Origins and extinctions: paleontology in Chicago.
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Biomedical subjects
Publications and source records attributed to R A Kerr.
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In 60 thiamine deficient patients, the mean erythrocyte transketolase activity after activation by thiamine diphosphate cofactor in vitro, representing the apparent sum of holoenzyme and apoenzyme activities, was 0.609 (SD 0.166) U/g Hb before thiamine therapy and rose to 0.772 (SD 0.152) U/g Hb immediately after the administration of thiamine to the patients. The difference between these values, 0.163 (SD 0.130) U/g, is the mean activity of transketolase protein which can be activated by thiamine in vivo but not by thiamine diphosphate in vitro. This difference correlated with low initial erythrocyte transketolase activity in these patients, but not with their alcohol intake, liver function or diagnoses.
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Patients (n = 104) were judged to be thiamine deficient by the criteria of erythrocyte transketolase activity (ETK) less than 0.6 U/g of hemoglobin, or greater than 17% increase in this activity on addition of thiamine pyrophosphate in vitro (TPP effect). ETK activated by TPP in vitro (AETK) was related to ETK by a linear regression of slope greater than or equal to 1, implying that transketolose apoenzyme (apoTK) was constant or decreased as ETK decreased. For most patient groups the value of apoTK was 0.1 U/g and the slope 1.033 to 1.050. In the subgroup of non-vomiting drinkers with Wernicke's encephalopathy (WE), the slope of the linear regression of AETK on ETK was 1.21, so that apoTK decreased as ETK decreased. Comparison of these data is consistent with a difference in the TK of WE drinkers from that of others. Generally, any variation of TPP effect was due only to variation of ETK. We recommend measurement of ETK, without TPP effect, for the assessment of thiamine nutrition.
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