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PubMed1979

A clinical scoring system for chronic inflammatory bowel disease in children.

A clinical scoring system for the assessment of children with chronic inflammatory bowel disease has been devised. A close correlation is demonstrated between severity of disease and the level of serum albumin. The clinical score is simple to perform, sensitive to changes in clinical status, reproducible by different observers, and specifically designed to evaluate inflammatory bowel disease in children and adolescents. The clinical score is a useful adjunct in the management of children with chronic inflammatory bowel disease and can be used in prospective studies of various therapeutic modalities.

Adolescent↗

PubMed1975

Lymphocytotoxic antibody in inflammatory bowel disease. A family study.

The prevalence of lymphocytotoxic antibody in inflammatory bowel disease is 40 per cent. Twenty-seven of 90 relatives of 23 probands with the disease (30 per cent) demonstrated lymphocytotoxic antibody, as contrasted with only three of 69 control family members (4 per cent) (P less than 0.0001). Decreased lymphocytotoxicity against lymphocytes from patients with inflammatory bowel disease as compared to normal donor lymphocytes previously demonstrated in the serum of probands was also observed in the serums from family members of the probands. Nineteen of the 48 household contacts of probands (40 per cent) were positive for antibody, whereas eight of 42 nonhousehold contacts (19 per cent) demonstrated it (P less than 0.05). Eight of 16 spouses (50 per cent) of probands showed antibody. The increased prevalence of lymphocytotoxic antibody in family members of probands and its occurrence mainly in household contacts (consanguineous and non-consanguineous) may indicate the exposure of probands and their family members to a common environmental agent.

Adult↗

PubMed1978

Serum lysozyme, serum proteins, and immunoglobulin determinations in nonspecific inflammatory bowel disease.

The serum levels of lysozyme, serum electrophoresis, and serum immunoglobulins were determined prospectively in 101 patients with ulcerative colitis, ulcerative proctitis, Crohn's disease, or nonclassifiable nonspecific inflammatory bowel disease. Although the mean serum lysozyme concentration of patients with Crohn's disease (10.5 +/- 6.8 microgram/ml) and ulcerative colitis (9.6 +/- 4.1 microgram/ml) performed by a standardized lysoplate method was significantly greater than normal controls (6.0 +/- 1.5 microgram/ml), the results did not correlate with the diagnosis nor with the degree of disease activity. Individually separated protein fractions and serum immunoglobulins also did not correlate with the serum lysozyme levels. This study indicates that measurement of the level of serum lysozyme in individual patients is not helpful in determining the cause or degree of activity of nonspecific inflammatory bowel disease.

Adult↗

PubMed1976

Urologic complications of inflammatory bowel disease.

Urologic complications occurred in 54 of 233 patients with inflammatory bowel disease followed during a 15-year period. Urinary calculi, enterovesical fistulas and ureteral obstruction were the most common problems. Urinary tract complications may arise many years after primary bowel disease has been diagnosed. Symptoms frequently may be absent or obscured by those of the gastrointestinal disorder. We recommend that urologic evaluation be included periodically in the long-term management of patients with inflammatory bowel disease.

Adult↗

PubMed1978

Skin test reactivity in inflammatory bowel disease in the United States and Czechoslovakia.

Inflammatory bowel disease (IBD) patients in the United States of America (USA) and Czechoslovakia (CSSR) were categorized by clinical, pathological, and radiological criteria as having Crohn's disease (CD) or ulcerative colitis (UC) and were tested with five skin test antigens [Candida, mumps, purified protein derivative (PPD), streptokinase-streptodornase (SK-SD), and trichophytin] at two different dilutions in an attempt to elicit some evidence of anergy. No significant differences were encountered between the USA and CSSR populations or between any patient group and its controls.

Allergens↗

PubMed1977

Assessment of the therapeutic value of an elemental diet in chronic inflammatory bowel disease.

