[Acute mesenteric adenitis and follicular ileitis. Development of the follicular ileitis].
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Humans↗
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Results for “ILEITIS”
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[Regional ileitis and pseudo-ileitis].
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Crohn Disease↗
[Ileitis and viral pneumopathy. Reactional ileitis].
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Humans↗
[Premonitory subacute mump ileitis: new example of reactional ileitis].
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Humans↗
[TERMINAL ILEITIS (REGIONAL ILEITIS, CROHN) IN THE PRACTICE].
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Crohn Disease↗
Interleukin-5 participates in the pathogenesis of ileitis in SAMP1/Yit mice.
SAMP1/Yit mice spontaneously develop ileitis resembling Crohn's disease (CD) without chemical or genetic manipulations. Since the focus of studies were Th1 cytokines, only Th1-type T cells were thought to be responsible for intestinal inflammation in these mice. To further characterize the pathogenesis of this ileitis, we investigated the implication of Th2 cytokines in ileitis of SAMP1/Yit mice. The expression of chemokine receptors (CCR) associated with both Th1 and Th2 lymphocytes, such as CCR2, CCR3, CCR4, CCR5, and CCR8, was increased. Among cytokines, IL-5 was remarkably increased in Peyer's patches, mesenteric lymph nodes, and mucosa involved in ileitis. Furthermore, infiltration of numerous eosinophils in ileitis was histologically evident. Severe combined immunodeficiency mice injected intraperitoneally with CD4(+) cells from SAMP1/Yit mice developed colitis and ileitis, with the infiltration of eosinophils. Administration of anti-IL-5 antibodies significantly attenuated ileitis in these mice. We suggest that IL-5 participates in the pathogenesis of ileitis and that anti-IL-5 antibodies are potentially useful for immunotherapy in CD patients. This is the first demonstration that IL-5 is crucial for the development of ileitis in this mouse model of CD.
Animals↗
[New development in Crohn's disease: ++unravelling the mystery and its reinstatement as a surgically treatable condition. Part 2. Potential etiopathogenesis of "terminal ileitis" and extension of the disease to mesenteric small intestine and the colon].
INTRODUCTION: The aetiopathogenesis of terminal ileitis is still unknown, as is the cause of its spread to the small and large bowel. The aim of this study was to shed light on these unknown aspects of Crohn's disease. CONCLUSIONS: The lack of patency of the ileal branch of the ileocolic lymphatic collector which causes terminal ileitis, usually in the earlier part of life, is likely to occur in the foetus around the 10th week of pregnancy as a result of a minor abnormality of the physiological regression of the vitelline duct. Excessive atrophy of the lymphatic network seems to occur, also affecting the rudimentary lymphatic vessels in the midgut destined to become the terminal ileum. The terminal ileitis spreads to the large bowel in an increasing percentage of cases and is directly related to duration of the disease, causing first ileitis plus right colitis, and then ileitis plus total colitis (which, however, does not include the rectum). It may also include the jejunum, causing skip lesions. This spread of lesions is not due to any genetic predisposition (that is to say, it is not predetermined in empirical terms), but rather to the extent of the lymphatic obstruction caused by the spread of immunocomplexes via the lymphatic network. This is shown by the fact that secondary lesions of the jejunum and large bowel are also typical of lymphoedema and that their spread is segmentary. In the light of these pathogenetic mechanisms, it is reasonable to assume that the spread of the process from the ileum to the colon might be prevented by prompt surgery during the initial phase of the ileitis. If these views are correct, the traditional subdivision of Crohn's disease forms into ileitis, ileocolitis and solitary colitis should be replaced by a very simple scheme showing the spread of the primary ileitis very often to ileocolitis, first confined to the right colon and then total. We cannot include either solitary colitis (not clearly defined in the literature) or anorectal Crohn's disease (whose forms have yet to be fully acknowledged) in this scheme.
