditions of the reference strain Lactobacillus plantarum NCIMB 8826. Not only was protection found to vary in function in different levels of colitis, but also repeated experiments showed a clear bacterial dose-dependent attenuation of colitis. The physiological stage of bacteria was shown to impact as well, with substantial, mild, or reduced improvement of inflammatory scores for exponentially growing, stationary-phase, or killed bacteria, respectively. A recombinant strain, secreting murine interleukin-10 (IL-10) and previously reported to successfully treat colitis in two different models of murine colitis (dextran sulfate sodium [DSS] and IL-10-deficient mice), was used to validate the final experimental conditions. In conclusion, we identified and optimized some of the key parameters that need to be controlled in order to ensure reliable comparison of results generated over a long period of time or independent experiments. The recommendations for an improved model presented here will prove to be helpful for reproducible, independent comparison of the anti-inflammatory potential of wild-type or recombinant candidate probiotic strains, whether administered as pure cultures or as blends.

Animals↗
PubMed2006

Dextran sulfate sodium-induced colitis is associated with enhanced low molecular mass polypeptide 2 (LMP2) expression and is attenuated in LMP2 knockout mice.

Low molecular mass polypeptide 2 (LMP2) is an inducible proteasome subunit. Our goals were to examine LMP2 expression in mice with dextran sulfate sodium (DSS)-induced colitis and to evaluate colitis in LMP2 knockout (LMP2-/-) mice. Mice were given 2.5% DSS in the drinking water. On day 0, 2, 4, or 6 after DSS treatment, LMP2 expression was determined in the distal colon by western blot and immunohistochemistry. Parameters of colitis were measured in LMP2-/- mice or wild-type mice. LMP2 expression was enhanced in the colon of DSS-treated mice at all time points. Symptoms of DSS-induced colitis were always lower in LMP2-/- mice. Normalized histology scores and colonic IL-1ss levels increased over the 6-day study period in wild-type mice. These parameters were significantly reduced in LMP2-/- mice that consumed DSS for 6 days. Enhanced LMP2 expression contributes to the pathogenesis of DSS-induced colitis in mice.

Animals↗
PubMed2006

Mechanism underlying the reversal of contractility dysfunction in experimental colitis by cyclooxygenase-2 inhibition.

Inflammatory bowel diseases are associated with reduced colonic contractility and induction of cyclooxygenase-2. In this study a possible role of cyclooxygenase-2 in and the underlying mechanism of the reduced contractility were investigated in experimental colitis. The effects of meloxicam, a cyclooxygenase-2 selective inhibitor were examined on colonic contractility and MAP kinase p38 and ERK(1/2) expression. Colitis was induced in Sprague-Dawley male rats by intra-colonic instillation of trinitrobenzenesulphonic acid (TNBS; 40 mg/rat in 50 ethanol). The animals were divided into three groups. Group 1 (n=9) received meloxicam (3 mg/kg-day) gavage 1 h before and 1 day (Group 2) after induction of colitis. Group 3 (n=9) received phosphate buffered saline (PBS) in a similar manner and served as colitic control. The non colitic control animals received meloxicam in a similar manner. The animals were sacrificed after 5 days of treatment, colon was cleaned with PBS and colonic smooth muscle was obtained which was used in this study. Meloxicam treatment given 1 h before or 1 day after administration of colitis restored the reduced colonic contractility without affecting the sensitivity to carbachol. The levels of colonic smooth muscle IL-1beta mRNA, PGE(2), ERK(1/2), p38, malondialdehyde, myeloperoxidase activity and colonic mass were increased, whereas the body weight was decreased due to TNBS. The changes except colonic muscle mass and p38 expression were reversed by meloxicam treatment. These findings indicate that restoration of reduced colonic contractility by meloxicam is mediated by ERK(1/2), and that ERK(1/2) may serve as an important anti inflammatory target for treatment of colitis.

Animals↗
PubMed1985

Intensive intravenous treatment of ulcerative colitis.

