SEARCH · Search PubMed

Results for “INFLAMMATORY BOWEL DISEASE”

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.

SourceResearch connectionFrom yearThrough year

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 667 records · Page 37Linked to original sources

PubMed1995

Gynecologic history of women with inflammatory bowel disease.

OBJECTIVE: To describe the gynecologic history of women with inflammatory bowel disease. METHODS: Questionnaires were sent to the 1000 women age 20-60 who had been hospitalized for inflammatory bowel disease at the Cleveland Clinic Foundation during 1989-1993. There were 692 responses, and those from 662 women who had undergone surgery for inflammatory bowel disease were analyzed. Of the 117 women who had undergone hysterectomy, 85 responded to follow-up questionnaires. RESULTS: Three hundred sixty women had Crohn disease, 251 had ulcerative colitis, and 51 had inflammatory bowel disease of indeterminate or unknown type. Menstrual abnormalities were reported by 58%. Symptomatic vaginal discharge, reported by 40%, was more likely to occur in those with Crohn disease than with ulcerative colitis (odds ratio [OR] 2.09, 95% confidence interval [CI] 1.47-2.99; P < .001). Infertility was reported by 25% of the women in this series. Abdominal pain with sexual intercourse (50% overall) was more common in women with Crohn disease than in those who had ulcerative colitis (OR 1.64, 95% CI 1.13-2.40; P = .01), but pain with penetration (55% overall) did not differ statistically by type of inflammatory bowel disease. Half of the women reported the loss of pleasure or desire for sex. Ovarian cysts had been diagnosed in 39% of women and resulted in surgical treatment in 57% of these. One hundred seventeen women (18%) had undergone hysterectomy, 52 (44% of total) at age 35 or younger. CONCLUSION: Gynecologic conditions are common in women with inflammatory bowel disease, including menstrual abnormalities, vaginal discharge, infertility, and gynecologic surgery. All physicians providing care for women with inflammatory bowel disease should be familiar with the frequency and nature of concurrent gynecologic conditions.

Adult↗

PubMed2005

Inflammatory bowel disease in patients with celiac disease.

BACKGROUND: Several case reports and series report an association between celiac disease and inflammatory bowel disease (IBD); however, there is no current data assessing this association. We therefore studied the occurrence of these conditions in a cohort of patients with celiac disease seen at a referral center. METHODS: A database of patients with celiac disease seen between 1981 and 2002 was analyzed. Only biopsy-proven adults were included. Patients who had endoscopic and pathologic evidence of IBD were identified, and their pathology was reviewed. Age- and sex-adjusted prevalence rate ratios were determined by comparing results with population-based prevalence data. RESULTS: Among 455 patients with celiac disease, IBD was identified in 10 (5 had ulcerative colitis and 5 had Crohn's disease). This represented an age- and sex-adjusted prevalence rate ratio for ulcerative colitis of 3.56 (95% confidence interval, 1.48-8.56) and for Crohn's disease of 8.49 (95% confidence interval, 3.53-20.42). CONCLUSION: Within our cohort of patients with celiac disease, IBD was significantly more common than in the general population.

Adult↗

PubMed1997

Role of animal models for the pathogenesis and treatment of inflammatory bowel disease.

The etiology of chronic inflammatory bowel diseases (IBD) such as Crohn's disease and ulcerative colitis is still unknown. Recent studies including animal models of intestinal inflammation have identified interactions between the mucosal immune system, host genetic susceptibility and environmental factors, including normal intestinal microflora. Although the ideal animal model of IBD has not been found, each model can study pathogenetic factors such as acute intestinal injury and healing, acute and chronic inflammation, regulation by key cytokines, T-lymphocyte mediation, the role of luminal bacteria, immunoregulatory factors and genetic susceptibility. The relevance of these studies for the treatment of IBD is also discussed.

Animals↗

PubMed2006

The role of tacrolimus in inflammatory bowel disease: a systematic review.

