Low holotranscobalamin II is the earliest serum marker for subnormal vitamin B12 (cobalamin) absorption in patients with AIDS

Abstract

In AIDS, as previously found in pernicious anemia (PA), the earliest serum marker of subnormal vitamin B₁₂ (cobalamin) absorption, and therefore of negative B₁₂ balance, is low serum holotranscobalamin II (holo‐TC II; B₁₂‐TC II) despite normal total serum B₁₂ level, normal serum homocysteine, and normal classic (oral free radio‐B₁₂) Schilling test. This may be accompanied by subtle and insidious damage to hematopoietic, immunologic, neuropsychiatric, nutritional and alimentary systems, confirmed by correction on therapeutic trial with B₁₂ therapy. Our studies suggest such selective B₁₂ deficiency occurs in about half of the HIV‐1 infected, in part due to frequent depression of B₁₂ absorption by HIV‐1 attack on the gastric mucosa and/or opportunistic infection attack on the small bowel, and in part due to a telescoping of the continuum of the stages of negative B₁₂ balance in relation to damage to B₁₂ delivery by the infective and/or systemic disease process. In AIDS, when total serum B₁₂ is normal despite tissue depletion of B₁₂, if the classic Schilling test does not reveal subnormal food B₁₂ absorption, the food Schilling test does. We hypothesize that DNA‐synthesizing cells of the hematopoietic, immunologic, neurologic and other systems which have surface receptors solely for holo‐TC II, and which have low B₁₂ stores, rapidly become dysfunctional due to B₁₂ deficiency when holo‐TC II is low, while cells (such as liver cells) which also have surface receptors for holohaptocorrin (B₁₂‐haptocorrin) remain B₁₂‐replete. We believe this to be another example of the concept of selective nutrient deficiency in one cell line but not another.