Two hundred four courses of intensive intravenous treatment were given to 158 patients with ulcerative colitis. The remission rates in the severe, moderate, or mild attacks were 55.7%, 86.9%, and 91.8%. Total colitis had a great impact on the results, especially in severe attacks. Of these patients, 52.8% were operated on within 3 wk. The relapse rate was exponential, and during the first year 48.1% of the patients in remission relapsed. The extent of the colitis, severity of the attack, or duration of intensive intravenous treatment had no influence on the time of relapse. Twelve patients with chronic continuous disease were given intensive intravenous treatment. No long-term benefit was seen in patients with total ulcerative colitis, but half of those with less extensive colitis showed a good to excellent response to treatment.

Adult↗
PubMed1990

Misoprostol provides a colonic mucosal protective effect during acetic acid-induced colitis in rats.

This study determined if intracolonically applied prostaglandin E1 analogue (misoprostol) had a mucosal protective effect in rats with 4% acetic acid-induced colitis. The effects of misoprostol were compared with those of 5-aminosalicylic acid and betamethasone. A single application of 4% acetic acid induced an experimental colitis which was maximal at 2 days and showed spontaneous macroscopic and histologic healing by 12 days. Misoprostol (100 micrograms/kg), but not 5-aminosalicylic acid or betamethasone, administered 30 min before induction of colitis, provided macroscopic and histologic colonic mucosal protection but not protection of in vivo fluid absorption. The mucosal protective effect of misoprostol was time, dose, and diluent volume dependent. In the presence of misoprostol-induced colonic morphologic but not functional absorptive mucosal protection, in vitro unidirectional sodium and chloride flux measurements showed protection of theophylline-stimulated chloride secretion but not sodium absorption. Protection of in vivo colonic fluid absorption, in addition to morphologic protection, could be achieved when misoprostol was administered between 2 and 16 min before induction of colitis or when the highest dose (1000 micrograms/kg) of misoprostol was examined. We conclude that intracolonic misoprostol administration provides unique mucosal protective effects in experimental colitis.

Acetates↗
PubMed1990

Epithelial deposition of immunoglobulin G1 and activated complement (C3b and terminal complement complex) in ulcerative colitis.

The epithelial destruction seen in ulcerative colitis remains unexplained. Complement activation has been proposed to be involved, but no definite evidence has been available to this end. In the present study, we examined immunohistochemically ulcerative colitis lesions with monoclonal antibodies to activation neoepitopes in the complement component C3b and in the cytolytically active terminal complement complex. Colonic tissue specimens from 23 patients with ulcerative colitis were examined by indirect two-color immunofluorescence staining with monoclonal antibodies to the four human immunoglobulin G subclasses and to activated complement C3b or terminal complement complex. All except two patients had activated C3b deposited apically on the surface epithelium of involved mucosa. Immunoglobulin G1 was found on the epithelium in extensively prewashed specimens from 7 of 11 patients, and a striking colocalization of immunoglobulin G1, C3b, and terminal complement complex was observed in 4. Immune deposits were not observed in 31 noninflamed specimens from the same ulcerative colitis patients. Only 1 of 44 histologically normal mucosae from 17 controls and 1 of 10 colonic adenomas contained some epithelial complement deposits. It is concluded that activated complement is often deposited along the brush border of the surface epithelium in active ulcerative colitis lesions and may be associated with immunoglobulin G1 autoantibody.

Adolescent↗
PubMed1991

Ulcerative colitis in the autotransplanted neovagina.

A 33-year-old woman had undergone a radical surgical excision for carcinoma of the vagina at age 11. Vaginal reconstruction using a pedicled transplant of the sigmoid colon was successfully accomplished at age 19. Fourteen years later she developed vaginal bleeding, and a biopsy of the neovagina revealed changes consistent with ulcerative colitis. Within 2 weeks the patient developed bleeding per ano, and a rectal biopsy also revealed changes consistent with ulcerative colitis. Symptoms responded to sulfasalazine. This is believed to be the first case report of ulcerative colitis developing in colonic tissue used for a neovagina. The etiology, natural history, and surveillance of ulcerative colitis in relation to this unique case are reviewed. This case argues against the hypothesis that chronic ulcerative colitis is causally related to direct exposure to alimentary antigens.

Adenocarcinoma↗
PubMed1992

Recombinant interleukin-1 receptor antagonist blocks the proinflammatory activity of endogenous interleukin-1 in rabbit immune colitis.