Colonic Diseases↗
Ileitis in ulcerative colitis: is it a backwash?
PURPOSE: This study aims to determine the incidence, demography, pathologic nature, and clinical significance of ileitis in ulcerative colitis patients who underwent restorative proctocolectomy. METHODS: A prospectively collected pouch database and the case notes of 100 consecutive patients who underwent restorative proctocolectomy for ulcerative colitis, under the care of a single surgeon, between 1988 and 2003 were reviewed. The original proctocolectomy specimens and pouch biopsies were reexamined and regraded blind, using the current diagnostic criteria. Patients were divided into two groups, those who had ileitis and those who had not. The demographic, clinical, and pathologic characteristics and the incidence of pouchitis of both groups were compared. RESULTS: Twenty-two patients had ileitis (22 percent). Compared with those with noninflamed ileum, patients with ileitis had a significantly shorter disease duration (P < 0.005), many of them presented or progressed to a fulminant state requiring acute surgical intervention (P < 0.01), had strong association with pancolitis and primary sclerosing cholangitis (P < 0.001), and had a higher incidence of subsequent development of pouchitis (P < 0.001). There was no correlation between the presence of ileitis and colitis severity. CONCLUSIONS: Ileitis in ulcerative colitis is not rare and does influence the prognosis, and the term "backw ash" is a misnomer. Ulcerative colitis with ileitis represents a distinct disease-specific subset of patients. Its true incidence and clinical significance can be determined only if detailed microscopic characterization of the terminal ileum is performed routinely in every patient with ulcerative colitis and the clinical outcome of these patients is audited prospectively.
Adolescent↗
Pre-pouch ileitis: a disease of the ileum in ulcerative colitis after restorative proctocolectomy.
OBJECTIVE: Ileal inflammation in ulcerative colitis can occur as backwash ileitis or prestomal ileitis. After restorative proctocolectomy (RPC), ileal inflammation may be present in the pouch (pouchitis) but inflammation proximal to the pouch in the neo-terminal ileum, so called pre-pouch ileitis (PI), has also been observed. As pouchitis is increasingly common and PI can mimic it, our aim was to characterize this condition. SUBJECTS AND METHODS: A review of prospectively collected data on 571 inflammatory bowel disease patients undergoing follow-up after RPC in a single centre over 22 years was performed. The histology of biopsy material was reviewed and staining for colonic mucosal phenotypic changes was undertaken. It was not routine practice to prospectively assess all patients for pre-pouch ileitis when the database was constructed. RESULTS: Of 19 patients with inflammation of the pre-pouch neo-terminal ileum (NTI) identified three had Crohn's disease and one a NSAID stricture. The remaining 15 had a characteristic diffuse inflammation extending from the NTI-pouch junction proximally: pre-pouch ileitis. The inflammation extended proximally for up to 50 cm. Fistula formation was seen in only one. Seven (47%) of 15 had pouchitis but only two had suffered backwash ileitis pre-operatively. Seven responded to medical therapy and four to surgery. The histological appearances including staining for colonic phenotypic change were similar in PI and pouchitis. CONCLUSION: Pre-pouch ileitis is uncommon. As the patients' previous diagnosis of UC was confirmed and there was no radiological or histological evidence of Crohn's disease, PI appears to have a distinct pathogenesis from Crohn's disease.
Adolescent↗
[Diffuse jejuno-ileitis of Crohn's disease: a separate form of the disease?].
