PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Inflammatory bowel disease”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

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

At least 19 recordsLinked to original sources
PubMed1977

Emotional factors in inflammatory bowel disease.

Inflammatory bowel diseases are not caused by emotional conflicts, but emotional factors influence both the pathogenesis and the course of the illness. Establishing a trusting physician-patient relationship is important in helping the patient to (1) avoid denial of illness or chronic illness behavior, (2) understand symptoms and diagnostic and treatment procedures, and (3) cope with loss of a key person or the threat of lessened self-control.

Adolescent↗
PubMed1978

Ankylosing spondylitis and inflammatory bowel disease. I. Prevalence of inflammatory bowel disease in patients suffering from ankylosing spondylitis.

To establish the prevalence of inflammatory bowel disease in ankylosing spondylitis (AS), 79 AS patients underwent detailed medical screening, including sigmoidoscopic and roentgenological examination, 48 had gastrointestinal symptoms and the others did not. In 3 patients a diagnosis of Crohn's disease was made which was previously established. In all other patients inflammatory bowel disease could be excluded. The prevalence of inflammatory bowel disease in this series of patients with AS therefore was 3.8%.

Enteritis↗
PubMed2026

The impact for causal associations between common diseases and inflammatory bowel disease: a disease-wide bidirectional Mendelian randomization study.

OBJECTIVES: Observational studies on associations between various diseases and inflammatory bowel disease (IBD) are often limited by confounding and reverse causation. We aimed to assess potential causal relationships between a wide range of diseases and IBD, including Crohn's disease (CD) and ulcerative colitis (UC). METHODS: We performed a comprehensive bidirectional Mendelian randomization (MR) analysis of 104 common diseases and IBD traits using the generalized summary-data-based MR (GSMR) approach. Genome-wide association study (GWAS) summary statistics for diseases were obtained from the MRC Integrative Epidemiology Unit, and IBD data from the International IBD Genetics Consortium. Summary-data-based MR (SMR) integrating GWAS and expression quantitative trait locus data was applied to identify pleiotropic genes associated with IBD. RESULTS: MR analyses identified 38, 34, and 52 exposures significantly associated with IBD, UC, and CD, respectively. Childhood- and adult-onset asthma showed distinct causal effects on UC and CD. Reverse MR indicated associations between IBD traits and 15 diseases, including multiple sclerosis. SMR identified RGS14 and CARD9 as pleiotropic genes linked to IBD, suggesting shared genetic mechanisms with asthma and multiple sclerosis. CONCLUSIONS: These findings provide evidence for causal links and shared immune-related genetic mechanisms underlying IBD, highlighting potential targets for future research.

Humans↗
PubMed2025

Possible linking and treatment between Parkinson's disease and inflammatory bowel disease: a study of Mendelian randomization based on gut-brain axis.

BACKGROUND: Mounting evidence suggests that Parkinson's disease (PD) and inflammatory bowel disease (IBD) are closely associated and becoming global health burdens. However, the causal relationships and common pathogeneses between them are uncertain. Furthermore, they are uncurable. Thus, we aimed to identify the causal relationships and novel therapeutic targets shared between them based on their common pathophysiological mechanisms in gut-brain-axis (GBA). METHODS: A meta-analysis on bidirectional Mendelian randomization (MR) utilizing various datasets was performed to estimate their causal relationship. Then, pleiotropic analysis under the composite null hypothesis (PLACO) with functional mapping combined with annotation of genetic associations (FUMA) analysis were conducted to identify pleiotropic genes. Next, blood, brain and intestine expression quantitative trait locus (eQTL) were taken to perform drug-target MR finding common causal genes in two diseases. Colocalization analysis ensured the eQTLs of corresponding gene colocalized with disease. Enrichment analysis and protein‒protein interaction (PPI) network were done to explore common pathogenesis pathways. Genes passed all analysis were regarded as drug targets. RESULTS: Our MR meta-analysis revealed the bidirectional causal relationship between diseases, with combined ORs for PD on IBD, CD, UC (1.050 [95% CI 1.014-1.086], 1.044 [95% CI 0.995-1.095], 1.063 [95% CI 1.016-1.120]); for IBD, CD, UC on PD (1.003 [95% CI 0.973-1.034], 1.035 [95% CI 1.004-1.067], 1.008 [95% CI 0.977-1.040]). Overall, 277, 216 and 201 genes were identified as pleiotropic genes between PD and IBD, CD, UC. Total of 733 genes were classified as tier 3 (found in only one tissue) druggable targets, 57 as tier 2 (found in two tissues, 51 protein-coding genes) and 9 as tier 3 (found in three tissues). Among 60 protein-coding druggable targets over tier 2, 18 overlapped with pleiotropic genes and enriched in mitochondria, antigen presentation, processing and immune cell regulation pathways. Three druggable genes (LRRK2, RAB29 and HLA-DQA2) passed colocalization analysis. LRRK2 and RAB29 were reported to be pleiotropic genes, and RAB29 and HLA-DQA2 were reported for the first time as potential drug targets. CONCLUSIONS: This study established a reliable causal relationship, possible shared drug targets and common pathogenesis pathways of two diseases, which had important implications for intervention and treatment of two diseases simultaneously.

