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Vitamin E Deficiency

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Last Update: February 14, 2019.

Introduction

Vitamin E is all the following eight compounds alpha, beta, gamma, and delta-tocopherol and alpha, beta, gamma, and delta-tocotrienol. Alpha-tocopherol is the only compound of the eight that are known to meet human dietary needs. All of the vitamin E forms are absorbed in the small intestine, and then the liver metabolizes only alpha-tocopherol. The liver then removes and excretes the remaining vitamin E forms.[1][2][3][4]

Vitamin E deficiency is extremely rare in humans as it is unlikely caused by a diet consisting of low vitamin E. Rather, it tends to be caused by irregularities in dietary fat absorption or metabolism. Vitamin E is a lipid-soluble nutrient. Vitamin E may have a role in reducing atherosclerosis and lowering rates of ischemic heart disease. Premature infants have low vitamin E reserves due to vitamin E only able to cross the placenta in small amounts.

Etiology

In developed countries, it is unlikely that vitamin E deficiency occurs due to diet intake insufficiency and the more common causes are below.

  • Premature low birth weight infants with a weight less than 1500 grams (3.3 pounds)
  • Mutations in the tocopherol transfer protein causing impaired fat metabolism
  • Disrupted fat malabsorption as the small intestine requires fat to absorb vitamin E
  • Patients with cystic fibrosis patients fail to secrete pancreatic enzymes to absorb vitamins A, D, E, and K
  • Short-bowel syndrome patients may take years to develop symptoms. Surgical resection, mesenteric vascular thrombosis, and pseudo-obstruction are a few examples of this issue
  • Chronic cholestatic hepatobiliary disease leads to a decrease in bile flow and micelle formation that is needed for vitamin E absorption
  • Crohn's disease, exocrine pancreatic insufficiency, and liver disease may all not absorb fat
  • Abetalipoproteinemia an autosomal-recessive disease causes an error in lipoprotein production and transportation
  • Isolated vitamin E deficiency syndrome an autosomal recessive disorder of chromosome arm 8q

In developing countries, the most common cause is inadequate intake of vitamin E.

Epidemiology

Serum levels of alpha-tocopherol in 0.1% of United States adults over the age of 20 have been found to be deficient. Surveys of the same data set have shown that 89.8% of men and 96.3% of women 19 years of age or older have insufficient intake of alpha-tocopherol. Some studies have shown alpha-tocopherol to be lower in pediatric populations and higher in pregnancy.[5]

Pathophysiology

Vitamin E works as an antioxidant, immunomodulation and antiplatelet effects.

Antioxidant Effect

Vitamin E prevents propagated oxidation of saturated fatty acids within membranes. Also, vitamin E may prevent oxidative changes to LDLs, reducing coronary heart diseases.

Immunomodulation

Vitamin E decreases the production of prostaglandin E2 and serum lipid peroxides while enhancing lymphocyte proliferation.

Antiplatelet Effect

Vitamin E inhibits platelet adhesion by preventing oxidative changes to LDLs and inhibition of platelet aggregation by reducing prostaglandin E2. Another effect is inhibiting protein kinase C causing smooth-muscle proliferation.

Even though research has shown that vitamin E assists with the prevention of heart disease and atherosclerosis it has not been approved for this use by the United States Food and Drug Administration (FDA).

History and Physical

Patients may present with one of the causative histories listed along with symptoms of ataxia, difficulty with upward gaze, and hyporeflexia. Not as common symptoms include muscle weakness and visual-field constriction. The most severe symptoms are blindness, dementia, and cardiac arrhythmias.

If vitamin E deficiency is expected, a full neurological exam is recommended as well as a standard physical exam. Patients presenting early may show hyporeflexia, decreased night vision, loss/decreased vibratory sense, however, have normal cognition. A more moderate stage of this deficiency may show limb and truncal ataxia, profuse muscle weakness, and limited upward gaze. Late presentations may show cardiac arrhythmias and possible blindness with reduced cognition. Ataxia is the most common exam finding.

Patients that have abetalipoproteinemia have eye problems often including pigmented retinopathy and visual field issues. However, patients suffering from cholestatic liver disease often have personality and behavioral disorders.

Evaluation

A low alpha-tocopherol level or low ratio serum alpha-tocopherol to serum lipids measurement is the mainstay of diagnosis. In adults, alpha-tocopherol levels should be less than 5 mcg/mL. In an adult with hyperlipidemia, the abnormal lipids may affect the vitamin E levels and a serum alpha-tocopherol to lipids level, needing to be less than 0.8 mg/g) is more accurate. A pediatric patient with abetalipoproteinemia will have serum alpha-tocopherol levels that are not detectable.

Treatment / Management

Treatment addresses the underlying cause of the deficiency (fat malabsorption, fat metabolism disorders, among others) and then provide oral vitamin E supplementation. Also, a modification in diet can assist in the supplementation, increase intake of leafy vegetables, whole grains, nuts, seeds, vegetable oils and fortified cereals is highly recommended. Though normally presented in our diets, adults need 15mg of vitamin E per day. A supplement of 15 to 25 mg/kg once per day or mixed tocopherols 200 IU can both be used. If a patient has issues with the small intestine and/or oral ingestion intramuscular injection is necessary.[6][7][8][9] The recommended daily allowance of alpha-tocopherol is as follows.

