BIOCHEMICAL-EVIDENCE OF THIAMINE DEPLETION DURING THE CUBAN NEUROPATHY EPIDEMIC, 1992-1993

During an epidemic outbreak of neuropathy in Cuba during 1992-1993, bl ood and urine samples were collected from 107 persons with confirmed n europathy, from 106 control subjects without clinical abnormality who were broadly matched with the affected persons by age and domicile, an d from 537 unmatched subjects, also free from clinical abnormality. Th e unmatched subjects lived in two locations in Cuba; at each location they were drawn from two age ranges: 11-15-y-old secondary school stud ents and 16-64-y-old adults. Measurements of urinary thiamine and bloo d transketolase and its activation with thiamine pyrophosphate were ma de. For the neuropathy subjects, these measurements were repeated afte r 3 wk of rehabilitation. All groups showed biochemical evidence of th iamine depletion affecting 30-70% of their members, which is a high pr evalence. Severity of biochemical depletion was, however, no greater i n the neuropathy subjects than in the control subjects (P > 0.05). How ever, it was greater in Pinar del Rio, where the incidence of disease was higher, than in the city of Havana, where less disease was seen. A lthough the majority of the affected subjects responded biochemically to a daily oral multivitamin supplement containing thiamine (P < 0.001 ), in some cases normal biochemical status was not achieved even after 3 wk of intensive treatment. In the affected group, thiamine status w as inversely correlated with the amount of alcohol consumed (P = 0.007 ). Thiamine status at the outset was correlated with clinical outcome after treatment. Although neither thiamine depletion nor alcohol abuse were likely to have been the sole cause of the neuropathy epidemic, t hey may have been contributory factors. Thiamine supplementation or fo od fortification may therefore be necessary in Cuba.