Humans↗
PubMed1977

Influence of SRBC/lymphocyte ratio on T-cell rosettes in alcoholic liver disease and inflammatory bowel disease.

Thymus-derived (T) rosette-forming cells were enumerated in patients with alcoholic liver disease and in patients with inflammatory bowel disease using variable sheep red blood cell (SRBC)/lymphocyte ratios. SRBC/lymphocyte ratios of 60:1 and 32:1 did not reveal significant differences from controls in Crohn's disease. The percentage, but not absolute count, of T cells was significantly reduced in alcoholic hepatitis at the 60:1 ratio. Both the percentage and absolute count of T cells were reduced in alcoholic hepatitis and Crohn's disease with the 8:1 ratio. No significant reduction in T cells was seen at any ratio in patients with compensated alcoholic cirrhosis or ulcerative colitis. Use of a SRBC/lymphocyte ratio of 8:1 indentifies T cells which demonstrate an avidity for SRBC. This avidity may be related to the density of SRBC receptors on the surface of T cells and/or the affinity of these receptor sites for SRBC. Use of the 8:1 ratio may provide a more sensitive means by which to monitor changes in T-cell rosettes in patients suspected of having an altered cellular immune state.

Colitis, Ulcerative↗
PubMed1977

DNA-synthesizing cells in the blood in coeliac disease and inflammatory bowel disease.

The level of 3H-labelled thymidine ([3H]TdR) incorporation of blood cells of patients with coeliac disease was shown in two separate studies to be significantly lower than that of a normal control group. In the first study the 'background' DNA synthesis in unstimulated cultures containing a standard number of blood lymphocytes was measured on days 4, 5 and 6. In the second study a standard volume of freshly drawn whole blood was added to culture medium and the [3H]TdR incorporation measured over the first 24 hr and from 48 to 72 hr. In all cases the [3H]TdR incorporation of cells of coeliac patients on a normal or a gluten-free diet was lower than that of the control group. It is suggested that sequestration of DNA-synthesizing cells in the mucosa of the small bowel may partly explain these results. In whole-blood cultures from patients with inflammatory bowel disease in remission [3H]TdR incorporation over the first 24 hr was raised in Crohn's disease but normal in ulcerative colitis.

Blood Cell Count↗
PubMed1977

Colo-rectal biopsy in inflammatory bowel disease.

The term inflammatory bowel disease (IBD) is viewed as all-inclusive, covering the full panoply of intestinal disorders in which inflammatory changes are a prominent feature, including those of infectious, toxic, and intrinsic origin as well as the idiopathic entities ulcerative colitis and Crohn's disease. This chapter describes and discusses those aspects of colo-rectal biopsy in IBD which can help pathologists make optimal interpretations. The areas covered are: 1) methods used to prepare biopsy specimens for study, 2) normal histologic findings and common artefacts, 3) basic pathologic changes occurring in IBD, 4) a general approach to differential diagnosis in IBD, and 5) discussion of the various individual forms of IBD. The importance of full and reliable information exchange between the endoscopist and pathologist is stressed. Special attention is given to features in biopsy specimens which help in differentiating between ulcerative colitis and Crohn's disease. Other entities discussed are bacterial dysenteries; gonococcal proctitis; tuberculosis; Whipple's disease; amebiasis; balantidiasis; schistosomiasis; cryptosporidiosis; lymphopathia venereum; cytomegalovirus infection; histoplasmosis; antibiotic colitis; IBD due to cytotoxic drugs (5-FU), heavy metals, and foodstuffs; irradiation colitis; ischemic colitis; solitary ulcer syndrome; diverticulitis; and colitis secondary to obstruction. The term pseudomembranous enterocolitis is also considered.

