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Research Article

Diabetes Mellitus Increases the Risk of Active Tuberculosis: A Systematic Review of 13 Observational Studies

  • Christie Y Jeon mail,

    To whom correspondence should be addressed. E-mail: chjeon@hsph.harvard.edu

    Affiliation: Department of Epidemiology, Harvard School of Public Health, Boston, Massachusetts, United States of America

    X
  • Megan B Murray

    Affiliation: Department of Epidemiology, Harvard School of Public Health, Boston, Massachusetts, United States of America

    X
  • Published: July 15, 2008
  • DOI: 10.1371/journal.pmed.0050152

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Diabetes and tuberculosis activation

Posted by plosmedicine on 31 Mar 2009 at 00:28 GMT

Author: Heikki Savolainen
Position: Professor
Institution: Dept. of Occup. Safety & Hlth., Tampere, Finland
E-mail: heikki.savolainen@stm.fi
Submitted Date: August 08, 2008
Published Date: August 11, 2008
This comment was originally posted as a “Reader Response” on the publication date indicated above. All Reader Responses are now available as comments.

This highly interesting analysis is biologically plausible. Its metabolic mechanisms may include the accumulation of methylglyoxal (MG) from the excessive glucose. MG is known to interfere with signal transmission molecules like Raf-1, a protein ser/thr kinase (1). This could attenuate the macrophage functions.

An analogous example is the increased pulmonary tuberculosis risk in the occupational exposure to silica dust. Phagocytosed quartz particle induce the phagocytic cell death.

An idea of the circulating MG can be had by urinalysis for D-lactate (2).

1 Du J, Zen J, Ou X, et al. Methylglyoxal downregulates Raf-1 protein through a ubiquination-mediated mechanism. Int J Biochem Cell Biol, 2006; 38: 1084

2 Talasniemi JP, Pennanen S, Savolainen H, et al. Analytical investigation: Assay of D-lactate in diabetic plasma and urine. Clin Biochem, 2008, doi:10.1016/j.clinbiochem2008.06.11

No competing interests declared.