Thiamine participates as a cofactor in oxidative phosphorylation, and its absence is sorely missed.
Historically, this is a cause of lactic acidosis in the malnourished patient in who there is no other apparent cause of lactic acidosis.
Among its many uses, thiamine acts as a coenzyme with pyruvate dehydrogenase to form acetyl-CoA. So of course, if you completely abolish thiamine, there will be no entry for pyruvate into Krebs cycle. And even if it could enter, alpha-ketoglutarate dehydrogenase would also need thiamine as a coenzyme to convert alpha-ketoglutarate into succynyl coenzyme A. Thus, a deficiency of thiamine produces an excess of lactate by preventing pyruvate from becoming a substrate for oxidative metabolism.
It seems pretty difficult to become so thiamine deficient that it would produce a clinically relevant lactic acidosis. The case reports in the literature all seem to involve people on TPN in whom multivitamins are accidentally not administered.
One can easily envision a developing world environment where this sort of nutritional deficiency is commonplace. However, it seems this problem can also exist in the nutritionally competent West. Specifically, people on long-term frusemide (a huge proportion of the ICU population) seem to have a thiamine deficiency due to a constant urinary loss. And yes, it is a deficiency which is relevant to their outcome- the patients in that study all had an improvement in their systolic function once thiamine was replaced at 100mg IV per day, for 7 days.
In this way, one might argue that the hopelessly shocked cardiac patient could benefit from thiamine supplementation, and is unlikely to be harmed by it, which is a strong argument for supplementing everybody.
But of course these are occult thiamine deficits. Nobody expected those frusemide-intoxicated patients to develop a thiamine deficiency. The chronic alcoholic, on the other hand, is at risk of this every day; the term “wet beriberi” is used to describe the cardiovascular collapse which ensues, which is typically associated with a lactic acidosis.
Red cell transketolase is an enzyme of the pentose pathway which is affected by the presence of thiamine; its activity is decreased in the absence of thiamine (which it uses as a cofactor). Its increased activity with the addition of thiamine in the laboratory (measured by red cell NADH consumption) is used as an indirect evidence of thiamine deficiency.