The effects of human recombinant interleukin-1 receptor antagonist (IL-1ra) on inflammation, tissue damage, and production of inflammatory mediators in rabbit formalin-immune complex colitis were examined. Treatment of rabbits with intravenous administration of IL-1ra before and periodically throughout the first 43 hours after the induction of colitis (total 7 doses) suppressed inflammation and tissue damage in a dose-related manner. Maximum inhibition of inflammatory index (from 3.0 +/- 0.3 to 0.8 +/- 0.3, P less than 0.001), edema (from 2.3 +/- 0.2 to 0.6 +/- 0.2, P less than 0.001), percent of mucosal necrosis (from 44% +/- 7% to 7% +/- 3%, P less than 0.02) and myeloperoxidase (MPO) activity (from 4.9 +/- 1.0 U/g to 1.0 +/- 0.3 U/g, P less than 0.001) occurred with the dose of 5 mg/kg. Colonic prostaglandin E2 (PGE2) and leukotriene B4 (LTB4) production, measured in rectal dialysates by specific radioimmunoassays, was also dose dependently suppressed (from 1124 +/- 319 pg/mL to 190 +/- 75 pg/mL, P less than 0.001 and 568 +/- 192 pg/mL to 92 +/- 51 pg/mL, P less than 0.001, respectively, at 5 mg/kg). In contrast, colonic IL-1 alpha tissue levels measured by a specific radioimmunoassay after tissue extraction were similar in all groups. When only two doses of IL-1ra, 10 minutes before and 3 hours after the induction of colitis were given, there was no longer an inhibitory effect on inflammation or production of inflammatory mediators. However, delaying the initial IL-1ra treatment 3 hours after the induction of colitis (total 6 doses) was effective in reducing inflammatory index (by 60%), MPO activity (by 79%), PGE2 (by 62%), and LTB4 (by 72%) whereas colonic IL-1 alpha levels were unchanged compared with vehicle-treated animals. These studies show the ability of human recombinant IL-1 receptor antagonist to suppress the proinflammatory activity of IL-1 produced in the colon during the induction and progression of rabbit immune complex colitis.

Animals↗
PubMed1994

Neutrophil autoantibodies: a genetic marker in primary sclerosing cholangitis and ulcerative colitis.

BACKGROUND/AIMS: Perinuclear antineutrophil cytoplasmic antibodies (pANCA) were found at high frequency in patients with primary sclerosing cholangitis and ulcerative colitis. In this study, to accumulate further evidence for the importance of genetic factors in pathogenesis of inflammatory bowel disease, sera of patients with inflammatory bowel disease and primary sclerosing cholangitis and their unaffected family members were tested for pANCA. METHODS: Three hundred twenty-seven sera from 11 families of patients with primary sclerosing cholangitis, 43 families of patients with ulcerative colitis, 11 families of patients with Crohn's disease, and 11 healthy families were tested for pANCA in immunofluorescence on cytospin slides with isolated neutrophils. RESULTS: pANCA were found in 82% of the patients with primary sclerosing cholangitis and in 25% of their relatives. In ulcerative colitis, 70% of the patients and 30% of their relatives had pANCA. pANCA were found only in low titers in 27% of patients with Crohn's disease and in 6% of their relatives. pANCA were not detected in members of healthy families. Only 16% of the patients with ulcerative colitis and their families and none of the patients with primary sclerosing cholangitis and their families were completely negative for pANCA. CONCLUSIONS: These data show that pANCA may be a genetic marker in families of patients with ulcerative colitis and primary sclerosing cholangitis.

Adolescent↗
PubMed1995

Experimental colitis alters myenteric nerve function at inflamed and noninflamed sites in the rat.