Thirty-four patients with chronic inflammatory bowel disease, 23 with ulcerative colitis, and 11 with crohn's disease, weretreated with elemental diet. thirty-one patients had been on high dose prednisonetherapy one to four weeks prior to the diet with no or insufficient response. Fifteen patients (44%) went into remission when elemental diet was introduced as the only change of treatment. Furthermore six patients (18%) went into remission when the dietary treatment was supplemented with high dose prednisone treatment (2 cases) or an increase of prednisone dose (4 cases). Remission occurred in 16 of 21 patients with disease of moderate activity, but in only 5 of 13 cases with severe disease. Remission rate was higher in patients with a limited extent of the lesion, but 8 patients with extensive colitis responded to treatment. There was no significant change of haemoglobin serum iron, transferrin, albumin, orosomucoid, or renal excretion of creatinine. However, significant decreases were observed of sedimentation rate, renal urea excretion, faecal volume and daily number of bowel movements. Colectomy was performed in 8 patients whose condition remained unchanged or aggravated during treatment. Follow-up studies of non-operated patients who went into remission showed that 6 of 13 patients with ulcerative colitis were perfectly well 7-28 months after the study, 3 patients suffered a mild recurrence after 4-24 months, and 4 patients were colectomized 5-10 months later due to severe attack. Of 8 patients with Crohn's disease 4 remained unoperated and free of symptoms 22-35 months after the study.

Adolescent↗

PubMed1978

Significance of anergy to dinitrochlorobenzene (DNCB) in inflammatory bowel disease: family and postoperative studies.

To evaluate the pathogenetic significance of impaired cellular immunity in inflammatory bowel disease (IBD), we have measured the cutaneous responsiveness to dinitrochlorobenzene (DNCB) among 58 patients with IBD, 33 with Crohn's disease and 25 with ulcerative colitis, 63 of their clinically normal relatives, 24 additional ileitis and colitis patients who had undergone resection of all visibly diseased bowel, and 23 control subjects. Cutaneous anergy to DNCB was demonstrated among 70% of the patients with CD and 48% of those with UC, as against only 9% of the controls (p less than 0.001). There was no increased incidence of anergy among either 44 first-degree relatives (7%) or 19 spouses (3%), nor was there any special proclivity toward anergy among six pairs of patients with familial inflammatory bowel disease. In Crohn's disease, anergy was still present after bowel resection in six of 10 patients (60%), while in ulcerative colitis anergy was found after colectomy in only two of 14 patients (14%). Our data suggest that the immune defect in patients with inflammatory bowel disease may be a secondary phenomenon. In ulcerative colitis, the defect appears to reverse after colectomy, but in Crohn's disease it persists despite resection. This finding is consistent with the observed tendency of Crohn's disease, but not ulcerative colitis, to inexorable postoperative recurrence.

Colitis, Ulcerative↗

PubMed1979

A high incidence of chronic inflammatory bowel disease in patients with Turner's syndrome.

Four new cases of chronic inflammatory bowel disease in a series of 135 adult patients with Turner's syndrome observed over an average period of 11 years are reported. The diagnosis in 2 of the patients was ulcerative colitis; the other 2 had clinical and histological features consistent with a diagnosis of Crohn's disease. The incidence is considerably higher than any reported frequency of new cases of inflammatory bowel disease in the general population. Previously reported cases are described and attention is drawn to the severity of the bowel disorder. An apparent association with a karyotype abnormality which includes a structurally abnormal X chromosome is noted.

Adolescent↗

PubMedDate not supplied

Skeletal demineralization and growth retardation in inflammatory bowel disease.

Skeletal growth and mineralization in 54 adolescent and adult patients with inflammatory bowel disease have been analyzed comprehensively. Quantitative and qualitative radiologic techniques consisted of conventional roentgenography, photon absorptiometry, and radiographic morphometry. The data are correlated with the type, duration, and severity of disease, and with several modes of therapy. The results indicate the osteopenia and retardation of growth are common in patients with inflammatory bowel disease, particularly in adolescents, in whom the effects of corticosteroids on the skeleton are most deleterious.

Adolescent↗

PubMed1979

Co-existing coeliac and inflammatory bowel disease in a patient with Turner's syndrome.

