ArticleDiabetology & metabolic syndrome2023
Unraveling genetic causality between type 2 diabetes and pulmonary tuberculosis on the basis of Mendelian randomization.
Article in Diabetology & metabolic syndrome, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 11 citations in OpenAlex.
- Concurrent pulmonary candidiasis and tuberculosis in type 2 diabetes mellitus: immune pathogenesis and multidisciplinary management challenges: a case report.Journal of medical case reports · 2026Article
- Integrative transcriptomic and genomic insights into diabetic kidney disease: evidence from multi-omics analysis and experimental validation.Renal failure · 2025Article
- Assessing Causality Between Endocrine, Nutritional, and Metabolic Disease and Pulmonary Tuberculosis: A Mendelian Randomization Study.Health science reports · 2025Article
- The Role and Potential Application of IL-12 in the Immune Regulation of Tuberculosis.International journal of molecular sciences · 2025Review
- Diabetes and tuberculosis: a systematic review and meta-analyis of mendelian randomization evidence.Diabetology & metabolic syndrome · 2025Review
- Clinical and Mycobacterium tuberculosis strain characteristics of tuberculosis patients with diabetes mellitus in Changping District, Beijing, China.BMC infectious diseases · 2025Article
- Genetic Association between Lipid-Regulating Drug Targets and Diabetic Retinopathy: A Drug Target Mendelian Randomization Study.Journal of lipids · 2024Article
- Intersecting epidemics: deciphering the complexities of tuberculosis-diabetes comorbidity.Frontiers in tuberculosis · 2024Review
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Authors and funding
7 authors at 3 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
backgroundThe comorbidity rate between type 2 diabetes mellitus (T2DM) and pulmonary tuberculosis (PTB) is high and imposes enormous strains on healthcare systems. However, whether T2DM is causally associated with PTB is unknown owing to limited evidence from prospective studies. Consequently, the present study aimed to clarify the genetic causality between T2DM and PTB on the basis of Mendelian randomization (MR) analysis.
methodsGenetic variants for T2DM and PTB were obtained from the IEU OpenGWAS project. The inverse variance weighted method was used as the main statistical analysis method and was supplemented with MR-Egger, weighted median, simple mode, and weighted mode methods. Heterogeneity was analyzed using Cochran's Q statistic. Horizontal pleiotropy was assessed using the MR-PRESSO global test and MR-Egger regression. Robustness of the results was verified using the leave-one-out method.
resultsA total of 152 independent single-nucleotide polymorphisms (SNPs) were selected as instrumental variables (IVs) to assess the genetic causality between T2DM and PTB. Patients with T2DM had a higher risk of PTB at the genetic level (odds ratio (OR) for MR-Egger was 1.550, OR for weighted median was 1.540, OR for inverse variance weighted was 1.191, OR for simple mode was 1.629, OR for weighted mode was 1.529). There was no horizontal pleiotropy or heterogeneity among IVs. The results were stable when removing the SNPs one by one.
conclusionsThis is the first comprehensive MR analysis that revealed the genetic causality between T2DM and PTB in the East Asian population. The study provides convincing evidence that individuals with T2DM have a higher risk of developing PTB at the genetic level. This offers a significant basis for joint management of concurrent T2DM and PTB in clinical practice.
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