BACKGROUND AND AIMS: Diffuse jejuno-ileitis of Crohn's disease may be a homogeneous clinical subgroup. The aim of this work was to compare the demographic and clinical data at diagnosis and the initial treatments of patients with diffuse jejuno-ileitis of Crohn's disease and to the ones without this localization. PATIENTS AND METHODS: For demographic and clinical studies, 48 (32M/16F) incident cases of diffuse jejuno-ileitis of Crohn's disease diagnosed between 1988 and 1994 in the EPIMAD register were compared with 96 (48M/48F) controls diagnosed the same year. As far as for the therapeutic management, the 48 incident cases were compared with 48 controls. RESULTS: Diffuse jejuno-ileitis constituted 3.3% of the total incident cases. Median age at diagnosis was significantly lower (20 vs 23 years, P = 0.01) and an upper digestive involvement was more frequent (56% vs 34%, P = 0.03) in patients with diffuse jejuno-ileitis. These patients were more often treated by total parenteral nutrition (43.8% vs 19.6%, P = 0.01) or azathioprine (50% vs 20.8%, P = 0.005). Azathioprine was also introduced earlier (20.7 vs 40.3 months, P = 0.009). Surgery for resection was less often required in diffuse jejuno-ileitis than in controls (65.2% vs 99.8%, P = 0.02) while more stricturoplasties were performed (52.9% vs 10%, P = 0.003); overall surgical rates did not significantly differ in the 2 groups. CONCLUSION: Our series suggest that diffuse jejuno-ileitis of Crohn's disease is a subgroup of patients characterized by a young age at diagnosis, with more frequent and earlier requirement for azathioprine.
Adolescent↗
Backwash ileitis is strongly associated with colorectal carcinoma in ulcerative colitis.
BACKGROUND & AIMS: Commonly accepted risk factors for colorectal carcinoma (CRC) in ulcerative colitis are duration and extent of disease. By identifying still unknown risk factors, surveillance strategies may be improved further. We investigated whether backwash ileitis is also a factor associated with CRC in ulcerative colitis. METHODS: Five hundred ninety consecutive patients with ulcerative colitis who received restorative proctocolectomy were classified into 3 groups: (1) pancolitis with backwash ileitis, (2) pancolitis without backwash ileitis, and (3) left-sided colitis. The association with CRC was analyzed in these 3 groups of patients. As further risk factors, we investigated disease duration, dysplasia, primary sclerosing cholangitis, age at diagnosis of disease, disease activity, and gender. Univariate and multivariate logistic regression were used for analysis. RESULTS: CRC was diagnosed in 11.2% of all patients. CRC was found in 29.0% of 107 patients in group 1, compared with 9.0% of 369 patients in group 2, and in 1.8% of 114 patients in group 3 (P < 0.001). Cancer patients in group 1 showed significantly more multiple tumor growth (45.2%) than patients in group 2 (24.2%) and group 3 (0%) (P = 0.041). Estimating the relative risk for CRC in the multivariate analysis, patients in group 1 showed a significantly higher odds ratio than patients in groups 2 and 3 (odds ratio: 19.36 vs. 9.58 vs. 1; P < 0.001). High-grade dysplasia, low-grade dysplasia, disease duration of more than 10 years, and disease duration of less than 10 years in patients older than 45 years were further factors with significantly increased risk (odds ratios: 21.69, 6.36, 3.63, 4.37), but primary sclerosing cholangitis was not (P = 0.080). However, primary sclerosing cholangitis was strongly associated with backwash ileitis. CONCLUSIONS: There is a strong association of backwash ileitis with CRC in patients with ulcerative colitis who undergo proctocolectomy. The predictive value of backwash ileitis for CRC and premalignant dysplasia in patients with ulcerative colitis should be investigated in future studies based on colonoscopic surveillance.
Adolescent↗
The primary defect in experimental ileitis originates from a nonhematopoietic source.