BACKGROUND & AIMS: Studies in inflammatory bowel disease have shown extensive structural abnormalities in the enteric nervous system of inflamed and noninflamed gut; however, functional correlates are lacking. The aim of this study was to determine the effect of colitis on myenteric nerve function at inflamed and noninflamed sites in rat intestine. METHODS: Tritiated noradrenaline release was measured from longitudinal muscle myenteric plexus preparations from the distal and transverse colon and terminal ileum of rats with colitis induced by trinitrobenzene sulfonic acid or Trichinella spiralis larvae. RESULTS: As characterized by myeloperoxidase activity and histology, both models induced inflammation restricted to the distal colon. In distal colon in trinitrobenzene sulfonic acid colitis, KCl- or electrical field stimulation-evoked 3H release was suppressed by 56% and 60%, respectively; in T. spiralis-infected rats, the KCl-evoked release was suppressed by 58%. 3H release was also suppressed by similar magnitudes in noninflamed transverse colon and terminal ileum of each model. CONCLUSIONS: Experimental distal colitis alters myenteric nerve function in inflamed distal colon and noninflamed gut regions. These changes are independent of the manner in which colitis is induced and provide a basis for the extensive disruption of physiological function observed in inflammatory bowel disease.

Adrenergic Fibers↗
PubMed1995

Anti-inflammatory effects of CGP 47969A, a novel inhibitor of proinflammatory cytokine synthesis, in rabbit immune colitis.

BACKGROUND & AIMS: Proinflammatory cytokines such as interleukin (IL) 1, IL-8, and tumor necrosis factor (TNF) have been implicated as primary mediators of intestinal inflammation. The aim of the present study was to determine the effects of a novel cytokine antagonist (CGP 47969A) in a rabbit model of acute colitis. METHODS: Colitis was induced using the formalin-immune complex technique. Animals were pretreated intrarectally with CGP 47969A (30, 10, or 3 mg/kg), hydrocortisone (0.8 mg/kg), or vehicle (4 mL saline) 2 hours before the induction of colitis and twice daily thereafter until death 48 hours after the induction of colitis. The severity of inflammation of colonic tissue was assessed using histological analysis and myeloperoxidase activity assay, and IL-1 alpha, IL-8, TNF-alpha, and IL-1 receptor antagonist levels were determined. RESULTS: Compared with vehicle, CGP 47969A (10 mg/kg) significantly reduced the acute inflammatory index by 58%, edema by 67%, necrosis by 99%, and myeloperoxidase activity by 49% (all P < 0.02) with efficacy similar to that of steroids. These effects were associated with a significant inhibition of colonic IL-1 alpha and IL-8 by 56% and 90%, respectively (p < 0.01). CONCLUSIONS: Administration of CGP 47969A reduces inflammation and tissue damage in rabbit immune complex colitis through mechanisms involving the inhibition of mucosal proinflammatory cytokines.

Animals↗
PubMed1993

The occurrence of diversion colitis in patients with a sigmoid neovagina.

Diversion colitis is an inflammatory process occurring in segments of the colorectum surgically diverted from the fecal stream. Clinical symptoms of this condition are rectal discomfort, pain, discharge, and bleeding. We diverted isolated segments of sigmoid to create neovaginas in patients with aplasia vaginae and in male to female transsexuals. In contrast to what is reported in most studies of diversion colitis, the neovagina consists of an isolated segment not connected to the anus in patients without any pre-existing bowel disease. To investigate the occurrence of diversion colitis in these sigmoid-neovaginas we studied biopsy specimens from 13 patients. Most of the patients complained of discharge and slight blood loss from their sigmoid-neovagina. Microscopic examination of the biopsy specimens showed lymphocytic infiltration in all cases. Four cases showed an acute inflammatory infiltrate in the lamina propria. Our results indicate that the changes observed on clinical and histopathologic examinations represent the entity of mild diversion colitis. We conclude that diversion colitis also occurs in a sigmoid neovagina.

Adult↗
PubMed1993

The morphologic features of diversion colitis: studies of a pediatric population with no other disease of the intestinal mucosa.

