Plasma lysozyme and alpha1-acid glycoprotein as an index of disease activity in inflammatory bowel disease.
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Adult↗
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Immunological studies in inflammatory bowel disease.
Three aspects of immunological function were studied in patients with Crohn's disease and ulcerative colitis (inflammatory bowel disease): atopic status and serum IgE levels; serum concentration of C-reactive protein; and C3 activation. The incidence of atopy, assessed by prick testing with common allergens, did not differ in patients with inflammatory bowel disease from healthy controls. 12 of 39 patients with Crohn's disease and 5 of 20 with ulcerative colitis, among whom were some non-atopic subjects, had elevated serum levels of IgE. Serum levels of C-reactive protein in patients were significantly greater than normal, even in those in whom the disease was clinically quiescent. Symptomatic patients with Crohn's disease had significantly higher levels than similar patients with ulcerative colitis and in Crohn's disease the levels correlated well with an overall assessment of severity and disease activity. Although conversion of C3 was detected in fresh serum samples from inflammatory bowel disease patients and not controls, only minimal traces were present in just 7 of 89 samples of EDTA--plasma from 47 patients; this finding did not correlate with disease activity. However, there were low titres of immunoconglutinin in the sera of some patients, but not in controls, suggesting that complement activation may be occurring in vivo.
C-Reactive Protein↗
Multi-ancestry genome-wide and transcriptome-wide association analyses identified new risk loci and genes for inflammatory bowel disease.
To advance genetic understanding of inflammatory bowel disease (IBD), we conducted genome-wide association meta-analyses of 63,415 IBD cases of European and East Asian descendants and identified 90 previously unknown risk loci. Integrating multi-ancestry transcriptome-wide association studies (TWAS), cell type-specific TWAS, alternative splicing (AS-WAS), and alternative polyadenylation (APA-WAS) analyses using RNA-seq data from normal colon tissues of 707 European and 364 East Asian individuals, we uncovered 506 high-confidence IBD risk genes, including 384 not previously reported. These genes converge on immune regulation, microbial interaction, and other pathways central to IBD pathogenesis, with over half showing transcriptional dysregulation supported by single-cell and spatial omics analyses. Notably, 46 risk genes are targeted by 225 drugs that have been approved or in Phase II/III trials, including sulfasalazine already used in IBD therapy. Our study findings deepen the understanding of IBD genetics and support the development of precision medicine for its prevention and treatment.
GWAS↗
Ten years experience with intravenous hyperalimentation and inflammatory bowel disease.
A retrospective analysis was conducted on 74 patients with inflammatory bowel disease who were treated with intravenous hyperalimentation at the Hospital of the University of Pennsylvania between the years 1967-1976. Intravenous hyperalimentation can ameliorate the inevitable protein-calorie malnutrition present in patients with inflammatory bowel disease. Combined with complete bowel rest, intravenous hyperalimentation can effectively function as the primary treatment or as an adjunct to the surgical management of the complications of inflammatory bowel disease. Intravenous hyperalimentation can be safely administered to these severely ill patients, almost certainly improving survival rates in the patients treated.
Adult↗
Toxic dilatation of the colon in salmonella colitis and inflammatory bowel disease.
Toxic dilatation of the colon may be due to inflammatory bowel disease, either ulcerative colitis or Crohn's disease of the colon, but recent experience has shown that infective colitis due to salmonella can produce this complication. We present 13 cases with toxic dilatation (9 inflammatory bowel disease and 4 salmonellosis) and outline the diagnostic features and treatment in these patients. It is important to distinguish salmonellosis at an early stage because, whilst toxic dilatation in inflammatory bowel disease is an absolute indication for surgical treatment, cases with this complication due to salmonellosis may be treated conservatively in the majority of instances.
Adolescent↗
Characteristics of isolated intestinal mucosal lymphoid cells in inflammatory bowel disease.