The initiating etiologic factor in Crohn's disease (CD) remains unclear. SAMP1/YitFc (SAMP) mice develop chronic ileitis similar to human CD. We used bone marrow chimeras to determine if SAMP ileitis results from a primary immunological defect or from dysregulated mucosal immunity secondary to intrinsic, nonhematopoietic (e.g., epithelial) dysfunction. SAMP mice receiving wild-type (AKR) BM developed severe ileitis, whereas SAMP BM did not confer ileitis to WT recipients. WT lymphocytes from reconstituted SAMP mice resembled native SAMP populations in regard to surface phenotype and cytokine production. Ilea from native SAMP mice and SAMP recipients of wild-type BM displayed decreased epithelial barrier resistance ex vivo and increased epithelial permeability in vivo compared to native WT mice and AKR recipients of SAMP BM. This permeability defect preceded the development of ileal inflammation, was present in the absence of commensal bacteria, and was accompanied by altered ileal mRNA expression of the tight junction proteins claudin-2 and occludin. Our results provide evidence that the primary defect conferring ileitis in SAMP mice originates from a nonhematopoietic source. Generation of pathogenic lymphocytes is a consequence of this defect and does not reflect intrinsic proinflammatory leukocyte properties. Decreased barrier function suggests that defects in the epithelium may represent the primary source of SAMP ileitis susceptibility.
Animals↗
Utilization of monoclonal antibodies to evaluate the involvement of Campylobacter jejuni in proliferative ileitis in Syrian hamsters (Mesocricetis auratus).
The role of Campylobacter jejuni in the pathogenesis of proliferative ileitis in Syrian hamsters was evaluated with monoclonal antibodies of different specificities. Monoclonal antibodies were produced with two different specificities: one for all members of the genus Campylobacter tested (antibody 8322-2E6) and one for C. jejuni and Campylobacter coli (antibodies 841-2A11, 841-4C6, and 841-5B1). Heal sections from healthy hamsters, from hamsters with naturally occurring proliferative ileitis, and from hamsters with experimentally induced proliferative ileitis were examined by using fluorescein isothiocyanate-labeled, Campylobacter sp.-specific 8322-2E6 and tetramethylrhodamine isothiocyanate-labeled C. jejuni-C. coli-specific 841-2A11 for direct dual-labeling immunofluorescence. Organisms which stained with the C. jejuni-C. coli-specific monoclonal antibody were observed in the ileal lumens and along the distal tips of the villi of hamsters with either experimentally induced or naturally occurring proliferative ileitis. In contrast, organisms identified by the Campylobacter sp.-specific monoclonal antibody were present deep within the villus lumens and crypts and intracellularly within the apical portions of the epithelial cells. No organisms stained with the C. jejuni-C. coli-specific monoclonal antibody were observed in ileal sections from control hamsters; an occasional intracellular organism stained with the Campylobacter sp.-specific monoclonal antibody was observed in 2 of 10 control hamsters. Thus, at least two immunologically distinct patterns were identified in ileal sections from hamsters with proliferative ileitis. On the basis of these results, we conclude that the organism seen intracellularly in ileal sections from hamsters with proliferative ileitis is a member of the genus Campylobacter but that it probably is not C. jejuni or C. coli.
Animals↗
Systemic effects of acute terminal ileitis on uninflamed gut aggravate bile acid malabsorption.
BACKGROUND: Some patients with terminal ileitis suffer from significant bile acid malabsorption even if the inflammation is locally limited. We hypothesized that inflammation in the terminal ileum may lead to changes in mucosal absorption in more proximal intestinal segments and aggravate bile acid malabsorption. METHODS: Five hamsters underwent laparotomy and localized instillation of 2,4,6-trinitrobenzenesulfonic acid (TNBS) in 10% ethanol into the last 4 cm of ileum to create terminal ileitis. A control group (n = 5) underwent instillation of saline. Animals were sacrificed after 24 h. Active and passive transport of radiolabeled bile acids was measured in the proximal and terminal ileum and glucose absorption in the jejunum using an everted sleeve technique. Myeloperoxidase (MPO) activity and histomorphology were examined by standard methods. RESULTS: In animals with ileitis, active bile acid uptake decreased by 84% in the terminal ileum (t test, P <0.001) and by 58% in the proximal ileum (P < 0.05) compared with saline-treated controls. Jejunal glucose absorption decreased by 59% (P < 0.01). Passive bile acid and glucose absorption rates were not significantly changed in any segments of treated animals versus controls. Histological examination of the treated group revealed signs of acute terminal ileitis without changes in the proximal ileum and jejunum. All control tissues were uninflamed. MPO activity was 13-fold increased in the inflamed ileal samples compared with controls (P <0.001). No significant changes were seen in the proximal ileum and jejunum. There was no evidence of reflux of TNBS into proximal ileum. Nominal mucosal surface area values showed no significant changes between groups. Pretreatment of an additional group of hamsters (n = 5) with acetylsalicylic acid before TNBS instillation ameliorated the inflammatory response in the terminal ileum and largely abrogated the negative effects on ileal bile acid absorption. CONCLUSION: These data suggest that limited acute ileitis impairs active bile acid uptake in the terminal ileum. It also diminishes active bile acid and glucose absorption in more proximal segments of the small intestine, likely by a systemic effect. This systemic effect may aggravate bile acid malabsorption in patients with limited ileitis.
