1. Chromato-bioautographic analysis of cobalamins in Nigerian subjects showed that in patients with tropical ataxic neuropathy as in normal control subjects methylcobalamin was the major form of vitamin B12 in plasma. Plasma cyanocobalamin was significantly higher in patients than control subjects. The concentration of plasma adenosylcobalamin in patients was about twice that in control subjects.

2. Adenosylcobalamin was the predominant liver cobalamin in all subjects. Cyanocobalamin was not detected in liver from normal subjects, but a small proportion of cyanocobalamin was detected in the liver in the majority of the patients.

3. The raised cyanocobalamin levels may have resulted from the chronic cyanide intoxication known to exist in these patients. There was no evidence of tissue vitamin B12 deficiency or that conversion of metabolically active cobalamins into cyanocobalamin plays a part in the pathogenesis of tropical ataxic neuropathy. However, the increase in plasma adenosylcobalamin does indicate some disturbance of bodily handling of cobalamins in this disease.

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