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The effect of diabetes mellitus on organ dysfunction with sepsis: an epidemiological study

Annette M Esper email, Marc Moss email and Greg S Martin email

Critical Care 2009, 13:R18doi:10.1186/cc7717



See related commentary by Yende and van der Poll, http://ccforum.com/content/13/1/117

Infection susceptibility in diabetes

Heikki Savolainen   (20 February 2009)  Dept. of Occup. Safety & Hlth., Tampere, Finland email

The increased susceptibility to generalized infections in diabetes can be compared with the increased risk for active tuberculosis in the same patients (1).

As to the mechanism, it may be suggested that the downstream metabolites of the excessive glucose concentration are toxic to the immunological regulatory system. The principal intermediate methylglyoxal downregulates the Raf-1 thereby attenuating the system (2).

An idea of the circulating methylglyoxal concentration can be had by the urinalysis for D-lactic acid, its eventual metabolite (3).

1 Murray JCY. Diabetes mellitus increases the risk of active tuberculosis. A systematic review of 13 observational studies. PLoS Med 2008; 5: e152.

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

3 Talasniemi JP, Pennanen S, Savolainen H, et al. Assay of D-lactate in diabetic plasma and urine. Clin Biochem 2008; 41: 1099

Competing interests

None

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