Studies of diversion colitis have not shown a consistent pattern of histopathologic features, and many descriptions are difficult to interpret because of the presence of underlying intestinal mucosal disease. To define the histologic changes in patients free of other mucosal inflammatory disease, we studied the resected segments of bypassed colorectum from 37 patients with Hirschsprung's disease treated by a two-stage procedure, using rectal biopsy specimens taken for initial diagnosis and trimmings from proximal to the stoma as controls. Biopsy specimens from a further 14 patients of similar age but without colorectal mucosal disease were used as additional controls. The histology of the bypassed segment was abnormal in all patients. Twenty-six had diversion colitis characterized by diffuse follicular lymphoid hyperplasia; lamina propria expansion by plasma cells, lymphocytes, and some neutrophils; cryptitis; reactive epithelium; and mucin depletion. Crypt abscesses, aphthous ulcers, mild architectural distortion, and Paneth cell metaplasia were noted in more severe cases. The remaining 11 patients had mild follicular lymphoid hyperplasia and an increase in lymphoplasmacytic infiltrates, with absence of neutrophils, epithelial injury, and other changes seen in diversion colitis, a pattern we term "diversion reaction." Diversion colitis is common in children with a bypassed colorectum. It can be distinguished histologically from other mucosal diseases in most cases. We hypothesize that diversion reaction may be an inevitable consequence of colonocyte nutrient deficiency and that diversion colitis may be superimposed by a second insult, such as a low-grade pathogen.

Anastomosis, Surgical↗
PubMed1992

Randomised comparison of olsalazine and mesalazine in prevention of relapses in ulcerative colitis.

Sulphasalazine extends remissions and lessens disease activity during relapses of ulcerative colitis, but it also causes many adverse side-effects. The adverse reactions are mostly attributable to the sulphapyridine carrier moiety rather than the active principle 5-aminosalicylic acid (5-ASA), so agents to deliver 5-ASA to the colon by other means have been designed. We have compared the efficacy and tolerability of two such agents, olsalazine and mesalazine, in maintenance therapy of ulcerative colitis. 100 patients with ulcerative colitis in remission were recruited at one centre and assigned randomly to treatment with olsalazine (Dipentum; 1.0 g daily) or mesalazine (Asacol, with Eudragit-S coating; 1.2 g daily). Compliance, biochemical and haematological variables, and clinical evidence of disease activity were assessed every 3 months for 12 months by observers unaware of treatment allocation. In intention-to-treat analysis, which included as treatment failures patients withdrawn for protocol violations, adverse reactions, intercurrent illness, or non-compliance as well as those with relapses of ulcerative colitis, the olsalazine group had a significantly lower rate of treatment failure than the mesalazine group (12/49 [24%] vs 23/50 [46%]; p = 0.025). Analysis restricted to 64 patients still in remission at 1 year and 18 with relapses also showed a significant difference in relapse rate (olsalazine 5/42 [12%] vs mesalazine 13/40 [33%]; p = 0.024). Both drugs were well tolerated; only 9 patients reported substantial side-effects. Olsalazine was clearly superior to mesalazine in prevention of relapses in ulcerative colitis, especially in patients with left-sided disease.

Adolescent↗
PubMed1996

Aseptic cerebral venous thrombosis associated with idiopathic ulcerative colitis: a report of two cases.

Two cases of cerebral venous thrombosis with ulcerative colitis with complete autopsy findings are reported. The diagnosis of cerebral venous thrombosis with ulcerative colitis was made during life in one case and at autopsy showed active chronic ulcerative colitis with recent cerebral venous thrombosis with cerebral infarction. In the other case active chronic ulcerative colitis and old cerebral venous thrombosis with cerebral infarction were diagnosed at autopsy. Although rare the importance of recognising cerebral venous thrombosis as a complication of ulcerative colitis has been emphasised in view of the high mortality of this complication.

Adult↗
PubMed1992

Misoprostol therapy following trinitrobenzene sulfonic acid-induced colitis accelerates healing.

Prostaglandins have been demonstrated to have a mucosal protective effect when administered prior to the experimental induction of colitis in animals. We here determined whether prostaglandins would have a beneficial therapeutic effect when administered after colitis had been established. Diffuse, chronic, trinitrobenzene sulfonic acid-induced colitis was established in rats, and misoprostol was administered daily for up to 10 days following the induction of colitis. The effects of misoprostol therapy were compared to those obtained by treatment with 5-aminosalicylic acid and betamethasone. Misoprostol therapy following trinitrobenzene sulfonic acid-induced colitis accelerated colonic healing, as measured in terms of macroscopic ulceration area and fluid absorption, whereas 5-aminosalicylic acid and betamethasone therapy did not. Ileal fluid absorption impairment was repaired by betamethasone but not by misoprostol or 5-aminosalicylic acid therapy.

Aminosalicylic Acids↗