Therapeutic management of inflammatory bowel disease remains beyond the limits of conventional therapy in many cases. Novel therapies used include tacrolimus, a new powerful immunosuppressive drug, employed in some case reports and a few studies that have tried to evaluate its effectiveness in Crohn's disease and ulcerative colitis with promising results, but its role in the management of inflammatory bowel disease remains controversial. We performed a systematic review that analyzed a total of 23 reported experiences in 286 patients with inflammatory bowel disease treated with tacrolimus. Although most of the published studies are uncontrolled, short, and heterogeneous, promising results have been obtained in fistulizing disease, unresponsive cases of both ulcerative colitis and Crohn's disease, and even extraintestinal manifestations. The overall outcome was good enough to consider tacrolimus as a rationale therapeutic option. However, comparative studies with standard therapeutic options like infliximab are needed to assess the correct role that tacrolimus may play in these patients.

Humans↗

PubMed1989

Pregnancy and inflammatory bowel disease.

Conclusions about the relationship between the pathophysiology and treatment of inflammatory bowel disease and the physiology and management of pregnancy are based on the results of several large physician surveys and retrospective chart reviews. Patients with active disease fare worse than those with inactive disease. There is little evidence that pregnancy affects the course of inflammatory bowel disease or that inactive inflammatory bowel disease affects the course of pregnancy. Judicious medical therapy is effective in controlling inflammatory bowel disease during pregnancy. Sulfasalazine or steroid therapy should not be withdrawn in a patient who needs it to achieve or maintain a quiescent state of inflammatory bowel disease during the course of pregnancy. Immunosuppressive therapy should be avoided. Aggressive medical therapy with total parenteral nutrition in a team approach with a gastroenterologist, surgeon, and perinatologist usually avoids the need for surgical intervention during pregnancy with a good fetal outcome in a patient whose disease is active. Contraception against pregnancy need only be considered in those patients whose disease is so severe that operative therapy is imminent.

Adrenal Cortex Hormones↗

PubMed2002

Colonic epithelial cells are a major site of macrophage inflammatory protein 3alpha (MIP-3alpha) production in normal colon and inflammatory bowel disease.

BACKGROUND AND AIM: Macrophage inflammatory protein 3alpha (MIP-3alpha) is a recently described lymphocyte directed C-C chemokine expressed predominately at extralymphoid sites, including the intestine. The aim of this study was to determine whether colonic epithelial cells produce MIP-3alpha and whether its expression is upregulated in inflammatory bowel disease. METHODS AND RESULTS: We found that interleukin 1beta and tumour necrosis factor alpha dose dependently stimulated MIP-3alpha production in Caco-2 and HT-29 intestinal epithelial cells. In cytokine treated Caco-2 and HT-29 cells, a significant increase in MIP-3alpha protein production was observed after three hours and continued for at least 24 hours. Analysis of colonic tissues by quantitative real time polymerase chain reaction and ELISA revealed significantly elevated MIP-3alpha mRNA levels (7.9-fold; p<0.05) and protein levels (8.9-fold; p<0.05) in Crohn's disease compared with controls or ulcerative colitis. MIP-3alpha immunoreactivity in normal colon and inflammatory bowel disease was principally associated with crypt and surface epithelial cells. Moreover, MIP-3alpha protein levels were elevated in primary epithelial cells isolated from patients with inflammatory bowel disease. CONCLUSIONS: These findings indicate that increased enterocyte MIP-3alpha production may play an important role in lymphocyte activation and recruitment to the colonic epithelium in Crohn's disease and ulcerative colitis.

Biomarkers↗

PubMed2026

Hidradenitis Suppurativa and Smoking, Obesity, Psoriasis, Inflammatory Bowel Disease, and Systemic Sclerosis: Results From A 2-Sample Mendelian Randomization Study.