A patient, aged 20, with Turner's syndrome was found to have both coeliac disease and chronic ulcerative colitis. Although a gluten-free diet restored to normal the jejunal biopsy, persisting diarrhoea was found to be due to coexisting left-sided ulcerative colitis. A search of the literature revealed only three detailed reports of chronic inflammatory bowel disease in coeliac patients, one of coeliac disease in Turner's syndrome and three of inflammatory bowel disease in Turner's syndrome. Growth failure with coeliac or inflammatory bowel disease in females, may call for a chromosomal study, even in the absence of webbing of the neck. The reason for three uncommon disorders occurring in this patient remains obscure.

Adult↗

PubMed2024

Genetic and Microbial Analysis of Invasiveness for Escherichia coli Strains Associated With Inflammatory Bowel Disease.

BACKGROUND & AIMS: The adherent-invasive Escherichia coli (AIEC) pathotype is implicated in inflammatory bowel disease (IBD) pathogenesis. AIEC strains are currently defined by phenotypic measurement of their pathogenicity, including invasion of epithelial cells. This broad definition, combined with the genetic diversity of AIEC across patients with IBD, has complicated the identification of virulence determinants. We sought to quantify the invasion phenotype of clinical isolates from patients with IBD and identify the genetic basis for their invasion into epithelial cells. METHODS: A pangenome with core and accessory genes (genotype) was assembled using whole genome sequencing of 168 E coli samples isolated from 13 patients with IBD. A modified assay for invasion of epithelial cells (phenotype) was established with consideration of antibiotic resistance phenotypes. Isolate genotype was correlated to invasiveness phenotype to identify genetic factors that cosegregate with invasion. RESULTS: Pangenome-wide comparisons of E coli clinical isolates identified accessory genes that can cosegregate with invasion phenotype. These correlations found the acquisition of antibiotic resistance genes in clinical isolates compromised the traditional gentamicin protection assays used to quantify invasion. Therefore, an alternate assay, based on amikacin resistance, identified genes cosegregating with invasion. These genes encode an arylsulfatase, a glycoside hydrolase, and genetic islands carrying propanediol utilization and sulfoquinovose metabolism pathways. CONCLUSIONS: This study highlights the importance of incorporating antibiotic resistance screening for invasion assays used in AIEC identification. Accurately screened invasion phenotypes identified accessory genome elements among E coli IBD isolates that correlate with their ability to invade epithelial cells. These results help explain why single genetic markers for the AIEC phylotype are challenging to identify.

Humans↗

PubMed2025

FOSB is a key factor in the genetic link between inflammatory bowel disease and acute myocardial infarction: multiple bioinformatics analyses and validation.

BACKGROUND: Inflammatory Bowel Disease (IBD), which includes Crohn's disease and ulcerative colitis, is associated with an increased risk of Acute Myocardial Infarction (AMI). The genetic mechanisms underlying this link are not well understood. METHODS: We downloaded IBD and AMI-related microarray datasets from the NCBI Gene Expression Omnibus (GEO) database. Differentially expressed genes (DEGs) were identified and analyzed using enrichment analysis and Weighted Gene Co-expression Network Analysis (WGCNA). Machine learning techniques, including LASSO, random forest, and Boruta, were employed to screen for hub genes. These genes were validated through qRT-PCR and Western blotting. Single-cell sequencing was used to confirm findings. Additionally, potential therapeutic targets were identified using the Connectivity Map (CMap) database. RESULTS: Five key hub genes-THBD, FOSB, ADGPR3, IL1R2, and PLAUR-were identified as significantly involved in both IBD and AMI pathogenesis. A diagnostic model for AMI constructed using these hub genes demonstrated high predictive accuracy. Single-cell sequencing analysis and several potential drugs targeting these hub genes were identified, offering new therapeutic avenues. CONCLUSION: This study highlights the crucial role of FOSB and other hub genes in the comorbidity of IBD and AMI. The findings provide novel insights for early diagnosis and potential therapeutic strategies, emphasizing the importance of further investigation into these genetic links.

Humans↗

PubMed2026

S100P as a Shared Biomarker in Inflammatory Bowel Disease, Colorectal Cancer, and Pancreatic Adenocarcinoma: An Integrated Transcriptomic Analysis.

