Risks Challenged in Treating Tardive Dyskinesia with Vitamin E


The risks of vitamin E treatment seemed to outweigh the benefits in this particular case.

O. Greg Deardorff, PharmD

O. Greg Deardorff, PharmD

While daily vitamin E treatments seemed to ease one patient’s tardive dyskinesia (TD), the risk of prostate cancer in the patient overruled the benefits, according to a recent case report.

Researchers from Fulton State Hospital Pharmacy in Missouri, led by O. Greg Deardorff, PharmD, treated a 57-year-old male patient with a schizophrenia diagnosis and TD. Part of their treatment focused on the hypothesis that antipsychotics increases dopamine metabolism and turnover, leading to the formation of free radicals. In turn, they believed that these free radicals, as well as the oxidative stress, could lead to the development of TD.

Therefore, the doctors believed that antioxidants could accept electrons from free radicals which would neutralize them and prohibit them from causing damage. This lead the team to vitamin E, one of the many treatments for tardive dyskinesia. However, it is not sufficiently studied and can even cause harm in high doses, including risk of stroke or heart failure, and risk of prostate cancer in men after long term exposure.

In July 2008, the patient began receiving 1200 IU daily vitamin E treatments, increased to 1600 IU daily after 22 days. In November, his treatment was reduced to 800 IU daily, which continued for the next 24 months.

In November 2010, an elevated prostate specific antigen (PSA) was discovered, where it reached 4.89 ng/mL. The researchers wrote that this was “mildly elevated.” After a month, the patient’s PSA level increased to 6.37ng/ML. The PSA level dropped after the general practitioner introduced tamsulosin 0.4 mg daily, but the PSA did not disappear until vitamin E treatment was discontinued in October of 2011.

After 2 months of discontinuation, the PSA level in the patient was within normal limits, and stayed that way for nearly 3 years.

The researchers stressed that an elevated PSA level — between 4 and 10 ng/mL – was not a sufficient diagnosis for prostate cancer, but the correlation between elevated PSA levels and future development of prostate cancer is strong.

Prior to vitamin E therapy, and before tamsulosin treatment began, the patient’s PSA velocity was 1.9 ng/ mL/ year. However, rather than continuing testing, the general practitioner suggested discontinuing vitamin E treatment on the basis of the total PSA levels over time. Mr. A’s PSA velocity was 0.2 ng/ mL/ year for 3 years after the discontinuation of vitamin E therapy.

“The findings of this case report and the SELECT trial suggest that long-term vitamin E therapy may increase the risk of developing prostate cancer,” researchers wrote.

The Selenium and Vitamin E Cancer Prevention Trial (SELECT), published in JAMA in 2011, found that dietary supplements with vitamin E significantly increased the risk of prostate cancer in healthy men. Their study included more than 35,000 men from the United States and Canada observed between 2001 and 2004. Those researchers continued to collect data from the patients through 2011.

“This finding incites concern, primarily because a much higher dose of vitamin E is many times used to treat tardive dyskinesia,” the study authors concluded. “Health care providers should include patients in the decision-making process when assessing the risks and benefits of vitamin E therapy.”

The paper, titled “Tardive Dyskinesia: Is Vitamin E Singing the Prostate Blues?” was published in The Primary Care Companion for CNS Disorders.

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