scholarly journals Monocyte Human Leukocyte Antigen–DR Expression—A Tool to Distinguish Intestinal Bacterial Infections From Inflammatory Bowel Disease?

Shock ◽  
2013 ◽  
Vol 40 (2) ◽  
pp. 89-94 ◽  
Author(s):  
Wolfgang Tillinger ◽  
Ruth Jilch ◽  
Thomas Waldhoer ◽  
Walter Reinisch ◽  
Wolfgang Junger
Keyword(s):  
Inflammatory Bowel Disease ◽  
Human Leukocyte Antigen ◽  
Bowel Disease ◽  
Bacterial Infections ◽  
Human Leukocyte ◽  
Leukocyte Antigen ◽  
Inflammatory Bowel

scholarly journals Establishing a Causal Link between Ankylosing Spondylitis and Inflammatory Bowel Disease: A Review of the Literature

2016 ◽  
Vol 4 (2) ◽  
pp. 55-63
Author(s):  
Jaclyn Rivington ◽  
Michael Gillett
Keyword(s):  
Inflammatory Bowel Disease ◽  
Ankylosing Spondylitis ◽  
Human Leukocyte Antigen ◽  
Bowel Disease ◽  
Human Leukocyte ◽  
Active Role ◽  
Causal Link ◽  
Leukocyte Antigen ◽  
Pubmed Database ◽  
Inflammatory Bowel

The link between ankylosing spondylitis and inflammatory bowel disease is unclear, however it is hypothesized that there is a causal link between the inheritance of a human leukocyte antigen B27 allele and the development of inflammatory bowel disease symptoms in ankylosing spondylitis patients. Research articles assessing the relationship between ankylosing spondylitis, inflammatory bowel disease and the human leukocyte antigen B27 antigen were collected from the PubMed database. Patients expressing the human leukocyte antigen B27 allele have a demonstrated predisposition to developing symptoms of inflammatory bowel disease and sacroiliitis in ankylosing spondylitis. However, human leukocyte antigen B27 is considered to be just a contributing factor in the disease, as interleukin-23, natural killer cells, and alterations to the microbiome have also demonstrated an active role in the development of symptoms. More longitudinal studies using larger cohorts are needed to further substantiate a direct causal relationship between ankylosing spondylitis and inflammatory bowel disease.

scholarly journals Genetic polymorphism of HLA-G gene (G*01:03, G*01:04, and G*01:05N) in Iraqi patients with inflammatory bowel disease (ulcerative colitis and Crohn’s disease)

2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Sarah S. Abdul-Hussein ◽  
Ekhlass N. Ali ◽  
Neihaya H. Zaki ◽  
Ali H. Ad’hiah
Keyword(s):  
Ulcerative Colitis ◽  
Inflammatory Bowel Disease ◽  
Crohn’S Disease ◽  
Crohn's Disease ◽  
Bowel Disease ◽  
Human Leukocyte ◽  
Leukocyte Antigen ◽  
Increased Risk ◽  
Soluble Hla ◽  
Inflammatory Bowel

Abstract Background Human leukocyte antigen-G (HLA-G) has been proposed to influence susceptibility to inflammatory bowel disease (IBD). Therefore, the genetic association between HLA-G alleles and two clinical phenotypes of IBD (ulcerative colitis [UC] and Crohn’s disease [CD]) was evaluated in Iraqi patients. A case-control study was performed on 50 UC and 50 CD patients and 100 healthy controls (HC). Three HLA-G alleles (G*01:03, G*01:04, and G*01:05N) were determined using sequence-specific polymerase chain reaction assay followed by product digestion with restriction endonucleases (Hinf-I, BseR-I, and PpuM-I, respectively). Results The G*01:03 allele was not detected in IBD patients (UC and CD) or HC, while G*01:04 and G*01:05N alleles showed polymorphic frequencies. The allele G*01:04 was significantly associated with susceptibility to UC (odds ratio [OR] = 2.55; 95% confidence interval [CI] = 1.27–5.13; corrected probability [pc] = 0.018) and CD (OR = 4.45; 95% CI = 2.11–9.41; pc < 0.001). The allele G*01:05N was also associated with increased risk of UC (OR = 4.17; 95% CI = 1.32–13.21; pc = 0.032) and CD (OR = 4.75; 95% CI = 1.53–14.78; pc = 0.014). These associations were more pronounced in IBD (UC + CD), and a significantly increased risk for IBD was found with the alleles G*01:04 (OR = 3.32; 95% CI = 1.86–5.95; pc < 0.001) and G*01:05N (OR = 4.46; 95% CI = 1.59–12.47; pc = 0.008). A stratification of IBD patients according to some demographic and clinical characteristics revealed that frequencies of both alleles showed no significant differences between the subgroups of patients in each stratum. Soluble HLA-G was not influenced by HLA-G alleles in patients or HC. UC was an exception, and the presence of G*01:04 allele was associated with a significantly higher mean of soluble HLA-G compared to patients without the allele (189.6 ± 24.0 vs. 168.6 ± 27.2 ng/mL; p = 0.033). Conclusion This study indicated that HLA-G*01:04 and HLA-G*01:05N alleles may influence susceptibility to UC and CD in Iraqi patients.