Acute Disease↗
Pouch ileitis.
Pouch ileitis is the most poorly understood complication of ileal reservoir surgery. Variability in definition of this syndrome may account for differences in incidence rate, associated symptoms, and response rate to therapy present in the literature. Outcomes of 19 episodes of pouch ileitis in patients having undergone prior colectomy and continent ileostomy construction for presumed ulcerative colitis were analyzed. An episode of pouch ileitis was characterized by: (1) abdominal pain, (2) increased ileal output, (3) mucosal inflammation within the continent ileostomy, and (4) absence of other recognized concurrent postoperative complications. The mean time of occurrence after construction of the continent ileostomy was 25 months (range 3-54 months). The mean length of follow-up of patients included in this analysis was 49 months from the time of continent ileostomy construction (range 22-101 months). Associated clinical symptoms included bloody effluent (53%), nausea or emesis (47%), and fever (42%). Endoscopic features were often nonspecific, with mucosal erythema (84%), edema (79%), friability (58%), and mucosal ulceration (53%) the most common. In those episodes of pouch ileitis where ileoscopy revealed no evidence of mucosal ulceration, complete resolution of the episode occurred 89% of the time, with 78% treated with antibiotics alone. In those episodes where mucosal ulceration was described on ileoscopy, 40% of episodes completely resolved after medical treatment, 20% with antibiotics alone. The varied clinical symptoms, endoscopic findings, and response to treatment raises the possibility that what has previously been described in the literature as pouch ileitis may be a heterogeneous group not of single etiology.(ABSTRACT TRUNCATED AT 250 WORDS)
Colectomy↗
Relationship of backwash ileitis to ileal pouchitis after ileal pouch-anal anastomosis.
To assess whether the presence of backwash ileitis predisposed to the subsequent development of ileal pouchitis after ileal pouch-anal anastomosis, 131 patients who had the operation were studied. Fifteen patients had nonspecific inflammation in the terminal ileum noted at the time of the operation, while 20 patients subsequently developed pouchitis. No correlation between the two conditions was found. Pouchitis developed in two of 15 patients (13 percent) with backwash ileitis and in 18 of 116 patients (16 percent) without the ileitis (P greater than 0.05). Among the 20 patients with pouchitis only two (10 percent) had had previous backwash ileitis. It is concluded that the presence of backwash ileitis does not predispose to later development of pouchitis, and so does not contraindicate use of the inflamed terminal ileum for construction of the ileal pouch and anastomosis.
Adenomatous Polyposis Coli↗
Rabbit chronic ileitis leads to up-regulation of adenosine A1/A3 gene products, oxidative stress, and immune modulation.
