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  arrow  Zurier, R. B.
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REPLY

Potential Risk of Prolonged Gamma-linolenic Acid Use

right arrow Robert B. Zurier, MD

15 April 1994 | Volume 120 Issue 8 | Page 692


IN RESPONSE:

Dr. Phinney's remarks are well taken. Administration of {gamma}-linolenic acid might be expected to increase arachidonate levels by increasing conversion of dihomo-{gamma}-linolenic acid to arachidonate. Also, prostaglandin E1 reduces phospholipase A2 activity; thus, mobilization of arachidonate from phospholipid might be reduced. It is also possible that {gamma}- linolenic acid administration results in the movement of arachidonate from phospholipids, which normally provide arachidonate for prostablandin production. We have not observed increased concentrations of total or phospholipid arachidonate in plasma or in peripheral blood leukocytes after administration of {gamma}-linolenic acid but we have not analyzed fatty acids in cells from patients receiving {gamma}-linolenic acid for more than 24 weeks, nor have we examined tissue triglycerides.

We have noticed worsening of synovitis in several patients after withdrawal of {gamma}-linolenic acid. We have considered this finding to be due to absence of the anti-inflammatory effects of the fatty acid. Arachidonate accumulation may lead to increased synovitis in the manner suggested by Dr. Phinney. We are investigating {gamma}-linolenic acid and arachidonate movement and metabolism in cells from patients receiving long-term (24 to 48 weeks) {gamma}-linolenic acid.

We agree with Dr. Phinney's note of caution. Gamma-linolenic acid in the doses we use must be considered experimental and should be administered by physician-investigators in a controlled setting.


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University of Massachusetts Medical Center; Worcester, MA 01655

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