scholarly journals New Concepts of Pathogenesis in Inflammatory Bowel Disease

1995 ◽  
Vol 9 (5) ◽  
pp. 261-270
Author(s):  
Claudio Fiocchi
Keyword(s):  
Inflammatory Bowel Disease ◽  
Bowel Disease ◽  
Measles Virus ◽  
Human Leukocyte ◽  
Basic Research ◽  
Leukocyte Antigen ◽  
New Concepts ◽  
Inflammatory Bowel ◽  
Immunological Factors ◽  
Low Incidence

The precise etiology and mechanisms of inflammatory bowel disease (IBD) are still unclear. Nevertheless, several concepts are gaining acceptance and constitute the basis for a better understanding of its pathogenesis and for improved therapy. The association of Crohn’s disease (CD) and ulcerative colitis (UC) with ‘western’ lifestyle is well recognized, and is considered a reason for the increasing frequency of CD and UC in countries with previously low incidence. Proposed linkages of CD and UC with particular human leukocyte antigen haplotypes suggest a genetic predisposition, but no uniform or consistent patterns have emerged. Similarly, the study of susceptibility or disease markers has not offered reproducible results. The search for specific infectious agents is being pursued, and the measles virus is presently considered a possible culprit. A true explosion has occurred in the area of animal models, and a large number of chemically or genetically induced experimental colitides are at hand. Immunological factors continue to dominate the bulk of basic research in IBD. This area is vast and complex, and autoantibodies, immune, epithelial and mesenchymal cells, lipid mediators, cytokines, neuropeptides and oxygen metabolites are under investigation. Finally, other factors whose role in IBD is uncertain, including smoking and possible abnormalities of intestinal permeability or mucus composition, continue to receive attention. These extensive and varied efforts are yielding some profits, and new forms of therapy are being devised. Based mostly on studies of soluble mediators, a number of novel immunosuppressive and highly specific blocking agents are being developed and undergoing clinical trials.

scholarly journals Cholestatic Hepatocellular Injury with Azathioprine: A Case Report and Review of the Mechanisms of Hepatotoxicity

1998 ◽  
Vol 12 (7) ◽  
pp. 479-483 ◽  
Author(s):  
Joseph Romagnuolo ◽  
DC Sadowski ◽  
E Lalor ◽  
L Jewell ◽  
ABR Thomson
Keyword(s):  
Inflammatory Bowel Disease ◽  
Portal Hypertension ◽  
Bowel Disease ◽  
Cell Injury ◽  
Strong Association ◽  
Human Leukocyte ◽  
Peliosis Hepatis ◽  
Hepatocellular Injury ◽  
Inflammatory Bowel ◽  
Biochemical Abnormalities

Azathioprine is a drug commonly used for the treatment of inflammatory bowel disease, organ transplantation and various autoimmune diseases. Hepatotoxicity is a rare, but important complication of this drug. The cases reported to date can be grouped into three syndromes: hypersensitivity; idiosyncratic cholestatic reaction; and presumed endothelial cell injury with resultant raised portal pressures, veno-occlusive disease or peliosis hepatis. The components of azathioprine, 6-mercaptopurine and the imidazole group, may play different roles in the pathogenesis of hepatotoxicity. The strong association with male sex, and perhaps with human leukocyte antigen type, suggests a genetic predisposition of unknown type. Many of the symptoms of hepatotoxicity, such as nausea, abdominal pain and diarrhea, can be nonspecific and can be confused with a flare-up of inflammatory bowel disease. As well, the subtype resulting in portal hypertension can occur without biochemical abnormalities. A 63-year-old man with Crohn's disease who is presented developed the rare idiosyncratic form of azathioprine hepatotoxicity, but also had a severe disabling steroid myopathy, peripheral neuropathy, resultant deep venous thrombosis and pulmonary embolism related to immobility, and a nosocomial pneumonia. His jaundice and liver enzyme levels improved markedly on withdrawal of the drug, returning to almost normal in five weeks. Treating inflammatory bowel disease effectively while trying to limit iatrogenic disease is a continuous struggle. Understanding the risks of treatment is the first important step. There must be a low threshold for obtaining liver function tests, especially in men, and alertness to the need to discontinue the drug or perform a liver biopsy should patients on azathioprine develop liver biochemical abnormalities, unexplained hepatomegaly or signs of portal hypertension.

scholarly journals P815 Are hospitalised patients with inflammatory bowel disease at increased risk of invasive bacterial infections? Results from POLIBD 2-year cohort study