A rabbit model of chronic ileitis has helped decipher the mechanism of alteration of multiple electrolyte and nutrient malabsorptions in inflammatory bowel disease (IBD). This study examined alterations in the adenosine A1/A3 receptor, oxidant, antioxidant, and immune-inflammatory pathways in chronic ileitis. Chronic ileal inflammation was induced 13-15 days after infection with 10,000 Eimeria magna oocytes. Quantitative analysis in 16 rabbits was done for oxidants, antioxidants, A1 and A3 transcripts, transport, injury, and inflammatory mediators. Inflamed gut had villus blunting, crypt hyperplasia and fusion, and immune cell infiltration. Alkaline phosphatase and Na-glucose co-transport were reduced by 78% (P=0.001) and 89% (P=0.001), respectively. Real-time fluorescence monitoring (TaqMan)-polymerase chain reaction revealed a transcriptional up-regulation of 1.34-fold for A1 and 5.40-fold for A3 receptors in inflamed gut. Lipid peroxidation increased in the mucosa (78%, P=0.012), longitudinal muscle-myenteric plexus (118%, P=0.042), and plasma (104%, P=0.001). Mucosal antioxidants were altered by inflammation: reductions occurred in superoxide dismutase (32%, P=0.001) and catalase (43%, P=0.001), whereas increases occurred in glutathione (75%, P=0.0271) and glutathione reductase (86%, P=0.0007). Oxidant enzyme activities were elevated by 21% for xanthine oxidase (P=0.004), 172% for chloramine (P=0.022), 47% for gelatinase (P=0.041), and 190% for myeloperoxidase (P=0.002). Mast cell tryptase increased by 79% (P=0.006). Increases occurred in the plasma concentration of leukotriene B(4) (13-fold, P=0.003), thromboxane B(2) (61-fold, P=0.018), and tumor necrosis factor-alpha (9-fold, P=0.002). In conclusion, chronic ileitis and tissue injury are associated with discrete alterations in complex multi-level oxidant, antioxidant, and immune inflammatory components. The rabbit ileitis model is a suitable model to gain further insight into chronic inflammation and IBD. We hypothesize that adenosine A3 and A1 receptors may provide a novel target for therapy in chronic ileitis and perhaps IBD.
Animals↗
Ulcerative ileitis encountered at ileo-colonoscopy: likely role of nonsteroidal agents.
BACKGROUND & AIMS: Ileoscopy is increasingly practiced, but it is unclear what diagnostic and management decisions should ensue if ulcerations are encountered. METHODS: The lead author identified 40 patients with ulcerative ileitis during 1900 consecutive ileoscopies in a community practice. We analyzed the clinical, endoscopic, and histopathologic findings in these patients and related them to drug usage. RESULTS: Although most patients were asymptomatic, ileitis likely contributed to blood loss in 14 and to right lower quadrant pain in one. Endoscopy revealed multiple, discrete, fibrin-covered ulcerations in the prevalvular segment with patches of erythematous stippling, normal intervening mucosa, and occasional mucosal scars or webs. Histologic findings included focal superficial neutrophilic infiltrates, edema, mucosal hemorrhage, lymphatic dilatation, fibromuscular hyperplasia, prominence of the muscularis mucosae, and antral and Paneth cell metaplasia. Granulomas, fissure ulcers, and apoptosis were notably absent. No specific disease process developed in a median follow-up of 3.2 years. Thirty-three patients admitted recently taking nonsteroidal anti-inflammatory drugs (NSAIDs), notably: enteric-coated aspirin at 325 mg/day or less (19), selective cyclooxygenase-2 inhibitors (5), and nonacetylated salicylates (3). Three fourths of nonsteroidal users were taking agents with low or intermediate gastroduodenal toxicity. Lesions disappeared after drug withdrawal, and reappeared on resumption. CONCLUSIONS: Ileoscopy during colonoscopy may identify an ulcerative ileitis. This lesion likely contributes to gastrointestinal blood loss and other clinical manifestations, and likely is caused by NSAID use, including those usually associated with low toxicity or at low doses. Features of NSAID-ileitis overlap with Crohn's ileitis, but differentiation of the 2 entities is critical for appropriate management.
Adult↗