Inflammatory bowel disease (IBD) is associated with an increased risk of colorectal cancer (CRC) and pancreatic adenocarcinoma (PAAD), yet the molecular features shared among these diseases remain incompletely understood. This study aimed to identify common genes and biological pathways associated with IBD, CRC, and PAAD through integrated transcriptomic analysis and experimental validation. Gene expression datasets for IBD, CRC, and PAAD were obtained from The Cancer Genome Atlas and Gene Expression Omnibus databases. Weighted gene co-expression network analysis and differential expression analysis were performed to identify disease-associated and shared genes. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes (analyses were used to explore enriched biological functions and pathways. Immune cell infiltration was evaluated using Cell-type Identification by Estimating Relative Subsets of RNA Transcripts. Receiver operating characteristic analysis was performed to assess the diagnostic performance of common genes. Single-cell RNA sequencing analysis was conducted to examine the cellular distribution of S100P. In addition, the effects of S100P downregulation were evaluated in lipopolysaccharide (LPS)-stimulated colonic epithelial cells. A total of 162 disease-associated genes and four common genes were identified. Functional enrichment analyses indicated significant enrichment of immune- and inflammation-related pathways, including the interleukin-17 signaling pathway. Immune infiltration analysis revealed similar trends in several immune cell populations across IBD, CRC, and PAAD. Single-cell analysis showed elevated S100P expression in epithelial cells from all three diseases. Downregulation of S100P restored the proliferative capacity of LPS-stimulated colonic epithelial cells and reduced inflammatory cytokine expression. Integrated transcriptomic analysis identified S100P as a biomarker associated with IBD, CRC, and PAAD and highlighted shared immune-related features across these diseases.

Humans↗

PubMed1979

Urolithiasis and hyperoxaluria in chronic inflammatory bowel disease.

The incidence of urolithiasis was registered in 87 patients with chronic inflammatory bowel disease and compared with that of renal oxalate excretion. All patients were studied while on a standardized diet with fixed amounts of fat, calcium, and oxalate. Pyelography had been performed in all. Nine, or 35%, of 26 hyperoxaluric patients had urolithiasis, compared with 14, or 23%, of 61 patients were normal renal oxalate excretion, the difference being statistically insignificant. No significant difference in urinary oxalate or urinary calcium in stone-formers as compared with non-stone-formers could be demonstrated. Oxalate was a more frequent component of calculi in patients with normal renal oxalate excretion than in patients with hyperoxalura. Thus, we were unable to demonstrate an increased incidence of urolithiasis in patients with hyperoxaluria compared with a control group with normal renal oxalate excretion. Our results cast doubt on the concept that enteric hyperoxaluria per se is the cause of stone diathesis in chronic inflammatory bowel disease.

Adult↗

PubMed2025

Prevalence and predictors of low bone mineral density in pediatric inflammatory bowel disease.

OBJECTIVES: Bone health is at risk in children with inflammatory bowel disease (IBD). This study examined the prevalence and predictors of low bone mineral density (BMD) in a cohort of children and young adults with IBD. METHODS: This single-center retrospective study included patients with IBD, ages 3.5-22 years, with completed dual x-ray absorptiometry (DXA) scans from 2006 to 2019. Demographic, clinical, and laboratory data were collected. Logistic regression analysis identified predictors associated with low BMD (Z-scores ≤ -2 standard deviations [SDs]) for three outcomes. In an overlapping IBD cohort with available genetic data between 2002 and 2019 (n = 378), genetic risk for diminished bone health was calculated using published polygenic risk scores generated from genome-wide association studies based on DXA or heel ultrasound speed of sound (SOS). Linear regression analysis examined associations of low BMD and genetic risk. RESULTS: Low BMD prevalence was 7% in our cohort (n = 600) based on spine bone mineral apparent density (BMAD), which best accounts for growth delays. Median (interquartile range [IQR]) spine BMAD Z-score was -0.37 SD (-1.11 to 0.35). Predictors of low BMAD included lower BMI Z-score (odds ratio [OR]: 0.67, p value: 0.02) and decreased height Z-score (OR: 0.6, p value: 0.005). Of those with longitudinal data (n = 118), low BMI (OR: 0.44, p value: <0.001) and steroid use (OR: 3.42, p value: 0.01) were associated with suboptimal bone health (Z-scores ≤ -1SD). In the cohort with genetic data, heel genomic SOS (β [standard error] = 0.17 [0.35], p ≤ 0.01) was associated with BMD. CONCLUSIONS: Lower BMI should prompt DXA monitoring in pediatric IBD. Genetic predisposition may identify an at-risk subpopulation.

