Factors influencing the uptake of vitamin B 12 by normoblastic and vitamin B 12 -deficient bone marrow cells.
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Vitamin B(12) deficiency (B(12)D) has a wide variety of neurological symptoms and signs. However, cerebellar dysfunction and cranial neuropathies other than optic neuropathy have been rarely reported. Herein, we describe two cases of unusual neurological manifestations of B(12)D. One patient showed prominent hoarseness with vocal cord paralysis, myelopathy, and peripheral neuropathy. The other had gait disturbance, lateral gaze limitation and cerebellar dysfunction in addition to the typical manifestations of subacute combined degeneration. Vitamin B(12) deficiency can rarely affect cerebellum and cranial nerves other than optic nerve.
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1. The effect of the administration of vitamin B(12) and biotin on the metabolic pattern of vitamin B(12) in biotin-deficient rats was studied. 2. No significant changes in the absorption and excretion of orally administered [(58)Co]vitamin B(12) were noted either in vitamin B(12)-treated and or in biotin-fed rats. A significant decrease of the uptake of orally given [(58)Co]vitamin B(12) was observed in the liver and kidneys of biotin-treated rats, whereas an increase of uptake in the kidneys of vitamin B(12)-treated rats was noted as compared with biotin-deficient animals. 3. No significant difference in the excretion of radioactivity was noted between biotin deficient and biotin-fed rats when [(58)Co]vitamin B(12) was administered by injection. A small decrease was observed in vitamin B(12)-treated rats. The retention of injected [(58)Co]vitamin B(12) by major organs of biotin-treated rats was lower than that of biotin-deficient rats. A lower content of [(58)Co]vitamin B(12) was also detected in the organs, with the exception of the kidneys, of vitamin B(12)-treated rats. 4. These results are discussed in terms of an interrelationship between biotin and vitamin B(12).
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Serum vitamin B(12) radioimmunoassays may give falsely low results in patients with folate deficiency, multiple myeloma, megadose of vitamin C and following radioisotope organ scan. We evaluated 10 consecutive healthy women on oral contraceptives (OC) who had falsely low vitamin B(12) levels, as reflected by normal urine methylmalonic acid and plasma homocysteine. After 1-month cessation of OCs, vitamin B(12) returned to the normal range in all women. Transcobalamin I (TCI) blood level was decreased in 60% of patients. OCs may cause temporary low vitamin B(12) blood levels of no clinical significance that can be associated with low TCI levels
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Vitamin B(12) and folate are two vitamins that have interdependent roles in nucleic acid synthesis. Deficiencies of either vitamin can cause megaloblastic anemia; however, inappropriate treatment of B(12) deficiency with folate can cause irreversible nerve degeneration. Inadequate folate nutrition during early pregnancy can cause neural tube defects in the developing fetus. In addition, folate and vitamin B(12) deficiency and the compensatory increase in homocysteine are a significant risk factor for cardiovascular disease. Laboratory support for the diagnosis and management of these multiple clinical entities is controversial and somewhat problematic. Automated ligand binding measurements of vitamin B(12) and folate are easiest to perform and widely used. Unfortunately, these tests are not the most sensitive indicators of disease. Measurement of red cell folate is less dependent on dietary fluctuations, but these measurements may not be reliable. Homocysteine and methylmalonic acid are better metabolic indicators of deficiencies at the tissue level. There are no "gold standards" for the diagnosis of these disorders, and controversy exists regarding the best diagnostic approach. Healthcare strategies that consider the impact of laboratory tests on the overall costs and quality of care should consider the advantages of including methylmalonic acid and homocysteine in the early evaluation of patients with suspected deficiencies of vitamin B(12) and folate.
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