Biopsy↗
PubMed1977

Basal and stimulated serum growth hormone concentrations in inflammatory bowel disease.

Patients with inflammatory bowel disease (IBD) manifest growth failure which may antecede abdominal symptoms by some years. Eight of ten children with documented IBD had records of decreasing growth velocities. Investigation of growth hormone reserves showed excessive rather than impaired responses. Mean basal GH level was 6.2 +/- 0.75 (SEM) ng/ml. During sleep, the mean GH level rose to 26.0 +/- 4.7 ng/ml and following propranolol-glucagon stimulation, to 46.0 +/- 4.5 ng/ml. All values were significantly higher than levels obtained in a control population of 25 children investigated for short stature who were not GH deficient. The mean peak GH response following insulin in the IBD group (10.8 +/- 3.8 ng/ml), however, did not differ from the mean peak response in the control group (13.5 +/- 3.3 ng/ml). Growth failure in patients with IBD is not the result of GH deficiency and is not an irreversible phenomenon. On the contrary, judicious use of glucocorticoids aimed at the control of the disease usually produces compensatory growth acceleration ("catch-up growth").

Adolescent↗
PubMed1978

Ankylosing spondylitis and inflammatory bowel disease. II. Prevalence of peripheral arthritis, sacroiliitis, and ankylosing spondylitis in patients suffering from inflammatory bowel disease.

To establish the prevalence of peripheral arthritis, radiographic sacroiliitis, and ankylosing spondylitis in patients with inflammatory bowel disease, 58 consecutive patients suffering from ulcerative colitis (UC) and 51 with Crohn's disease (CD) underwent a detailed rheumatological examination. In addition, all patients were screened for the presence of the antigen HLA B27. Peripheral arthritis was found in 14 (8 UC, 6 CD) patients (12.8%); radiographic sacroiliitis was diagnosed in 11 (5 UC, 6 CD) (10.1%), of whom 10 were asymptomatic; and ankylosing spondylitis was diagnosed in 2 UC and 2 CD patients (3.7%). 18.9% of the UC and 3.9% of the CD patients were HLA B27 positive. One of the 11 patients with radiographic sacroiliitis and 2 of the 4 with ankylosing spondylitis had the HLA B27 antigen. Peripheral arthritis, radiographic sacroiliitis, and ankylosing spondylitis are apparently frequent manifestations in patients suffering from inflammatory bowel disease. Asymptomatic radiographic sacroiliitis in these patients appears to differ from idiopathic ankylosing spondylitis, both clinically and genetically. Evaluation of subjective rheumatological complaints, necessary for a confident diagnosis of ankylosing spondylitis, according to the New York criteria is difficult during a flare-up of the inflammatory bowel process, as was shown in 4 CD cases with marked limitation of lumbovertebral function and chest expansion, but no radiological abnormalities of the SI joints.

Adult↗
PubMed1978

Inherited deficiency of second component of complement and HLA haplotype A10,B18 associated with inflammatory bowel disease.

A patient with inflammatory bowel disease and sacroiliitis had haplotypes A10,B18 and Aw32,b18 at the major histocompatibility locus. Serum total complement and C2 hemolytic complement activities were undetectable; levels of the remaining C1-C9 components were normal. The parents, both siblings, and a child each had half-normal levels of C2 and either the A10,B18 or the Aw32,b18 hla haplotype. In a second unrelated family, an only child and both parents developed inflammatory bowel disease. The father and child had HLA haplotype A10,B18, but, along with the mother, each had normal serum levels of hemolytic C and C2. Homozygous C2 deficiency, often in association with the A10,B18 haplotype, has previously been linked with various autoimmune diseases and with propensity to infection. Our findings suggest that C2 deficiency or this haplotype also may predispose to inflammatory diseases of the intestine.

