Background

Molybdenum is a trace mineral which is required for the proper function of certain enzymes in the body.  

It is important in biological processes including metabolism of sulfur-containing amino acids, purines, and pyrimidines. 

Molybdenum is present in high amounts in legumes, grains, and organ meats. 

Molybdenum is component of some enzymes as follows: 

Sulfite oxidase 

Xanthine oxidase 

Aldehyde oxidase 

Molybdenum deficiency causes inability to form essential molybdenum coenzyme. 

It reduced sulfite enzyme activity and toxicity in patient with parenteral nutrition. The deficiency may cause intellectual disability, seizures, and lens dislocation. 

Epidemiology

Molybdenum deficiency is rare in the general population as minerals are available in many foods/products. 

Most populations consume adequate molybdenum levels. Molybdenum deficiency documented in patients on TPN. 

Recommended dietary allowance of molybdenum for adults is 45 mcg daily depending on age and gender. 

Long-term total parenteral nutrition (TPN) without proper mineral supplementation is risky to health. Insufficient molybdenum in TPN and IV reliance cause deficiency risks. 

Anatomy

Pathophysiology

Sulfite disrupts neurotransmitters to cause oxidative stress and damage brain development. 

Aldehyde oxidase promotes aldehyde oxidation to carboxylic acids in form of drug and toxin metabolism. 

Molybdenum enzyme disruption increases oxidative stress from reactive intermediate buildup. 

Aldehyde oxidase and mARC deficiency are responsible to cause toxic metabolite buildup in body.  

Etiology

• Causes for molybdenum deficiency are: 
• Prolonged Parenteral Nutrition 
• Inadequate Dietary Intake 
• Poor Soil Content 
• Gastrointestinal Disorders 
• Renal Disorders 

Genetics

Prognostic Factors

It has poor prognosis due to severe neurological damage, but early treatment can improve outcomes. 

Early detection helps to prevents long-term consequences of molybdenum deficiency. 

Delayed treatment worsens symptoms and prognosis in severe neurological cases. 

Neurological damage in molybdenum deficiency is a crucial factor in prognosis. 

Clinical History

Molybdenum deficiency affects individuals of any age group from infants to adults. 

Physical Examination

• Neurological Examination 
• Gastrointestinal Examination 
• Visual Examination 
• Cardiovascular Examination 

Age group

Associated comorbidity

Associated activity

Acuity of presentation

Acute symptoms are: 

Seizures, mental confusion, visual changes, rapid neurological decline 

Subacute to Chronic symptoms are: 

Headache, lethargy, and cognitive difficulties, Metabolic disturbances 

Differential Diagnoses

• Epileptic Disorders 
• Copper Deficiency 
• Celiac Disease 
• Xanthinuria 
• Inherited Metabolic Disorders 

Laboratory Studies

Imaging Studies

Procedures

Histologic Findings

Staging

Treatment Paradigm

Oral supplements in form of molybdenum used for dietary deficiency. 

Parenteral molybdenum for severe deficiency in TPN patients or unable to take oral supplements. 

Encourage molybdenum-rich foods such as legumes, grains, veggies, and organ meats.  

Monitor molybdenum levels and enzymes, adjust supplementation according to follow-up results. 

Anticonvulsants drugs should be recommended to control seizures and provide neurorehabilitation therapy to treat impairments. 

by Stage

by Modality

Chemotherapy

Radiation Therapy

Surgical Interventions

Hormone Therapy

Immunotherapy

Hyperthermia

Photodynamic Therapy

Stem Cell Transplant

Targeted Therapy

Palliative Care

use-of-non-pharmacological-approach-for-deficiency-of-molybdenum

Make molybdenum supplements accessible to those with deficiency or at-risk with dosage instructions. 

Collaborate with dietitian for balanced diet to achieve nutritional needs for deficiency-prone individuals. 

Regular check-ups and blood tests needed for those at risk of molybdenum deficiency. 

Promote balanced diets and trace nutrients in schools and workplaces through nutritional Programs. 

Proper education and awareness about molybdenum deficiency should be provided and its related causes with management strategies. 

Appointments with a physician and preventing recurrence of disorder is an ongoing life-long effort. 

Use of Enzymes/trace elements

Molybdenum: 

It is a cofactor present in xanthine, aldehyde, and sulfite oxidase. The tetra-thiomolybdate complexes combine copper in gastrointestinal tract and blood to decrease toxicity. 

Use of Anticonvulsants

Phenytoin: 

It is used to manage seizures associated with severe molybdenum deficiency. 

use-of-intervention-with-a-procedure-in-treating-deficiency-of-molybdenum

Intervention for molybdenum deficiency involves a combination of medical procedures, dietary adjustments, and supportive care.  

In medical interventions use of oral molybdenum supplements and enzyme replacement therapy is recommended. 

use-of-phases-in-managing-deficiency-of-molybdenum

In the initial diagnosis phase, evaluation of medical history and blood test to confirm diagnosis. 

Pharmacologic therapy is effective in the treatment phase as it includes use of enzymes, anticonvulsants and some therapy intervention. 

In supportive care and management phase, patients should receive required attention such as lifestyle modification and intervention therapies. 

The regular follow-up visits with the physician are scheduled to check the improvement of patients along with treatment response. 

Medication

Future Trends

Media Gallary

References

Molybdenum – PMC (nih.gov) 

Molybdenum Cofactor Deficiency – GeneReviews® – NCBI Bookshelf (nih.gov)