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1.
BMC Endocr Disord ; 24(1): 40, 2024 Mar 20.
Artículo en Inglés | MEDLINE | ID: mdl-38504196

RESUMEN

PURPOSE: Previous observational studies have revealed a potential link between non-alcoholic fatty liver disease (NAFLD) and gestational diabetes mellitus (GDM), but their causal relationship remains unclear. Thus, this study aimed to examine whether a causal link exists between genetically determined NAFLD and GDM. METHODS: Utilizing publicly accessible genome-wide association studies (GWAS), a two-sample bidirectional Mendelian randomization (MR) analysis was conducted. The GWASs data pertaining to NAFLD and GDM were obtained from the UK Biobank Consortium and FinnGen database in primary analysis, respectively. The random-effects inverse variance weighted (IVW) method was utilized as primary analysis method. Several sensitivity analyses were utilized to verify the robustness of the results. Additionally, we also analyzed the causal effect of potential shared influencing factors on these two conditions. RESULTS: The result of the IVW method showed that there was no significant causal relationship between genetically determined NAFLD and GDM (OR = 0.98, 95% CI: 0.90-1.07, P = 0.691). Similarly, our reverse MR analysis failed to detect a significant causal effect of GDM on NAFLD (OR = 1.14, 95% CI: 0.97-1.36, P = 0.118). Sensitivity analyses further confirmed the robustness of the results. Moreover, we found that genetically determined body mass index, waist-to-hip ratio, triglycerides, and television viewing time may be positively correlated with NAFLD and GDM, while high-density lipoprotein cholesterol and apolipoprotein A-I may both be negatively correlated with NAFLD and GDM. CONCLUSIONS: The current bidirectional MR study failed to provide sufficient genetic evidence for the causal relationship between NAFLD and GDM.


Asunto(s)
Diabetes Gestacional , Enfermedad del Hígado Graso no Alcohólico , Humanos , Femenino , Embarazo , Diabetes Gestacional/epidemiología , Diabetes Gestacional/genética , Enfermedad del Hígado Graso no Alcohólico/etiología , Enfermedad del Hígado Graso no Alcohólico/genética , Estudio de Asociación del Genoma Completo , Análisis de la Aleatorización Mendeliana , Índice de Masa Corporal
2.
Ther Adv Chronic Dis ; 14: 20406223231155119, 2023.
Artículo en Inglés | MEDLINE | ID: mdl-36890981

RESUMEN

Background and Objectives: Recent observational studies have investigated the association between Helicobacter pylori (H. pylori) infection and pancreatic cancer with conflicting data. Therefore, we conducted a systematic review and meta-analysis to assess the potential association. Design: This is a systematic review and meta-analysis. Methods: We searched three databases (PubMed, Embase, and Web of Science) from inception to 30 August 2022. The summary results as odds ratio (OR) or hazard ratio (HR) with 95% confidence interval (CI) were pooled by generic inverse variance method based on random-effects model. Results: A total of 20 observational studies involving 67,718 participants were included in the meta-analysis. Meta-analysis of data from 12 case-control studies and 5 nested case-control studies showed that there was no significant association between H. pylori infection and the risk of pancreatic cancer (OR = 1.20, 95% CI = 0.95-1.51, p = 0.13). Similarly, we also did not find significant association between cytotoxin-associated gene A (CagA) positive strains, CagA negative strains, vacuolating cytotoxin gene A (VacA) positive strains H. pylori infection, and the risk of pancreatic cancer. Meta-analysis of data from three cohort studies showed that H. pylori infection was not significantly associated with an increased risk of incident pancreatic cancer (HR = 1.26, 95% CI = 0.65-2.42, p = 0.50). Conclusion: We found insufficient evidence to support the proposed association between H. pylori infection and increased risk of pancreatic cancer. To better understand any association, future evidence from large, well-designed, high-quality prospective cohort studies that accounts for diverse ethnic populations, certain H. pylori strains, and confounding factors would be useful to settle this controversy.

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