IMPORTANCE: Smoking and obesity are associated with risk of hidradenitis suppurativa, and both are considered important environmental risk factors. However, a causal relationship remains unproven. OBJECTIVE: To primarily investigate the relationship between body mass index (BMI, calculated as weight in kilograms divided by height in meters squared) and smoking and HS, and secondarily to investigate potential relationships between 3 inflammatory diseases (psoriasis, inflammatory bowel disease [IBD], and systemic sclerosis [SSc]) and HS. DESIGN, SETTING, AND PARTICIPANTS: A mendelian randomization (MR) study conducted in 2024 on 5 exposure phenotypes (BMI, smoking, psoriasis, IBD, and SSc) on the outcome of phenotype HS was conducted. The MR analyses used large genetic White European cohorts from genome-wide association studies (GWAS) of each of the 6 phenotypes. Initial analyses were conducted May, 2024, and were updated in May, 2025. EXPOSURE: The 5 exposure phenotypes using predetermined genome-wide significant single-nucleotide variants as proxies for each particular exposure. RESULTS: The GWAS on HS included 4814 case patients and more than 1.2 million controls from Denmark, Iceland, Finland, the UK, and the US. The BMI GWAS involved 700 000 individuals from the UK Biobank and GIANT consortium. Smoking data were obtained from 1.23 million participants in an international consortium. The psoriasis GWAS analyzed 39 498 case patients and 286 769 controls from White European populations and a DNA genetic testing company. The IBD GWAS meta-analysis included 38 155 case patients and 48 485 controls from the International Inflammatory Bowel Disease (IBD) Genetics Consortium. The SSc GWAS included 9095 case patients and 17 584 controls from White European populations. Genetic correlations (rg) were found between HS and all exposure phenotypes except SSc (BMI: rg = 0.36, P < .001; smoking: rg = 0.33, P < .001; IBD: rg = 0.25, P < .001; psoriasis: rg = 0.34, P < .001; SSc: rg = 0.33, P = .22). MR analyses supported an effect of BMI on HS (β = 0.87; odds ratio [OR] per BMI unit, 1.20; 95% CI, 1.17-1.23; P < .001) without signs of pleiotropy (slope: β = 0.91, P < .001, P for intercept = .76). Smoking showed a significant causal estimate (β = 0.59, P < .001), but results became inconclusive in subsequent sensitivity analyses. Among IBD, psoriasis, and SSc, results supported a causal effect of IBD on HS (β = 0.18, OR = 1.20; 95% CI, 1.15-1.24; P < .001), without signs of pleiotropy. CONCLUSIONS AND RELEVANCE: These findings indicate causal effects of IBD and increased BMI on the risk of HS. This information may help physicians inform patients about disease risk contributed by modifiable lifestyle behaviors, which can be beneficial for planning lifestyle interventions.

Humans↗

PubMed2005

Peripheral neuropathy in patients with inflammatory bowel disease.

Peripheral neuropathy (PN) in inflammatory bowel disease (IBD) patients has been reported as individual cases or small series; however, its clinical and electrodiagnostic features have not been well characterized. We conducted a retrospective review of patients with PN and either Crohn's disease (CD) or ulcerative colitis (UC). Eighteen patients with CD and 15 patients with UC were identified after other PN causes were excluded. Male predominance and mean age of PN presentation in the fifties was seen in both groups. Demyelinating neuropathy (CIDP or MMN) occurred in close to 30% of the patients, in a higher percentage of women, than in the non-demyelinating patients. One-third of CD and UC patients had small-fibre or large-fibre sensory axonal PN, while approximately 40% of the CD and UC patients had large-fibre axonal sensorimotor PN. PN symptoms began earlier in the course of CD than in UC (P < 0.05). Patients with large-fibre axonal PN were older than patients with small-fibre sensory axonal PN (P < 0.05). Close to 60% of each group received immunotherapy with different agents. Half of those treated with CD and 40% with UC had demyelinating PN. Most of the patients who completed immunotherapy in both groups improved; all the patients with demyelinating neuropathy had either moderate or major improvement. The PN syndromes in IBD patients are diverse. Demyelinating forms may occur at any time, but early in the IBD course, pure sensory neuropathy is more common. Response to immunotherapy may occur in both demyelinating and axonal neuropathies.

Adult↗

PubMed2004

Human keratin 8 mutations that disturb filament assembly observed in inflammatory bowel disease patients.