Adult↗
PubMed1978

Ankylosing spondylitis and inflammatory bowel disease. III. Clinical characteristics and results of histocompatibility typing (HLA B27) in 50 patients with both ankylosing spondylitis and inflammatory bowel disease.

A study was made, in co-operation with several gastroenterology and rheumatology centres, of the clinical and genetic characteristics (HLA B27) of 50 patients suffering from both inflammatory bowel disease (38 Crohn's disease (CD), 12 ulcerated colitis (UC)) and ankylosing spondylitis (AS), the latter diagnosis being established according to the New York criteria. 20 CD (52.6%) and 8 UC (66.7%) patients were HLA B27 positive. The presence of HLA B27 was studied in relation to clinical parameters, such as first occurrence of symptoms of AS or inflammatory bowel disease (IBD), a history of peripheral arthritis, iridocyclitis, and a positive history of AS or IBD. Our patients were found to have heterogeneous clinical features: on one side of the spectrum a group of cases was distingiushed with the typical characteristics of idiopathic AS, often being HLA B27 positive. On the other side a smaller group of HLA B27 negative patients was observed, with severe intestinal inflammatory pathology, lacking most of the typical clinical features of idiopathic AS ('secondary' form of AS). Finally, between these two extremes a group of patients was found with less pronounced clinical or genetic characteristics. These different clinical and histocompatibility patterns suggest a mixed aetiopathogenesis of AS in IBD patients. Such a 'syndrome' of AS might harbour both idiopathic AS and forms of AS 'secondary' to the intestinal inflammatory pathology.

Adult↗
PubMed1979

Inflammatory bowel disease in the West Indies.

Inflammatory bowel disease is generally assumed to be rare among negroes and Indians. Over 10 years 34 cases of ulcerative colitis and 14 cases of Crohn's disease were seen in one medical and one surgical unit in Port-of-Spain, Trinidad. Twenty-six patients were Negroes, 18 were Indians, three were of mixed race, and one was Caucasian. In many of these patients the disease was extensive and several of those with Crohn's disease suffered severe complications. The assumption that inflammatory bowel disease is rare among West Indians of African and Indian origin therefore seems to be wrong.

Adolescent↗
PubMed1978

Cholangiographic abnormalities in patients with inflammatory bowel disease.

Twenty patients with inflammatory bowel disease, abnormal liver function tests and abnormal endoscopic retrograde cholangiograms were found to have a spectrum of abnormalities affecting the intra- and extrahepatic biliary trees. The intrahepatic systems were abnormal in all patients and demonstrated ductal stenosis, ectasia, decreased arborization and major duct obstruction. The extrahepatic systems were abnormal in 75 percent of cases with stenosis, diverticula formation and mural irregularity being the most frequent abnormalities. The value of endoscopic retrograde cholangiography in this patient group is to exclude extrahepatic obstruction, establish a nonoperative diagnosis, and assist in determining the method of treatment.

Adenoma, Bile Duct↗
PubMed1977

Influence of an elemental diet in protein exudation in chronic inflammatory bowel disease.

13 patients with chronic inflammatory bowel disease were treated with an elemental diet (Vivasorb). Intestinal protein exudation was studied during the treatment by means of of 131I-albumin. 131I-albumin studies showed no significant change of albumin degradation and, by inference, of intestinal protein loss in the group as a whole. A high initial albumin degradation rate augured treatment with elemental diet and prednisone to be unsuccessful. It is concluded that measurement of intestinal protein leakage is of no predictive value as regards the effect of treatment of chronic inflammatory bowel disease with elemental diet. Apparently, diminishing protein exudation is a late phenomenon during a course of clinical remission.

Adolescent↗
PubMed2026

Global gut microbiome atlas identifies epidemiologic-stage-specific signatures in inflammatory bowel disease.

