What is the pathophysiology of vitamin E toxicity?

Updated: Jun 01, 2020
  • Author: Mark Rosenbloom, MD, MBA; Chief Editor: Michael A Miller, MD  more...
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Vitamin E can prolong the prothrombin time (PT) in animal models by inhibiting vitamin K–dependent carboxylase, although administration of vitamin K corrects this. High doses of vitamin E increase the vitamin K requirement; coagulopathy can occur in patients who are deficient in vitamin K. [19, 20] (Concomitant use of vitamin E and anticoagulants can also increase the risk of bleeding complications). [19, 20]

Vitamin E at dosages of 1600 IU/day reduces platelet thromboxane production. Vitamin E supplementation may impair the hematologic response to iron in children with iron-deficiency anemia.

In the Heart Protection Study, a combination of vitamin E (600 IU alpha-tocopherol only), vitamin C, and beta-carotene did not affect mortality. However, it did cause a significant, albeit small, increase in total cholesterol, low-density lipoprotein (LDL) cholesterol, and triglycerides, as well as a decrease in high-density lipoprotein (HDL) cholesterol. In 2 randomized trials, an antioxidant cocktail that included vitamin E (form not specified) blunted the beneficial increase in HDL2 levels associated with niacin and simvastatin therapy. [21, 22]

Vitamin E can depress leukocyte oxidative bactericidal activity and mitogen-induced lymphocyte transformation.

Although adverse effects usually are observed only at very high dosages of vitamin E, a meta-analysis showed a possible increase in mortality at dosages of 400 IU/d and higher (alpha-tocopherol only). [11]

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