Immunologic characteristics of intestinal mucosal lymphoid cells from patients with inflammatory bowel disease and controls have been compared. Mononuclear cells isolated by enzymatic means from intestinal tissues involved with inflammatory bowel disease were present in greater numbers, with increased proportions of macrophages and B-lymphocytes, particularly cells bearing intrinsic membrane immunoglobulin G. Synthesis of immunoglobulin G, measured by radioimmunoassay, was increased tenfold in inflammatory bowel disease, while immunoglobulin A synthesis per 10(6) cells was unchanged. "Null" or K-lymphocytes were absent from all populations, and antibody-dependent cellular cytotoxicity (a K-cell-mediated function) was not demonstrable. Taken together, the results fail to support a role for antibody-dependent cellular cytotoxicity or a defect in secretory immunoglobulin A, but rather focus attention upon possible forms of immunoglobulin G-mediated tissue damage in the pathogenesis or perpetuation of inflammatory bowel disease.
Antibody-Dependent Cell Cytotoxicity↗
Pharmacogenomic Assessment of Genes Implicated in Thiopurine Metabolism and Toxicity in a UK Cohort of Pediatric Patients With Inflammatory Bowel Disease.
BACKGROUND: Thiopurine drugs are effective treatment options in inflammatory bowel disease and other conditions but discontinued in some patients due to toxicity. METHODS: We investigated thiopurine-induced toxicity in a pediatric inflammatory bowel disease cohort by utilizing exome sequencing data across a panel of 46 genes, including TPMT and NUDT15. RESULTS: The cohort included 487 patients with a median age of 13.1 years. Of the 396 patients exposed to thiopurines, myelosuppression was observed in 11%, gastroenterological intolerance in 11%, hepatotoxicity in 4.5%, pancreatitis in 1.8%, and "other" adverse effects in 2.8%. TPMT (thiopurine S-methyltransferase) enzyme activity was normal in 87.4%, intermediate 12.3%, and deficient in 0.2%; 26% of patients with intermediate activity developed toxicity to thiopurines. Routinely genotyped TPMT alleles associated with defective enzyme activity were identified in 28 (7%) patients: TPMT*3A in 4.5%, *3B in 1%, and *3C in 1.5%. Of these, only 6 (21%) patients developed toxic responses. Three rare TPMT alleles (*3D, *39, and *40) not assessed on routine genotyping were identified in 3 patients, who all developed toxic responses. The missense variant p.R139C (NUDT15*3 allele) was identified in 4 patients (azathioprine 1.6 mg/kg/d), but only 1 developed toxicity. One patient with an in-frame deletion variant p.G13del in NUDT15 developed myelosuppression at low doses. Per-gene deleteriousness score GenePy identified a significant association for toxicity in the AOX1 and DHFR genes. CONCLUSIONS: A significant association for toxicity was observed in the AOX1 and DHFR genes in individuals negative for the TPMT and NUDT15 variants. Patients harboring the NUDT15*3 allele, which is associated with myelosuppression, did not show an increased risk of toxicity.
Humans↗
Association of inflammatory bowel disease and large vascular lesions.
A case of inflammatory bowel disease with associated multiple large vessel vascular lesions similar to that seen in Takayasu's arteritis is described in a 15-year-old female. It is suggested that this type of vascular lesion may represent another rare systemic manifestation of inflammatory bowel disease.
Adolescent↗
Escherichia coli antibodies in patients with inflammatory bowel disease.
Sera from 30 patients with inflammatory bowel disease (IBD) (16 with Crohn's disease (CD) and 14 with ulcerative colitis (UC) were assayed for the presence of antibodies against 159 Escherichia coli O-antigens and compared with sera from 16 matched control subjects. The majority of patients with IBD had agglutinating antibodies to a higher number of Escherichia coli O-antigens and in higher titres than the control group. The number of positive agglutinins was O-33 mean 13.8 in CD, O-26 mean 7.9 for UC, and O-7 mean 1.5 in controls. Eight patients with IBD and arthropathy had antibodies to fewer O-antigens (O-7 mean 3.2). The antibodies were in the IgG and IgM, in titres corresponding to original values. No specific O-serotypes were associated with IBD. Common serotypes, R-plasmid carrying serotypes, and those associated with shigella-like adult diarrhoea were detected. O14 was detected only in five patients and O119 in none. There was no correlation between the number of Escherichia coli agglutinins and the site and severity of the disease or type of therapy. It is suggested that the presence of the high numbers of Escherichia coli antibodies is secondary to the disease process and is unlikely to be causally involved in the pathogenesis of the disease, but may play a role in the perpetuation of the disease and in the extraintestinal complications.
