Published online Jul 7, 2015. doi: 10.3748/wjg.v21.i25.7672
Peer-review started: February 25, 2015
First decision: March 26, 2015
Revised: April 7, 2015
Accepted: May 21, 2015
Article in press: May 21, 2015
Published online: July 7, 2015
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.
Core tip: Functional dyspepsia is a common disorder with complex pathophysiology. Recent evidence has shown that certain gene polymorphisms might be implicated in its pathogenesis; however, results are inconsistent. Further studies are required to develop new data that provide novel insights regarding the mechanisms of genetic susceptibility in functional dyspepsia.