[Acute mesenteric adenitis and follicular ileitis. Development of the follicular ileitis].
Explore the source record for details and available documents.
Humans↗
SEARCH · Search PubMed
Results for “ILEITIS”
Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
[Ileitis and viral pneumopathy. Reactional ileitis].
Explore the source record for details and available documents.
Humans↗
[Premonitory subacute mump ileitis: new example of reactional ileitis].
Explore the source record for details and available documents.
Humans↗
[TERMINAL ILEITIS (REGIONAL ILEITIS, CROHN) IN THE PRACTICE].
Explore the source record for details and available documents.
Crohn Disease↗
[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↗
[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↗
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↗
CD40/CD154 ligation is required for the development of acute ileitis following oral infection with an intracellular pathogen in mice.
BACKGROUND & AIMS: Acute inflammatory ileitis occurs in C57BL/6 mice after oral infection with Toxoplasma gondii. We evaluated the role of CD40/CD154 interaction in the development of acute ileitis in this experimental model. METHODS: CD154-/- and anti-CD154 antibody-treated mice as well as chimeric mice, either C57BL/6 or CD40-/- reconstituted with bone marrow from C57BL/6 or CD40-/- mice, were orally infected with cysts. Inflammation was assessed by qualitative histologic and phenotypic analysis of the intestinal compartment at day 7 after infection. Intestinal chemokine and cytokine production was assayed by ribonuclease protection assay. RESULTS: CD154-/- and anti-CD154 monoclonal antibody-treated mice failed to develop an acute, lethal ileitis after oral infection and survived. Chimeric mice reconstituted with bone marrow from C57BL/6 mice developed ileitis and died, whereas those recipient mice deficient in CD40 survived. CD40 expression in the intestine after infection was found principally within the B-cell compartment. A modest increase in CD40 expression in both the macrophage and dendritic cell compartments was also observed. Both chemokine and cytokine expression was up-regulated in those recipients of wild-type bone marrow. Impairment of CD40/CD154 interaction abrogated the production of these proinflammatory productions. CONCLUSIONS: CD40/CD154 interaction is essential to the development of inflammation in this pathogen-driven experimental model of acute ileitis.
Acute Disease↗
Salmonella- and Shigella-induced ileitis: CT findings in four patients.
PURPOSE: The purpose of this study is to describe and illustrate the CT appearance of four cases of acute terminal ileitis induced by nontyphoidal Salmonella and Shigella infection and to review the radiographic and endoscopic findings of these entities. METHOD: The medical records, CT examinations, and small bowel examinations of three patients with Salmonella ileitis and one patient with Shigella ileitis were retrospectively reviewed. CT examinations were done in four patients, colonoscopy in three patients, and small bowel examinations in two patients. Stool cultures established the diagnosis of nontyphoidal Salmonella enteritis in three patients and Shigella enteritis in one patient. The patients' symptoms and clinical findings resolved promptly following supportive therapy and appropriate antibiotic therapy. RESULTS: CT showed slight circumferential and homogeneous thickening of the terminal ileum over a segment of 10-15 cm in patients with Salmonella ileitis. Associated mild thickening of the wall of the colon was present in addition. Small bowel examination performed in one patient revealed a spastic terminal ileum with thickened mucosal folds. Colonoscopy revealed acute colitis involving the colon diffusely in one case, but sparing the distal 50 cm of the colon in one case. CT showed more pronounced thickening of the terminal ileum and a target configuration in the patient with Shigella ileitis. Small bowel examination revealed narrowing, irregular contour, several large nodular defects (thumbprinting), and a severely ulcerated mucosa affecting the terminal ileum. Colonoscopy revealed a normal colon and large ulcerations with fibropurulent exudate in the terminal ileum. CONCLUSION: In patients with severe Salmonella or Shigella infections or persistent and/or confusing clinical presentations, CT can play a complementary but important role in the initial diagnostic evaluation. It avoids clinical mismanagement, circumvents unnecessary invasive procedures, and contributes to the efficient workup and therapy in this group of individuals.
AIDS-Related Opportunistic Infections↗
Experimental production of proliferative ileitis in Syrian hamsters (Mesocricetus auratus) by using an ileal homogenate free of Campylobacter jejuni.