We have identified miss-sense mutations in keratin 8 in a subset of patients with inflammatory bowel disease (Crohn disease and ulcerative colitis). Inflammatory bowel diseases are a group of disorders that are polygenic in origin and involve intestinal epithelial breakdown. We investigated the possibility that these keratin mutations might contribute to the course of the disease by adversely affecting the keratin filament network that provides mechanical support to cells in epithelia. The mutations (Gly62 to Cys, Ile63 to Val and Lys464 to Asn) all lie outside the major mutation hotspots associated with severe disease in epidermal keratins, but using a combination of in vitro and cell culture assays we show that they all have detrimental effects on K8/K18 filament assembly in vitro and in cultured cells. The G62C mutation also gives rise to homodimer formation on oxidative stress to cultured intestinal epithelial cells, and homodimers are known to be polymerization incompetent. Impaired keratin assembly resulting from the K8 mutations found in some inflammatory bowel disease patients would be predicted to affect the maintenance and re-establishment of mechanical resilience in vivo, as required during keratin cytoskeleton remodeling in cell division and differentiation, which may lead to epithelial fragility in the gut. Simple epithelial keratins may thus be considered as candidates for genes contributing to a risk of inflammatory bowel disease.

Actin Cytoskeleton↗

PubMedDate not supplied

Thromboembolism in inflammatory bowel disease.

Thromboembolism represents a severe complication of inflammatory bowel disease occurring in young patient, with active disease. Deep venous thrombosis and pulmonary embolism are the most frequent thromboembolism manifestations. Arterial complications and unusual sites for thromboembolism are more rare. Overall, inflammatory bowel disease is a real prothrombotic state as almost all parameters of coagulation are enhanced. Anticoagulation during the episode of thromboembolism is mandatory, and sometimes may ameliorate the course of inflammatory bowel disease.

Adult↗

PubMed2006

Do patients with inflammatory bowel disease want genetic testing?

BACKGROUND: Inflammatory bowel disease (IBD) is a complex genetic disorder characterized by nonmendelian inheritance, incomplete penetrance, and disease susceptibility but not disease certainty. Genotype and phenotype associations are described, but the level of interest of patients with IBD in genetic testing for themselves or at-risk family members remains unknown. Thus, the goal of this study was to assess the interest of patients with IBD in genetic testing and their willingness to accept the uncertainty inherent in complex genetics. MATERIALS AND METHODS: Consecutive outpatients with IBD were recruited to complete a 57-item self-administered survey. The survey included a layperson explanation of the limits of IBD genetics. A 5-point Likert scale was used to determine willingness to undergo genetic testing to determine diagnosis, prognosis, and treatment; to help their family; and to advance medical knowledge. The IBD Questionnaire, a validated measure of the health status attitudes of patients with IBD, was used. To determine limits of patient interest in testing family members, the standard reference gamble paradigm was used. Patients were presented with situations for the genetic test with various levels of certainty in 10% decrements starting with 100%. They indicated the lowest degree of certainty that they would accept to test their family member. RESULTS: One hundred fourteen patients (mean age 38.4 years; 48.2% women) completed the survey. Of these 114, 71.9% (82) had Crohn's disease. Among the patients who answered questions on self-willingness, 76.8% (86 of 112) would undergo testing for diagnostic confirmation, 81.3% (91 of 112) for prognostic value, 88.4% (99 of 112) for therapeutic decision making, and 85.0% (96 of 113) for advancement of medical knowledge. We found that 28.1% of patients (32 of 114) had a first-degree relative with IBD. Those patients with a first-degree relative with IBD were more willing to undergo genetic testing than those without a first-degree relative with IBD (raw score on self-willingness 4.62 vs 4.36; P=0.026). There was no significant association between patients' health status and their willingness to undergo genetic testing (IBD Questionnaire score and raw score on self-willingness; Spearman's correlation coefficient -0.06; P=0.51). We also found that 88.6% of patients (93 of 105) indicated an interest in testing family members if the test provided absolute certainty of future disease. The average lowest level of certainty these patients were willing to accept was 42.2%. CONCLUSIONS: Despite the complexity of IBD genetics, most patients with IBD are interested in testing and willing to accept a variable degree of uncertainty about the results. An important minority of patients does not wish to be tested. Future work should better identify the reasons for these different attitudes. This information should be factored into plans for widespread clinical testing.

Adult↗

PubMed1994

Microalbuminuria in inflammatory bowel disease.

