[The assessment of the nutritional status of patients with epidemic neuropathy in the year of its evolution. The biochemical indicators]. / Evaluación del estado nutricional de enfermos con neuropatía epidémica al año de evolución. Indicadores bioquímicos.

The nutritional status of a group of patients with epidemic neuropathy (EN) was reevaluated after a one-year follow-up to observe the changes occurred and to assess their relationship with the individual clinical evolution. 71 patients (40 men and 31 women) were examined. 28 had optic epidemic neuropathy and 43 mixed epidemic neuropathy. Vitamins thiamine, niacin, A and E were determined and the values were compared with those of risk 21 days later. There was an improvement of these indicators after 21 days as a response to the treatment, and an increase one year later of the percentage of individuals deficient in or situated at the margin of thiamine and niacin, which reflects a nutritional unbalance without an apparent association with the clinical evolution that showed a trend towards the recovery of the patients. This disassociation between the clinics and the nutritional and vitamin status suggest that the pathogeny of the EN may be connected with non-nutritional factors. The deficiency found in the nutritional vitamin state could anticipate a worsening of the clinical picture and/or the appearance of clinical manifestations corresponding to deficiency diseases.

Biochemical evidence of thiamine depletion during the Cuban neuropathy epidemic, 1992-1993.

During an epidemic outbreak of neuropathy in Cuba during 1992-1993, blood and urine samples were collected from 107 persons with confirmed neuropathy, from 106 control subjects without clinical abnormality who were broadly matched with the affected persons by age and domicile, and from 537 unmatched subjects, also free from clinical abnormality. The unmatched subjects lived in two locations in Cuba; at each location they were drawn from two age ranges: 11-15-y-old secondary school students and 16-64-y-old adults. Measurements of urinary thiamine and blood transketolase and its activation with thiamine pyrophosphate were made. For the neuropathy subjects, these measurements were repeated after 3 wk of rehabilitation. All groups showed biochemical evidence of thiamine depletion affecting 30-70% of their members, which is a high prevalence. Severity of biochemical depletion was, however, no greater in the neuropathy subjects than in the control subjects (P > 0.05). However, 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. Although 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 was 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, they may have been contributory factors. Thiamine supplementation or food fortification may therefore be necessary in Cuba.