• S J Bakker, J C ter Maaten, S J Hoorntje, and R O Gans.
• Department of Medicine, University Hospital Vrije Universiteit, Amsterdam, The Netherlands.
• J. Intern. Med. 1997 Aug 1;242(2):179-83.

AbstractHyperlactataemia due to thiamine deficiency has so far only been reported in the setting of full-blown cardiovascular beriberi with congestive heart failure and systemic vasodilatation. Poor tissue oxygenation and impaired lactate clearance by the liver are generally accepted as underlying causes of the elevated lactate levels. We present an alcoholic patient with thiamine deficiency-induced hyperlactataemia and accompanying alcoholic ketoacidosis, who did not display the circulatory disturbances that are characteristic of cardiovascular beriberi. The hypothesis will be presented that the concomitant presence of alcoholic ketoacidosis has prevented haemodynamic deterioration. Putative mechanisms that could explain such an effect are discussed in detail, with special reference to the role of acetyl-CoA and adenosine.

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