Interrelationships between the B-vitamins in B₁₂-deficiency neuromyelopathy. A possible malabsorption-malnutrition syndrome

Abstract

Five patients presenting clinically with a form B₁₂-deficiency neuromyelopathy, with cord involvement in all and proximal muscle weakness in two of them, were investigated for their neurologic, hematologic and vitamin status. Megaloblastosis and achlorhydria were present in all, and impaired absorption of ⁵⁷Co vitamin B₁₂ and of D- xylose was detected in four. Total cyanide extracted vitamin B₁₂ (A) was lowered in all cases and noncyanide extractable (B) in four of the five, being zero in three. All five responded to injections of hydroxocobalamin. In two patients sequential estimations showed that both A and B, especially the latter, rose steeply initially, normalizing at 50% of A after some weeks. Moiety B is suggested to be physiologically the more active and dissociable form of vitamin B₁₂. Markedly elevated initial serum folate levels, and their subsequent fall under treatment with B₁₂, indicated the operation of the "methyltetrahydrofolate trap". Blood levels of thiamin, nicotinic acid and pantothenic acid were within normal limits. However, serum riboflavin (B₂) total vitamin B₆ and pyridoxal were reduced in all where tested. Vitamin B₆ deficiency could have resulted from its own malabsorption and have contributed to be B₁₂ deficiency. Vitamin B₂ and B₆ levels also corrected themselves on B₁₂ therapy. The B-vitamin deficiencies in our patients probably resulted from intestinal malabsorption, with a possible factor of malnutrition consequent to their strictly vegetarian diet.