Genetic and nutritional molybdenum deficiency have been documented in rare cases. A genetically caused Sulfitoxidasemangel was described in 1967 in a child. It resulted from the inability to form the Molybdäncoenzym although molybdenum was plentiful. The shortage led to mental retardation, seizures, opisthotonos and lens luxation.

Molybdenum (Mo) is a component of coenzymes, which are necessary for the activity of xanthine oxidase, aldehyde oxidase and sulfite oxidase. Genetic and nutritional molybdenum deficiency have been documented in rare cases. A genetically caused Sulfitoxidasemangel was described in 1967 in a child. It resulted from the inability to form the Molybdäncoenzym although molybdenum was plentiful. The shortage led to mental retardation, seizures, opisthotonos and lens luxation. A molybdenum deficiency, which led to a Sulfitintoxikation, occurred in a completely parenteral nutrition for long-term patients. As symptoms tachycardia, tachypnea, headache, nausea, vomiting and coma showed. Laboratory tests pointed to high sulfite and xanthine levels as well as to low sulfate and uric acid levels in the blood and urine. Intravenous administration of 300 micrograms daily ammonium led to very rapid recovery. A case of molybdenum toxicity has occurred may 1,961th This produced gout symptoms and abnormalities of the digestive tract, liver and kidneys.

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