Jun Qian1,2, Zhangfa Song3, Yinxiang Lv4, Xuefeng Huang3, Binliang Mao5. 1. Department of Colorectal Surgery, Xinchang People's Hospital, Xinchang, China. 2. Department of Colorectal Surgery, Xinchang Affiliated Hospital of Wenzhou Medical University, Xinchang, China. 3. Department of Colorectal Surgery, Sir Run Run Shaw Hospital, Hangzhou, China. 4. Department of Oncology Surgery, Xinchang People's Hospital, Xinchang, China. 5. Department of Surgery, Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Abstract
BACKGROUND: The published literature contains conflicting results regarding the impact of the glutathione S-transferase T1 (GSTT1) null genotype on the susceptibility to inflammatory bowel disease. Therefore, we conducted a meta-analysis of observational studies to assess the association. METHODS: We searched four online databases for eligible studies. The odds ratio (OR) with 95% CI was used to assess the gene-disease association. We also performed subgroup analyses by type of inflammatory bowel disease and ethnicity. RESULTS: There were 16 individual studies from 11 publications included in the analysis. There were 3366 cases with inflammatory bowel disease and 6013 controls. The meta-analysis of all 16 studies showed the GSTT1 null genotype was associated with increased susceptibility to inflammatory bowel disease (OR = 1.98, 95%CI 1.39-2.84, P < 0.001). The subgroup analysis by ethnicity further identified an association between the GSTT1 null genotype and inflammatory bowel disease in Caucasians, Asians, and Africans. The GSTT1 null genotype was associated with both ulcerative colitis (OR = 1.96, P = 0.004) and Crohn's disease (OR = 2.01, P = 0.022). The GSTT1 null genotype was still significantly associated with ulcerative colitis (OR = 1.63, P < 0.0001) and Crohn's disease (OR = 1.40, P = 0.023) after adjusting for study heterogeneity. CONCLUSION: The GSTT1 null genotype is significantly associated with an increased susceptibility to inflammatory bowel disease and is a risk factor for both ulcerative colitis and Crohn's disease.
BACKGROUND: The published literature contains conflicting results regarding the impact of the glutathione S-transferase T1 (GSTT1) null genotype on the susceptibility to inflammatory bowel disease. Therefore, we conducted a meta-analysis of observational studies to assess the association. METHODS: We searched four online databases for eligible studies. The odds ratio (OR) with 95% CI was used to assess the gene-disease association. We also performed subgroup analyses by type of inflammatory bowel disease and ethnicity. RESULTS: There were 16 individual studies from 11 publications included in the analysis. There were 3366 cases with inflammatory bowel disease and 6013 controls. The meta-analysis of all 16 studies showed the GSTT1 null genotype was associated with increased susceptibility to inflammatory bowel disease (OR = 1.98, 95%CI 1.39-2.84, P < 0.001). The subgroup analysis by ethnicity further identified an association between the GSTT1 null genotype and inflammatory bowel disease in Caucasians, Asians, and Africans. The GSTT1 null genotype was associated with both ulcerative colitis (OR = 1.96, P = 0.004) and Crohn's disease (OR = 2.01, P = 0.022). The GSTT1 null genotype was still significantly associated with ulcerative colitis (OR = 1.63, P < 0.0001) and Crohn's disease (OR = 1.40, P = 0.023) after adjusting for study heterogeneity. CONCLUSION: The GSTT1 null genotype is significantly associated with an increased susceptibility to inflammatory bowel disease and is a risk factor for both ulcerative colitis and Crohn's disease.
Authors: Andrew Y F Li Yim; Nicolette W Duijvis; Mohammed Ghiboub; Catriona Sharp; Enrico Ferrero; Marcel M A M Mannens; Geert R D'Haens; Wouter J de Jonge; Anje A Te Velde; Peter Henneman Journal: J Clin Med Date: 2020-04-08 Impact factor: 4.241
Authors: Katarzyna Dziąbowska-Grabias; Małgorzata Sztanke; Przemysław Zając; Michał Celejewski; Katarzyna Kurek; Stanisław Szkutnicki; Patryk Korga; Włodzimierz Bulikowski; Krzysztof Sztanke Journal: Antioxidants (Basel) Date: 2021-03-09