The role of other vitamin deficiencies

The clinical syndrome of beri-beri is seen sporadicedly in Nigeria, and an aetiological relationship to thiamine deficiency presumed from the therapeutic response to this vitamin. An implied relationship to the W. African ataxic neuropathy is sometimes suggested, but has been rejected because abnormalities of pyruvate metabolism are usually slight [39]. 

As mentioned earlier, Moore suggested that riboflavin deficiency was, in part, responsible for the occurrence of the syndrome, and certainly riboflavin intake tends to be low because of the limited intake of animal protein. The clinical signs of riboflavin deficiency—angular stomatitis and flexural dermatitis—are almost certainly non-specific effects of depressed tissue oxidation, and could be a direct or an indirect effect of cyanide itself. Although one report [39] suggested that riboflavin deficiency was slight in this area, more refined studies are required to decide whether or not coexisting riboflavin deficiency and delayed cyanide detoxication may not potentiate their adverse effect on neuronal metabolism. 

The infrequent development of major neurological abnormalities in a small proportion of patients with vitamin B12 deficiency is still unexplained. 

Under normal conditions, there is an equilibrium between cyanide and thiocyanate in blood dependent on  

It has been suggested that the equilibrium is upset when vitamin Bj2 is deficient, but that the equilibrium is restored through the reduction in red cell mass as anaemia develops. 

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