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Genetic polymorphism patterns suggest a genetic driven inflammatory response as pathogenesis in appendicitis
Jönköping University, School of Health and Welfare, HHJ, Dep. of Natural Science and Biomedicine. Jönköping University, School of Health and Welfare, HHJ. Biomedical Platform.ORCID iD: 0000-0003-2328-7334
Department of Clinical and Experimental Medicine, Linköping University, Linköping, Sweden.
Department of Laboratory Medicine, Division of Clinical Microbiology, Region Jönköping County, Jönköping, Sweden.
Department of Clinical and Experimental Medicine, Linköping University, Linköping, Sweden, and County Hospital Ryhov, Region Jönköping County, Department of Surgery, Jönköping, Sweden.
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2019 (English)In: International Journal of Colorectal Disease, ISSN 0179-1958, E-ISSN 1432-1262Article in journal (Refereed) Epub ahead of print
Abstract [en]

PURPOSE: The pathogenesis of appendicitis is not well understood. Environmental factors are regarded most important, but epidemiologic findings suggest a role of inflammatory and genetic mechanisms. This study determines the association of single nucleotide polymorphisms (SNPs) of inflammatory genes with appendicitis.

METHODS: As part of a larger prospective study on the diagnostic value of inflammatory variables in appendicitis, the genotype frequency of 28 polymorphisms in 26 inflammatory response genes from the appendicitis and control patients was analyzed in blood samples from 343 patients, 100 with appendicitis, and 243 with non-specific abdominal pain, using TaqMan SNP genotyping assays.

RESULTS: Associations with appendicitis were found for SNPs IL-13 rs1800925 with odds ratio (OR) 6.02 (95% CI 1.52-23.78) for T/T versus C/C + T/T, for IL-17 rs2275913 with OR 2.38 (CI 1.24-4.57) for A/A vs G/G + GA, for CCL22 rs223888 with OR 0.12 (0.02-0.90), and for A/A vs G/G + GA. Signs of effect modification of age for the association with appendicitis were found for IL-13 rs1800925 and CTLA4 rs3087243. Stratified analysis showed difference in association with severity of disease for IL-17 rs2275913 and CD44 rs187115.

CONCLUSIONS: The association of gene variants on risk of appendicitis and its severity suggest an etiologic role of genetically regulated inflammatory response. This may have implications for understanding the prognosis of untreated appendicitis as a possible self-limiting disorder and for understanding the inverse association of appendicitis with ulcerative colitis.

Place, publisher, year, edition, pages
Springer, 2019.
Keywords [en]
Appendicitis, Gene polymorphism, Inflammatory bowel disease, Pathophysiology
National Category
Gastroenterology and Hepatology
Identifiers
URN: urn:nbn:se:hj:diva-47189DOI: 10.1007/s00384-019-03473-1PubMedID: 31845023Scopus ID: 2-s2.0-85076627049OAI: oai:DiVA.org:hj-47189DiVA, id: diva2:1381174
Available from: 2019-12-20 Created: 2019-12-20 Last updated: 2020-01-02

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Dimberg, Jan

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