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By Larry E. Johnson, MD, PhD, Associate Professor of Geriatrics and Family and Preventive Medicine; Medical Director, University of Arkansas for Medical Sciences; Central Arkansas Veterans Healthcare System

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Molybdenum (Mo) is a component of coenzymes necessary for the activity of xanthine oxidase, sulfite oxidase, and aldehyde oxidase.

Genetic and nutritional deficiencies of molybdenum have been reported but are rare. Genetic sulfite oxidase deficiency was described in 1967 in a child. It resulted from the inability to form the molybdenum coenzyme despite the presence of adequate molybdenum. The deficiency caused intellectual disability, seizures, opisthotonus, and lens dislocation.

Molybdenum deficiency resulting in sulfite toxicity occurred in a patient receiving long-term TPN. Symptoms were tachycardia, tachypnea, headache, nausea, vomiting, and coma. Laboratory tests showed high levels of sulfite and xanthine and low levels of sulfate and uric acid in the blood and urine. Ammonium molybdate 300 mcg/day IV caused dramatic recovery.

A case of molybdenum toxicity may have occurred in 1961; it caused goutlike symptoms and abnormalities of the GI tract, liver, and kidneys.