Molybdenum is a trace metal. Severe deficiency in molybdenum can cause clinical findings.
Molybdenum cofactor is required for activity of sulfite oxidase. Sulfite oxidase normally oxidizes the sulfite to nontoxic sulfate. Sulfite is produced during catabolism of methionine and cysteine, and it is neurotoxic.
Molybdenum also impacts xanthine oxidase-dehydrogenase, interfering with the metabolism of purines to uric acid.
Risk factors for developing a deficiency:
(1) total parenteral nutrition
(2) severe malnutrition
(3) severe short bowel syndrome
Clinical findings:
(1) headache
(2) disorientation and lethargy
(3) altered mental status
(4) night blindness
(5) tachycardia
(6) nausea and vomiting
(7) possibly symptoms resembling amyotrophic lateral sclerosis
Symptoms may worsen if a sudden load of purines or sulfites is delivered.
Laboratory findings:
(1) elevated serum methionine
(2) low serum and urine uric acid
(3) low serum molybdenum
The diagnosis is supported if the clinical findings reverse upon administration of molybdenum (ammonium molybdate).