  • Age 0 to 6 months: 3 mg
  • Age 6 to 12 months: 4 mg
  • Age 1 to 3 years: 6 mg
  • Age 4 to 10 years: 7 mg
  • Adults and elderly patients: 10 mg

Differential Diagnosis

While developing a differential diagnosis, clinicians must consider other possible vitamin deficiencies as well as the following: 

  • Friedreich ataxia
  • Ataxia with vitamin E deficiency (AVED)
  • Stroke
  • Cerebral palsy
  • Paraneoplastic syndrome
  • Biliary disease
  • Short-Bowl syndrome
  • Mutations in the tocopherol transfer protein causing impaired fat metabolism 
  • Cystic fibrosis 
  • Chronic cholestatic hepatobiliary disease 
  • Crohn's disease
  • Exocrine pancreatic insufficiency
  • Liver disease 
  • Abetalipoproteinemia
  • Isolated vitamin E deficiency

Prognosis

If left untreated, symptoms may worsen. However, once diagnosed, the outcome is very good as most symptoms will resolve quickly. However, as the deficiency becomes more pronounced, the therapy will be more restricted. Patients who are at risk for vitamin E deficiency should be tested and evaluated regularly.

Complications

Vitamin E has a few interactions with medications that are listed below:

  • Anticoagulation and antiplatelet medications: due to vitamin E inhibiting platelet aggregation and disrupting vitamin K clotting factors there is a protentional increase risk of bleeding combining these two.
  • Simvastatin and niacin: Vitamin E can reduce the amount of high-density lipoprotein (HDL) which is the opposite desired effect of taking simvastatin and/or niacin.

Consultations

Depending on the cause many consultations may be required. However, if the biliary problem is discovered a gastroenterologist should be consulted. 

Deterrence and Patient Education

Replacement recommendations vary by causing disease and are as follows:

  • Abetalipoproteinemia: 100 to 200 IU/kg per day
  • Chronic cholestasis: 15 to 25 IU/kg per day
  • Cystic fibrosis: 5 to 10 IU/kg per day
  • Short-bowel syndrome: 200 to 3600 IU per day
  • Isolated vitamin E deficiency: 800 to 3600 IU per day

Vitamin E is safe for pregnancy and breastfeeding. Both vitamin K and omega-6 fatty acids requirements may increase with high doses of vitamin E.

Enhancing Healthcare Team Outcomes

Vitamin E deficiency is not common in North America but when it occurs, healthcare workers including the nurse practitioner should work the patient up for additional mineral deficiencies. The goal is to address the underlying cause of the deficiency (fat malabsorption, fat metabolism disorders, among others) and then provide oral vitamin E supplementation. A dietary consult should be sought and the patient educated about the foods that contain vitamin E. The outlook for patients treated for vitamin E deficiency is good provided the patient is compliant with the dietary changes and/or supplements. (Level V)

Questions

To access free multiple choice questions on this topic, click here.

References

1.
Kim HK, Han SN. Vitamin E: Regulatory role on gene and protein expression and metabolomics profiles. IUBMB Life. 2019 Apr;71(4):442-455. [PubMed: 30632663]
2.
Suzuki H, Kume A, Herbas MS. Potential of Vitamin E Deficiency, Induced by Inhibition of α-Tocopherol Efflux, in Murine Malaria Infection. Int J Mol Sci. 2018 Dec 24;20(1) [PMC free article: PMC6337606] [PubMed: 30586912]
3.
Jilani T, Iqbal MP. Vitamin E deficiency in South Asian population and the therapeutic use of alpha-tocopherol (Vitamin E) for correction of anemia. Pak J Med Sci. 2018 Nov-Dec;34(6):1571-1575. [PMC free article: PMC6290196] [PubMed: 30559825]
4.
Khadangi F, Azzi A. Vitamin E - The Next 100 Years. IUBMB Life. 2019 Apr;71(4):411-415. [PubMed: 30550633]
5.
Sapiejka E, Krzyżanowska-Jankowska P, Wenska-Chyży E, Szczepanik M, Walkowiak D, Cofta S, Pogorzelski A, Skorupa W, Walkowiak J. Vitamin E status and its determinants in patients with cystic fibrosis. Adv Med Sci. 2018 Sep;63(2):341-346. [PubMed: 30081288]
6.
Boltshauser E, Weber KP. Laboratory investigations. Handb Clin Neurol. 2018;154:287-298. [PubMed: 29903445]
7.
Tokgöz Y, Terlemez S, Karul A. Fat soluble vitamin levels in children with newly diagnosed celiac disease, a case control study. BMC Pediatr. 2018 Apr 09;18(1):130. [PMC free article: PMC5890346] [PubMed: 29631542]
8.
Teriaky A, Mosli M, Chandok N, Al-Judaibi B, Marotta P, Qumosani K. Prevalence of fat-soluble vitamin (A, D, and E) and zinc deficiency in patients with cirrhosis being assessed for liver transplantation. Acta Gastroenterol. Belg. 2017 Apr-Jun;80(2):237-241. [PubMed: 29560688]
9.
Gomez-Pomar E, Hatfield E, Garlitz K, Westgate PM, Bada HS. Vitamin E in the Preterm Infant: A Forgotten Cause of Hemolytic Anemia. Am J Perinatol. 2018 Feb;35(3):305-310. [PubMed: 29017181]
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Bookshelf ID: NBK519051PMID: 30085593

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