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Article: Functional dyspepsia susceptibility is associated with TGFB1 gene polymorphisms (RS4803455, RS1800469) in H pylori‐negative Chinese population

TitleFunctional dyspepsia susceptibility is associated with TGFB1 gene polymorphisms (RS4803455, RS1800469) in H pylori‐negative Chinese population
Authors
KeywordsDyspepsia
Low‐grade inflammation
SNP
TGFB1
Issue Date2019
PublisherWiley-Blackwell. The Journal's web site is located at http://www.wiley.com/bw/journal.asp?ref=1350-1925&site=1
Citation
Neurogastroenterology and Motility, 2019, v. 31 n. 10, p. article no. e13681 How to Cite?
AbstractBackground We previously published that altered expression of gastric TRPV1, BDNF, and peripheral cytokines was present in patients with functional dyspepsia. We herein examine whether genetic predisposition in altered biomarkers influences dyspeptic, sleep, and mood symptoms in patients with FD without previous infection. Methods Consecutive adult FD patients (Rome III) with no recent history of gastroenteritis and asymptomatic age‐ and sex‐matched healthy controls were recruited for upper endoscopy. Subjects with GERD and IBS as predominant symptoms, diabetes mellitus, current or previous H pylori infection, psychiatric illness, and recent use of NSAID or PPI were excluded. The genetic associations with dyspeptic symptoms, sleep quality, and mood symptoms were evaluated. Genetic polymorphisms in TRPV1, TGFB1, TNF, COMT, BDNF, IL6, IL8, IL10, and IL12 were analyzed. Key results Twenty‐nine male FD patients and 104 female FD patients were age matched (±3 years) with 81 healthy subjects. All had postprandial distress syndrome (PDS) as predominant subtype (PDS: 130, EPS: 3). SNPs in TGFB1 showed significant associations in dyspeptic patients after age and sex adjustment [for RS4803455: in the codominant model (C/A, OR = 0.34 (0.18‐0.65), P = .004); in the dominant model (genotype C/C vs C/A‐A/A, OR = 0.42 (0.23‐0.77), P = .004); and in the overdominant model (genotype C/C‐A/A vs C/A, OR = 0.38 (0.21‐0.70), P < .001)] [for RS1800469: in dominant model (genotype A/A vs A/G‐G/G, OR = 0.52 (0.27‐0.99), P = .043)]. A allele in RS4803455 was associated with higher HADS depression score (P = .05) and epigastric burning sensation(P = .01). Conclusions and inferences Our data showed that dyspeptic patients predispose genetic difference in TGFB1 which may influence the severity of dyspepsia.
Persistent Identifierhttp://hdl.handle.net/10722/290607
ISSN
2023 Impact Factor: 3.5
2023 SCImago Journal Rankings: 1.312
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorCheung, CKY-
dc.contributor.authorLan, LL-
dc.contributor.authorChan, Y-
dc.contributor.authorYuen, K-
dc.contributor.authorCheong, PK-
dc.contributor.authorFan, F-
dc.contributor.authorWu, JCY-
dc.date.accessioned2020-11-02T05:44:37Z-
dc.date.available2020-11-02T05:44:37Z-
dc.date.issued2019-
dc.identifier.citationNeurogastroenterology and Motility, 2019, v. 31 n. 10, p. article no. e13681-
dc.identifier.issn1350-1925-
dc.identifier.urihttp://hdl.handle.net/10722/290607-
dc.description.abstractBackground We previously published that altered expression of gastric TRPV1, BDNF, and peripheral cytokines was present in patients with functional dyspepsia. We herein examine whether genetic predisposition in altered biomarkers influences dyspeptic, sleep, and mood symptoms in patients with FD without previous infection. Methods Consecutive adult FD patients (Rome III) with no recent history of gastroenteritis and asymptomatic age‐ and sex‐matched healthy controls were recruited for upper endoscopy. Subjects with GERD and IBS as predominant symptoms, diabetes mellitus, current or previous H pylori infection, psychiatric illness, and recent use of NSAID or PPI were excluded. The genetic associations with dyspeptic symptoms, sleep quality, and mood symptoms were evaluated. Genetic polymorphisms in TRPV1, TGFB1, TNF, COMT, BDNF, IL6, IL8, IL10, and IL12 were analyzed. Key results Twenty‐nine male FD patients and 104 female FD patients were age matched (±3 years) with 81 healthy subjects. All had postprandial distress syndrome (PDS) as predominant subtype (PDS: 130, EPS: 3). SNPs in TGFB1 showed significant associations in dyspeptic patients after age and sex adjustment [for RS4803455: in the codominant model (C/A, OR = 0.34 (0.18‐0.65), P = .004); in the dominant model (genotype C/C vs C/A‐A/A, OR = 0.42 (0.23‐0.77), P = .004); and in the overdominant model (genotype C/C‐A/A vs C/A, OR = 0.38 (0.21‐0.70), P < .001)] [for RS1800469: in dominant model (genotype A/A vs A/G‐G/G, OR = 0.52 (0.27‐0.99), P = .043)]. A allele in RS4803455 was associated with higher HADS depression score (P = .05) and epigastric burning sensation(P = .01). Conclusions and inferences Our data showed that dyspeptic patients predispose genetic difference in TGFB1 which may influence the severity of dyspepsia.-
dc.languageeng-
dc.publisherWiley-Blackwell. The Journal's web site is located at http://www.wiley.com/bw/journal.asp?ref=1350-1925&site=1-
dc.relation.ispartofNeurogastroenterology and Motility-
dc.rightsPreprint This is the pre-peer reviewed version of the following article: [FULL CITE], which has been published in final form at [Link to final article using the DOI]. This article may be used for non-commercial purposes in accordance with Wiley Terms and Conditions for Use of Self-Archived Versions. Postprint This is the peer reviewed version of the following article: [FULL CITE], which has been published in final form at [Link to final article using the DOI]. This article may be used for non-commercial purposes in accordance with Wiley Terms and Conditions for Use of Self-Archived Versions.-
dc.subjectDyspepsia-
dc.subjectLow‐grade inflammation-
dc.subjectSNP-
dc.subjectTGFB1-
dc.titleFunctional dyspepsia susceptibility is associated with TGFB1 gene polymorphisms (RS4803455, RS1800469) in H pylori‐negative Chinese population-
dc.typeArticle-
dc.identifier.emailCheung, CKY: ckyc@hku.hk-
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1111/nmo.13681-
dc.identifier.pmid31386263-
dc.identifier.scopuseid_2-s2.0-85070706857-
dc.identifier.hkuros318304-
dc.identifier.volume31-
dc.identifier.issue10-
dc.identifier.spagearticle no. e13681-
dc.identifier.epagearticle no. e13681-
dc.identifier.isiWOS:000480102500001-
dc.publisher.placeUnited Kingdom-
dc.identifier.issnl1350-1925-

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