Molybdenum deficiency refers to the clinical consequences of inadequate intake of molybdenum in the diet.
Molybdenum deficiency | |
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Molybdenum | |
Specialty | Endocrinology ![]() |
The amount of molybdenum required is relatively small, and molybdenum deficiency usually does not occur in natural settings.[1] However, it can occur in individuals receiving parenteral nutrition.[2][3]
Signs and symptoms
editDescriptions of human molybdenum deficiency are few. A patient receiving prolonged parenteral nutrition acquired a syndrome described as ‘acquired molybdenum deficiency.’ This syndrome, exacerbated by methionine administration, was characterized by high blood methionine, low blood uric acid, and low urinary uric acid and sulfate concentrations. The patient suffered mental disturbances that progressed to a coma.[1] Pathological changes occurring in individuals with a genetic disease that results in a sulfite oxidase (a molybdoenzyme) deficiency include increased plasma and urine sulfite, sulfate, thiosulfate, S-sulfocysteine and taurine; seizures and brain atrophy/lesions; dislocated lenses; and death at an early age.
Diagnosis
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Treatment
edit300 mcg Ammonium Molybdate per day can bring about recovery of acquired molybdenum deficiency.[4]
See also
editReferences
edit- ^ a b "Molybdenum". Linus Pauling Institute. Oregon State University. Retrieved 2008-11-29.
- ^ Sardesai VM (December 1993). "Molybdenum: an essential trace element". Nutrition in Clinical Practice. 8 (6): 277–81. doi:10.1177/0115426593008006277. PMID 8302261.
- ^ Johnson LE (October 2018). "Molybdenum: Mineral Deficiency and Toxicity". Merck Manual Professional. Merck Sharp & Dohme Corp. Retrieved 2008-11-29.
- ^ "Ammonium molybdate Advanced Patient Information". Drugs.com. Retrieved 2024-02-01.
Further reading
edit- Nielsen FH (April 2003). "Trace Elements". In Caballero B, Finglas P, Toldra F (eds.). Encyclopedia of Food Sciences and Nutrition (Second ed.). Academic Press. pp. 5820–28. doi:10.1016/B0-12-227055-X/01204-9. ISBN 978-0-12-227055-0.