Microalbuminuria independently predicts the development of nephropathy and increased cardiovascular morbidity and mortality in diabetic patients, but it may be an indicator of the acute phase response. This study examined microalbuminuria as a marker of the acute phase response in patients with inflammatory bowel disease and correlated it with the disease activity in 95 patients with inflammatory bowel disease (ulcerative colitis (n = 52), Crohn's disease (n = 43)) determined by the simple index of Harvey and Bradshaw. Fifty patients were in complete clinical remission and 45 patients had active disease. Microalbuminuria was detected in all patients with inflammatory bowel disease (147 (17) v 18 (2) microgram/min, inflammatory bowel disease v controls mean (SEM), p < 0.007). Patients with active inflammatory bowel disease had higher concentrations of microalbuminuria compared with patients in remission (206 (19) v 65 (8) microgram/min, mean (SEM), p < 0.0001). Eight patients with active inflammatory bowel disease who were sequentially followed up with measurements of microalbuminuria had significantly lower values, when the disease was inactive (active inflammatory bowel disease 192 (44) v inactive inflammatory bowel disease 64 (14) microgram/min, p < 0.03). There was a significant correlation with the simple index of Harvey and Bradshaw (r = 0.818, p < 0.0001). Microalbuminuria values were significantly lower in inflammatory bowel disease patients in remission, maintained with olsalazine compared with those patients maintained with mesalazine and salazopyrine, but no significant difference was seen in values of microalbuminuria in active inflammatory bowel disease patients receiving different salicylates. This study also measured serum amyloid-A as an indicator of the acute phase response in the same patients. Serum amyloid-A was significantly increased in active disease compared with inactive disease (151 (43) v 33 (7) or controls 11 (2) micrograms/ml, p < 0.05). In conclusion microalbuminuria is present in abnormal amounts in all patients with active inflammatory bowel disease, and values fall when the disease is quiescent. Microalbuminuria is probably a consequence of an acute phase response and provides a simple, rapid, and inexpensive test, which has the potential to monitor inflammatory bowel disease activity and response to treatment.

Acute-Phase Reaction↗

PubMed2002

Turner syndrome associated with acquired von Willebrand disease, primary biliary cirrhosis, and inflammatory bowel disease.

We report a unique case of Turner syndrome associated with acquired von Willebrand disease (AvWD), primary biliary cirrhosis (PBC), and inflammatory bowel disease (IBD). During 7 years of close follow-up, the patient presented with multiple major episodes of upper and lower gastrointestinal bleeding caused by different pathogenic mechanisms, such as IBD, AvWD, gastric varices, and thrombocytopenia. AvWD mimicking familial vWD type III on laboratory testing was most probably triggered by autoimmune mechanism associated with PBC. Therapy of PBC with ursodeoxycholic acid (UDCA) resulted in significant decrease of liver enzymes followed by normalization of vWF and FVIII levels. Portosystemic shunt placement with ligation of gastric varices improved hypersplenism and severe thrombocytopenia and led to clinical stability for more than 24 months. The clinicopathological features of these disorders and of the recurrent bleeding episodes are discussed in the text along with a review of the literature.

Adult↗

PubMed2001

Differential alterations in tachykinin NK2 receptors in isolated colonic circular smooth muscle in inflammatory bowel disease and idiopathic chronic constipation.

Inflammatory bowel disease (IBD) and idiopathic chronic constipation (ICC) are intestinal disorders which disrupt normal colonic motility. Enteric tachykinins are well-recognised to play a role in the motor control of the gut, and increased colonic levels of substance P are seen in IBD, whereas decreased levels have been reported in ICC. In this investigation, we have characterised the tachykinin receptor population of normal human colonic circular smooth muscle and examined any changes that occur in IBD and ICC. The selective tachykinin NK2 receptor agonist, [beta-Ala8]neurokinin A(4-10), caused concentration-dependent contractions in healthy tissues; neither NK1 receptor-selective nor NK3 receptor-selective agonists were contractile. In diseased preparations also, only [beta-Ala8]neurokinin A(4-10) caused contractions with EC50 values similar to health. The maximum contractile responses (Emax), however, were significantly decreased in both forms of IBD but significantly increased in ICC. The muscarinic acetylcholine receptor agonist, carbachol, also caused contractions in diseased tissues, but EC50 and Emax values were not significantly different from health. The differential changes in contractility found in IBD and ICC are specific to NK2 receptors, and may reflect the altered levels of substance P or other tachykinins found in these intestinal disorders.

Adult↗

PubMed2000

The IL-10 gene is not involved in the predisposition to inflammatory bowel disease.

