Drug Induced Vitamin B2 Deficiency

It was noted in Section 10.8.1 that nitrous oxide causes inhibition ofmethionine synthetase, as a result of irreversible oxidation of the cobalt of methylcobal-amin. Patients with hitherto undiagnosed vitamin B12 deficiency can develop neurological signs after surgery when nitrous oxide is used as the anesthetic agent. There are a number of reports of neurological damage because of vitamin B12 depletion among people occupationally exposed to nitrous oxide (especially dental surgeons).

The histamine H2 receptor antagonists and proton pump inhibitors used to treat gastric ulcers and gastroesophageal reflux act by reducing the secretion of gastric acid considerably. Prolonged use will result in impairment of protein-bound vitamin B12 absorption. A number of studies have shown that even prolonged use of these drugs does not lead to significant depletion of vitamin B12 reserves.


A number of methods have been developed to permit assessment of folate and vitamin B12 nutritional status and to differentiate between deficiency of the vitamins as a cause of megaloblastic anemia. Obviously, detection of antibodies to intrinsic factor or gastric parietal cells will confirm autoimmune pernicious anemia rather than nutritional deficiency of either vitamin.

In addition to the methods described here, measurement of urinary ac-etamido p-aminobenzoyl glutamate will reflect folate turnover (Section 10.2.3) and incorporation of uracil, instead of thymidine into the DNA in leukocytes or lymphocytes may provide a sensitive index of folate status.

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