2020 ◽  
Vol 14 (Supplement_1) ◽  
pp. S635-S635
Author(s):  
R Filip ◽  
J Gruszecka
Keyword(s):  
Risk Factors ◽  
Inflammatory Bowel Disease ◽  
Length Of Stay ◽  
Bowel Disease ◽  
Bacterial Infections ◽  
Coagulase Negative Staphylococcus ◽  
Beta Lactam ◽  
Hospitalised Patients ◽  
Increased Risk ◽  
Inflammatory Bowel

Abstract Background The disease itself as well as immunomodulatory and biological therapy are risk factors for invasive bacterial infections in patients with inflammatory bowel disease (IBD). However, there are limited data on risk factors for bacteraemia in the general population of hospitalised patients with inflammatory bowel disease. The aim of the study was to assess the rate of bacteraemia in hospitalised patients with Inflammatory Bowel Disease and risk factors. Methods An observational cohort of hospitalised patients with Inflammatory Bowel Disease, aged 23–65 years, from 2017 to 2019 in a large tertiary hospital localised in Rzeszow (south-eastern Poland). Patients with one or more positive blood culture were reviewed. Those with Carlson comorbidity index of 2 or greater were excluded. Basic descriptive statistic and logistic regression to evaluate risk factors for bacteraemia were used. Results Of 727 admitted patients, only 1.24% had bacteraemia (9/727) (8, Crohn’s Disease; 1, Ulcerative Colitis). The most common pathogens were Staphylococcus epidermidis (MRCNS - methicillin-resistant coagulase-negative Staphylococcus - strain resistant to all beta-lactam antibiotics: penicillins, penicillins with a B-lactamase inhibitor, cephalosporin and carbapenem) (4/9 patients) and Escherichia coli (3/9 patients). The mortality rate at 30 days of patients with bacteraemia was 0% (no deaths in IBD patients with bacteraemia observed). Longer hospitalisation (mean length of stay for patients with CD was 42 ± 33 vs. 7.95 ± 17.3, p &lt;0.001; mean length of stay for a patient with UC 15 ± 23 vs. 6.25 ± 15.4, p = 0.004) was associated with an increased risk of bacteraemia. Older age was not associated with an increased risk of bacteraemia (P&gt;0.05). In multivariate analysis, treatment with either anti-tumour necrosis factor α, purine analogues, steroids or amino salicylates was not associated with an increased risk of bacteraemia. Conclusion Prolonged hospitalisation, but not Inflammatory Bowel Disease-related treatment, is associated with an increased risk of bacteraemia in hospitalised patients with Inflammatory Bowel Disease.

Non– Clostridium difficile Bacterial Infections Are Rare in Patients With Flares of Inflammatory Bowel Disease

2018 ◽  
Vol 16 (4) ◽  
pp. 528-533 ◽  
Author(s):  
Yuri Hanada ◽  
Sahil Khanna ◽  
Edward V. Loftus ◽  
Laura E. Raffals ◽  
Darrell S. Pardi
Keyword(s):  
Inflammatory Bowel Disease ◽  
Clostridium Difficile ◽  
Bowel Disease ◽  
Bacterial Infections ◽  
Inflammatory Bowel

scholarly journals Inflammatory Bowel Disease: Progress Towards a Gene

2000 ◽  
Vol 14 (3) ◽  
pp. 207-218 ◽  
Author(s):  
David A van Heel ◽  
Jack Satsangi ◽  
Alisoun H Carey ◽  
Derek P Jewell
Keyword(s):  
Inflammatory Bowel Disease ◽  
Candidate Genes ◽  
Bowel Disease ◽  
Animal Studies ◽  
Interleukin 1 ◽  
Twin Studies ◽  
Human Leukocyte ◽  
Epidemiological Data ◽  
Nucleotide Polymorphisms ◽  
Inflammatory Bowel

The pathogenesis of ulcerative colitis (UC) and Crohn’s disease (CD) is still unknown, but the importance of genetic susceptibility has been clearly shown by epidemiological data from family and twin studies. Linkage studies have identified two susceptibility loci for inflammatory bowel disease (IBD) on chromosomes 12 and 16. Importantly, these linkages have been replicated by independent investigators, and studies of positional candidates within these regions continue, together with fine mapping strategies. Regions of ’suggestive’ linkage on chromosomes 1, 3, 4, 6, 7, 10, 22 and X have also been reported in individual studies. Other important candidate genes investigated include the interleukin-1 receptor antagonist, MUC3 and genes of the human leukocyte antigen (HLA) system. The apparently conflicting data in different studies from around the world may be explained by ethnic differences, case mix and genetic heterogeneity. Replicated class II HLA associations include HLA DRB1*0103 and DR2 (DRB1*1502), involved in UC susceptibility, and HLA DRB1*03 and DR4 as resistance alleles for CD and UC respectively. Animal studies have provided insights from targeted mutations and quantitative trait locus analysis. The goals of continuing research include narrowing the regions of linkages and analysis of candidate genes, and possibly the application of newly developed methods using single nucleotide polymorphisms. Advances in IBD genetics hold the potential to provide knowledge about the disease pathogenesis at the molecular level, with ensuing benefits for clinical practice.

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