Although genetic predisposition for inflammatory bowel disease (IBD) is well established, little is known about the accountable genes. The pathogenesis of IBD is characterized by an imbalanced activation of Th1- and Th2-lymphocytes. IL-10 represents an anti-inflammatory cytokine which downregulates the production of Th1-derived cytokines. To evaluate the role of the IL-10 gene in IBD, two polymorphisms in the promoter region (G/A at position -1082 and C/A at position -592) were genotyped in 142 patients with Crohn's disease (CD), 104 patients with ulcerative colitis (UC), and 400 healthy controls. Significant differences were not apparent, neither in the allele frequencies of either polymorphism, nor in the haplotype frequencies. Screening of the coding region of the IL-10 gene by polymerase chain reaction--single strand conformation polymorphism (PCR-SSCP) analysis revealed a rare sequence variation in exon 1 leading to an amino acid exchange (G-->A; G15R) in two patients with CD and five healthy controls. Therefore, polymorphisms of the IL-10 gene are not demonstrably involved in the predisposition of IBD in our cohorts of patients.

Colitis, Ulcerative↗

PubMed2000

Chemokines and cytokines in inflammatory bowel disease and their application to disease treatment.

The term inflammatory bowel disease refers to two chronic, relapsing or remitting, inflammatory disorders of the intestinal tract that although somewhat similar clinically represent two markedly different and distinct disorders histologically, endoscopically, immunologically, and by many other means. The pathogenesis of these diseases, ulcerative colitis and Crohn's disease, remains unknown and medical and surgical therapy is limited. Approximately 70% of individuals with Crohn's disease require surgery with another 40% to 45% requiring reoperation, whereas approximately 20% to 25% of patients with ulcerative colitis undergo surgical intervention. This review highlights the specific clinical features of the disease as well as some of the recent insights into the cause of the disease. Standard medical therapy is highlighted and more recent biologic therapies including the use of anti-tumor necrosis factor-alpha antibodies are described. The changing focus of therapy from nonspecific anti-inflammatory medications to targeted biologic therapies is reviewed. A number of novel therapeutic targets are highlighted and future directions for research and clinical testing are discussed.

Journal Article↗

PubMed1995

Increased expression of cell adhesion molecule P-selectin in active inflammatory bowel disease.

The pathogenic changes of inflammatory bowel disease (IBD) depend on migration of circulating leucocytes into intestinal tissues. Although leucocyte rolling and tenuous adhesion are probably regulated by inducible selectins on vascular endothelia, little is known about the expression of these molecules in Crohn's disease and ulcerative colitis. Using immunohistochemistry on surgically resected specimens, this study investigated endothelial P-selectin (CD62, granular membrane protein-140) in frozen sections of histologically uninvolved tissues adjacent to inflammation (Crohn's disease = 10; ulcerative colitis = 10), from highly inflamed areas (Crohn's disease = 20; ulcerative colitis = 13), and from normal bowel (n = 20). By light microscopy, two forms of P-selectin immunoreactivity were detected that apparently corresponded ultrastructurally to stored and released distributions. Compared with the normal gut, there was a 3.7-fold increase of P-selectin immunoreactivity on veins (p < 0.0001), venules (p < 0.0001), and capillaries (p < 0.05) in the highly inflamed gut, without differences between Crohn's disease and ulcerative colitis. In the uninvolved gut, P-selectin expression was similar to that seen in normal controls, except for a focal increase of P-selectin in the vicinity of small lymphocyte aggregates. The dramatic upregulation of P-selectin in the inflamed tissue and its potential role in leucocyte trafficking support the concept of P-selectin blocking therapy for the control of active IBD.

Adolescent↗

PubMed2002

Intestinal microflora as a therapeutic target in inflammatory bowel disease.

Although the causes of inflammatory bowel disease (IBD) remain incompletely understood, increasing evidence implicates intestinal microflora in the pathogenesis of these disorders. Alteration of intestinal flora therefore may offer a plausible therapeutic approach. Although recent data support a potential therapeutic role for probiotics and prebiotics in patients with IBD, such treatments need to be further assessed by large, double-blind controlled trials. A better understanding of the intestinal microflora and the mechanisms of their action may help us to develop more effective treatment for IBD.

Biopsy, Needle↗