The role of Campylobacter jejuni in the pathogenesis of proliferative ileitis of Syrian hamsters (Mesocricetus auratus) has been uncertain. C. jejuni has been implicated as the etiologic agent on the basis of the campylobacter-type morphology of the intracellular organism and the repeated microbiologic isolation of C. jejuni from hamsters with proliferative ileitis. The inability to reproduce the disease with pure culture inocula, coupled with immunohistochemical studies, however, has suggested that although C. jejuni may be present in the ilea of infected hamsters, its involvement in the pathogenesis of proliferative ileitis is questionable. In this study hamsters were inoculated with infective ileal homogenates prepared from ilea which were extensively washed to remove the ileal contents before grinding. The ilea from hamsters inoculated with this homogenate were also washed before being ground and used to experimentally inoculate a second group of hamsters. Of the 20 hamsters from this second group, 12 developed lesions typical of proliferative ileitis. Extensive microbiologic cultures from these hamsters were negative for C. jejuni. Immunofluorescence studies with a C. jejuni-specific monoclonal antibody were also negative. The use of a Campylobacter genus-specific monoclonal antibody, however, revealed numerous campylobacter-type organisms within the ileal epithelial cells of the crypts and villi. The presence of C. jejuni is therefore apparently not necessary for the production of proliferative ileitis in hamsters, and the intracellular campylobacter-type organism present in the ileal epithelial cells of infected hamsters is probably not C. jejuni.
Animals↗
Radiological findings in Yersinia ileitis.
Bacteriological and clinical studies of patients with acute retional ileitis indicate that numerous patients with this diagnosis have a benign ileitis of short duration, caused by Yersinia enterocolitica, whereas others develop chronic Crohn's disease. Yersinia ileitis has some clinical and radiological features in common with Crohn's disease, but the two conditions are basically separate. In Yersinia ileitis, three stages are apparent: (a) the nodular stage, lasting up to three weeks; (b) the edematous stage (4th-5th week); and (c) resolution, observed during the 5th-8th week. The radiological findings in 25 patients with Yersinia ileitis and their distinction from Crohn's disease are described.
Adolescent↗
The relationship and epidemiology of acute terminal ileitis and Crohn's disease.
The frequency of admission for acute terminal ileitis, Crohn's disease, and acute mesenteric lymphadenitis has been compared from the years 1951 to 1970, and the long-term results of operation for acute terminal ileitis in 1951-1965 have been examined. Whereas the admission rates for both acute terminal ileitis and Crohn's disease rose during the review period, that for acute lymphadenitis tended to fall slightly. Sixty-eight of 72 patients operated upon by appendicectomy who had acute terminal ileitis were followed up. One of these, with small intestinal stenosis at the initial operation, proved to have histological evidence of Crohn's disease, and a further nine have since developed unequivocal evidence of the disease. A cutaneous fistula developed in only one patient after appendicectomy. It is concluded that appendicectomy can safely be performed in acute terminal ileitis provided that the caecum is not inflamed and that Crohn's disease seldom develops as a sequel.
Acute Disease↗
Cholecystectomy in patients with Crohn's ileitis.
PURPOSE: Gallstone disease is reported to be higher in patients with Crohn's disease than in the general population. This study was designed to determine the prevalence of cholecystectomy in patients with Crohn's ileitis, attempt to identify any associated risk factors, and determine whether it is justified to perform prophylactic cholecystectomy during ileocolic resection. METHODS: A total of 191 patients with Crohn's ileitis who were treated medically or who had an ileocolic resection were retrospective reviewed. A questionnaire survey was performed. Telephone interviews were conducted for the non respondents. Further review of medical records was performed to determine the details of admissions for any gallstone disease and/or subsequent cholecystectomy. A control group matched for age and gender was obtained. RESULTS: A total of 191 questionnaires were mailed, and the overall response rate was 70.2 percent (134/191) after telephone interview follow-up. There were 2 of 45 medical and 18 of 89 surgical patients with symptomatic cholelithiasis, i.e., 14.9 percent (20/134) of respondents. As a result, 2 patients (1.5 percent) required endoscopic sphincterotomy, 17 patients (12.7 percent) needed cholecystectomy, and 1 patient (0.7 percent) did not have any intervention. Only five patients had a cholecystectomy after their ileal resections. In the control group of 150 patients, 15 patients (14 females; mean age, 51.9 years; range, 34-78 years) had previous cholecystectomy. There was no significant difference with prevalence of cholecystectomy in Crohn's patients compared with controls (17/134 vs. 15/150; P = not significant). Furthermore, the number of ileal resections did not affect the cholecystectomy rate, but patients who had >30 cm of ileum resected were more likely to have cholecystectomy (P = 0.056). CONCLUSIONS: The prevalence of gallstone disease in Crohn's ileitis requiring cholecystectomy is similar to that of the general population with a female predominance. In addition, the number of patients requiring cholecystectomy after ileal resection was low. Thus, synchronous prophylactic cholecystectomy during ileocolic resection for Crohn's ileitis is not justified.
Adolescent↗