Дефіцит молібдену

ЗаLarry E. Johnson, MD, PhD, University of Arkansas for Medical Sciences
ПереглянутоGlenn D. Braunstein, MD, Cedars-Sinai Medical Center
Переглянуто/перевірено Змінено трав. 2025
v886419_uk

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 (1). 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 decreased activity of sulfite oxidase and sulfite toxicity occurred in a patient receiving long-term total parenteral nutrition. 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.

Довідковий матеріал

  1. 1. Johannes L, Fu CY, Schwarz G. Molybdenum Cofactor Deficiency in Humans. Molecules. 2022 Oct 14;27(20):6896. doi: 10.3390/molecules27206896