| Literature DB >> 26167069 |
Anastasia Kourikou1, George P Karamanolis1, George D Dimitriadis1, Konstantinos Triantafyllou1.
Abstract
Functional dyspepsia (FD) is a constellation of functional upper abdominal complaints with poorly elucidated pathophysiology. However, there is increasing evidence that susceptibility to FD is influenced by hereditary factors. Genetic association studies in FD have examined genotypes related to gastrointestinal motility or sensation, as well as those related to inflammation or immune response. G-protein b3 subunit gene polymorphisms were first reported as being associated with FD. Thereafter, several gene polymorphisms including serotonin transporter promoter, interlukin-17F, migration inhibitory factor, cholecystocynine-1 intron 1, cyclooxygenase-1, catechol-o-methyltransferase, transient receptor potential vanilloid 1 receptor, regulated upon activation normal T cell expressed and secreted, p22PHOX, Toll like receptor 2, SCN10A, CD14 and adrenoreceptors have been investigated in relation to FD; however, the results are contradictory. Several limitations underscore the value of current studies. Among others, inconsistencies in the definitions of FD and controls, subject composition differences regarding FD subtypes, inadequate samples, geographical and ethnical differences, as well as unadjusted environmental factors. Further well-designed studies are necessary to determine how targeted genes polymorphisms, influence the clinical manifestations and potentially the therapeutic response in FD.Entities:
Keywords: Functional dyspepsia; Gene polymorphism; Genetic susceptibility; Pathophysiology
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Year: 2015 PMID: 26167069 PMCID: PMC4491956 DOI: 10.3748/wjg.v21.i25.7672
Source DB: PubMed Journal: World J Gastroenterol ISSN: 1007-9327 Impact factor: 5.742