The global rise of inflammatory bowel disease (IBD) reflects environmental shifts, yet how these changes are embedded in the gut microbial ecology remains unclear. We construct a microbiome atlas comprising 245,627 profiles. By classifying countries into three epidemiologic stages, we establish a framework. As the IBD burden increases, the gut microbial alpha diversity declines, and community structures form distinct clusters. This transition is characterized by a gradient of core genera. Integrating six shotgun metagenomic cohorts, we identify the depletion of anabolic pathways in IBD patients. Strain-level analysis reveals that epidemiologic staging shapes genetic architecture within species, identifying an IBD-enriched subclade of Eisenbergiella associated with elevated fecal cholic acid. We develop a microbial inflammatory risk score (MIRS), based on 19 genera, that discriminates IBD from controls (area under the curve [AUC] = 0.92). MIRS correlates with IBD prevalence. Our study provides an atlas linking epidemiology to microbiome ecology and strain evolution, offering a foundation for population-level surveillance and interventions in IBD.

Humans↗
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&#x202f;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&#x202f;498 case patients and 286&#x202f;769 controls from White European populations and a DNA genetic testing company. The IBD GWAS meta-analysis included 38&#x202f;155 case patients and 48&#x202f;485 controls from the International Inflammatory Bowel Disease (IBD) Genetics Consortium. The SSc GWAS included 9095 case patients and 17&#x202f;584 controls from White European populations. Genetic correlations (rg) were found between HS and all exposure phenotypes except SSc (BMI: rg&#x2009;=&#x2009;0.36, P&#x2009;<&#x2009;.001; smoking: rg&#x2009;=&#x2009;0.33, P&#x2009;<&#x2009;.001; IBD: rg&#x2009;=&#x2009;0.25, P&#x2009;<&#x2009;.001; psoriasis: rg&#x2009;=&#x2009;0.34, P&#x2009;<&#x2009;.001; SSc: rg&#x2009;=&#x2009;0.33, P&#x2009;=&#x2009;.22). MR analyses supported an effect of BMI on HS (&#x3b2;&#x2009;=&#x2009;0.87; odds ratio [OR] per BMI unit, 1.20; 95% CI, 1.17-1.23; P&#x2009;<&#x2009;.001) without signs of pleiotropy (slope: &#x3b2;&#x2009;=&#x2009;0.91, P&#x2009;<&#x2009;.001, P for intercept&#x2009;=&#x2009;.76). Smoking showed a significant causal estimate (&#x3b2;&#x2009;=&#x2009;0.59, P&#x2009;<&#x2009;.001), but results became inconclusive in subsequent sensitivity analyses. Among IBD, psoriasis, and SSc, results supported a causal effect of IBD on HS (&#x3b2;&#x2009;=&#x2009;0.18, OR&#x2009;=&#x2009;1.20; 95% CI, 1.15-1.24; P&#x2009;<&#x2009;.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↗
PubMed1978

Decreased suppressor cell activity in inflammatory bowel disease.

Studies were performed on eleven patients with inflammatory bowel disease to determine if there was an alteration in concanavalin A (Con A) induced suppressor cell activity. Similar investigations were also performed on twenty-one control subjects and five patients with other inflammatory conditions. Supressor cells were generated by pre-incubation of peripheral blood mononuclear cells with a mitogenic concentration of Con A, followed by treatment with mitomycin C and alpha-methyl mannoside. Under these conditions, cells obtained from normal individuals are then capable of suppressing the Con A-stimulated blast transformation responses of fresh allogeneic lymphocytes in new cultures. We found that in twenty out of twenty-one control subjects, and all five patients with other inflammatory disorders, Con A-stimulated suppressor cell activity was demonstrable. Four patients with inflammatory bowel disease, whose disease was mildly active or was in clinical remission, had elicitable suppressor cell activity which fell within the normal range. In contrast, suppressor cell activity was markedly diminished or absent in seven patients with severe and active inflammatory bowel disease. These studies suggest that an alternation in Con A-stimulated suppressor cells exists in patients with active inflammatory bowel disease, which may contribute, in part, to the persistent inflammation in the gastrointestinal tract.

Adolescent↗