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]
Descriptions 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.
Diagnosisedit
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300 mcg Ammonium Molybdate per day can bring about recovery of “acquired molybdenum deficiency” [3]
molybdenum, deficiency, this, article, about, molybdenum, deficiency, humans, same, deficiency, plants, plant, disorder, refers, clinical, consequences, inadequate, supplies, molybdenum, diet, molybdenumspecialtyendocrinology, amount, molybdenum, required, rel. This article is about molybdenum deficiency in humans For the same deficiency in plants see Molybdenum deficiency plant disorder Molybdenum deficiency refers to the clinical consequences of inadequate supplies of molybdenum in the diet Molybdenum deficiencyMolybdenumSpecialtyEndocrinology 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 Contents 1 Signs and symptoms 2 Diagnosis 3 Treatment 4 See also 5 References 6 Further reading 7 External linksSigns 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 editThis section is empty You can help by adding to it November 2017 Treatment editThis section is empty You can help by adding to it November 2017 300 mcg Ammonium Molybdate per day can bring about recovery of acquired molybdenum deficiency 3 See also editMolybdenum cofactor deficiencyReferences 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 amp Dohme Corp Retrieved 2008 11 29 Further reading editNielsen 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 External links edit nbsp This article about an endocrine nutritional or metabolic disease is a stub You can help Wikipedia by expanding it vte Retrieved from https en wikipedia org w index php title Molybdenum deficiency amp oldid 1121548217, wikipedia, wiki, book, books, library,