Humans↗

PubMed2024

No causal relationship between glucose and inflammatory bowel disease: a bidirectional two-sample mendelian randomization study.

BACKGROUND: Association between glucose and inflammatory bowel disease (IBD) was found in previous observational studies and in cohort studies. However, it is not clear whether these associations reflect causality. Thus, this study investigated whether there is such a causal relation between elevated glucose and IBD, Crohn's disease (CD) and ulcerative colitis (UC). METHODS: We performed a two-sample Mendelian Randomization (MR) with the independent genetic instruments identified from the largest available genome-wide association study (GWAS) for IBD (5,673 cases; 213,119 controls) and its main subtypes, CD and UC. Summarized data for glucose which included 200,622 cases and glycemic traits including HbA1c and type 2 diabetes(T2DM) were obtained from different GWAS studies. Primary and secondary analyses were conducted by preferentially using the radial inverse-variance weighted (IVW) approach. A number of other meta-analysis approach and sensitivity analyses were carried out to assess the robustness of the results. RESULTS: We did not find a causal effect of genetically predicted glucose on IBD as a whole (OR 0.858; 95% CI 0.649-1.135; P = 0.286). In subtype analyses glucose was also suggestively not associated with Crohn's disease (OR 0.22; 95% CI 0.04-1.00; P = 0.05) and ulcerative colitis (OR 0.940; 95% CI 0.628-1.407; P = 0.762). In the other direction, IBD and its subtypes were not related to glucose and glycemic traits. CONCLUSIONS: This MR study is not providing any evidence for a causal relationship between genetically predicted elevated glucose and IBD as well as it's subtypes UC and CD. Regarding the other direction, no causal associations could be found. Future studies with robust genetic instruments are needed to confirm this conclusion.

Humans↗

PubMed1979

The spectrum of hepatic dysfunction in inflammatory bowel disease.

The spectrum and incidence of liver disease is described among a large series of patients with inflammatory bowel disease. The incidence of significant liver disease identified by the presence of serial biochemical abnormalities of liver function was 8.2 per cent. Transient peri-operative changes in liver function tests are common and usually relate to underlying intra-abdominal sepsis. Percholangitis, sometimes termed portal triaditis, is one of the commoner lesions, and is usually associated with extensive colitis and improves with resection of the underlying bowel disease. Cirrhosis of the liver is an important but uncommon complication and is usually associated with extensive long-standing disease. Stenosing cholangitis and biliary tract carcinoma are both important though rare associations. They are both associated with extensive disease of long-standing, but resection of the underlying inflammatory bowel disease does not necessarily protect the individual from these complications. Although stenosing cholangitis is a diffuse lesion of the biliary tree it is important to exclude strictures of the extra-hepatic biliary tree which may be amenable to surgical correction. Hepatic dysfunction is rarely the sole indication for advising surgery for the underlying bowel disease but the identification of the nature of the hepati- dysfunction provides a rational basis for such a decision and opportunities for the surgical correction of the hepatic lesion itself.

Adolescent↗

PubMed1979

Ileorectal anastomosis for inflammatory bowel disease: 15-year follow-up.

A personal series (E.S.R.H.) of 37 patients with inflammatory bowel disease, treated by colectomy and ileorectal anastomosis 15 years or more ago, is reviewed. Twenty-one patients (57 per cent) continue to be in satisfactory condition. Patients subjected to the two-stage operation have a notably lower rate of conversion to ileostomy than those treated by one-stage colectomy. One patient developed a carcinoma of the rectal stump. This 15-year review leads support to the opinion that ileorectal anastomosis has an important place in the treatment of inflammatory bowel disease.

Colectomy↗