Adult↗
Randomized Trial of Intensive Nurse-Led Follow‑Up Versus Standard Care in Inflammatory Bowel Disease.
BACKGROUND:  Nurses play a key role in inflammatory bowel disease (IBD) management. This randomized controlled trial evaluated intensive nurse-led program in patients with IBD starting advanced therapy. METHODS:  Patients were randomized (1:1) to intensive nurse follow‑up (Arm A) or standard care (Arm B). Both arms received baseline nurse education; Arm A additionally had scheduled nurse calls and visits. Primary outcome was reduction in IBD‑Disk score in W12. Secondary outcomes were W52 reduction, robust response (> 20-point improvement), and IBD-Disk remission (score < 40). RESULTS: Overall, 98 patients were randomized (Arm A: n = 50; Arm B: n = 48) with similar baseline characteristics. Mean baseline IBD‑Disk scores were 49.2 ± 20.7 in Arm A and 42.0 ± 19.8 in Arm B (p = 0.07). At W12, both groups improved, with greater IBD-Disk reductions in Arm A (16.1 ± 22.9 vs. 10.1 ± 20.1, p = 0.09). At W52, improvement was greater in Arm A (18.4 ± 20.7 vs 9.4 ± 17.8; p = 0.08). More patients achieved robust response in Arm A (49% vs 21%, p = 0.013) at W12. By W52, IBD-Disk remission was achieved by 22/25 (88%) patients in Arm A vs 18/28 (64%) in Arm B (p = 0.045). CONCLUSIONS:  In this pilot randomized trial, intensive nurse-led follow-up did not significantly improve IBD-Disk at week 12, yet favorable trends of functional outcomes were observed. Intensive nurse‑led follow‑up program may improve quality of life in patients with IBD. These findings support the integration of specialist IBD nurses to improve patient‑centered outcomes.
Humans↗
Deciphering microbial and metabolic influences in gastrointestinal diseases-unveiling their roles in gastric cancer, colorectal cancer, and inflammatory bowel disease.
INTRODUCTION: Gastrointestinal disorders (GIDs) affect nearly 40% of the global population, with gut microbiome-metabolome interactions playing a crucial role in gastric cancer (GC), colorectal cancer (CRC), and inflammatory bowel disease (IBD). This study aims to investigate how microbial and metabolic alterations contribute to disease development and assess whether biomarkers identified in one disease could potentially be used to predict another, highlighting cross-disease applicability. METHODS: Microbiome and metabolome datasets from Erawijantari et al. (GC: n = 42, Healthy: n = 54), Franzosa et al. (IBD: n = 164, Healthy: n = 56), and Yachida et al. (CRC: n = 150, Healthy: n = 127) were subjected to three machine learning algorithms, eXtreme gradient boosting (XGBoost), Random Forest, and Least Absolute Shrinkage and Selection Operator (LASSO). Feature selection identified microbial and metabolite biomarkers unique to each disease and shared across conditions. A microbial community (MICOM) model simulated gut microbial growth and metabolite fluxes, revealing metabolic differences between healthy and diseased states. Finally, network analysis uncovered metabolite clusters associated with disease traits. RESULTS: Combined machine learning models demonstrated strong predictive performance, with Random Forest achieving the highest Area Under the Curve(AUC) scores for GC(0.94[0.83-1.00]), CRC (0.75[0.62-0.86]), and IBD (0.93[0.86-0.98]). These models were then employed for cross-disease analysis, revealing that models trained on GC data successfully predicted IBD biomarkers, while CRC models predicted GC biomarkers with optimal performance scores. CONCLUSION: These findings emphasize the potential of microbial and metabolic profiling in cross-disease characterization particularly for GIDs, advancing biomarker discovery for improved diagnostics and targeted therapies.
Humans↗
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↗
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↗
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↗
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↗
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↗
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↗
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↗