Manku M S, Horrobin D F, Morse N, Kyte V, Jenkins K, Wright S, Burton J L
Prostaglandins Leukot Med. 1982 Dec;9(6):615-28. doi: 10.1016/0262-1746(82)90019-1.
In the plasma phospholipids of a group of 50 young adults with atopic eczema, there was an elevation of cis-linoleic acid associated with a deficit of gamma-linolenic acid and of the prostaglandin precursors, dihomogammalinolenic acid and arachidonic acid. This suggests that atopics have a deficit in the function of the delta-6-desaturase enzyme which converts linoleic acid to gamma-linolenic acid. Carriers of cystic fibrosis tend to be phenotypically atopic, supporting previous suggestions that in homozygote cystic fibrosis patients the key defect may be in the delta-6-desaturase enzyme. Atopic patients may be exceptionally sensitive to side effects of non-steroidal anti-inflammatory agents. They fail to flush in response to application of niacin compounds to the skin, a reaction mediated by prostaglandins. A deficit of prostaglandin precursors would explain both of these observations. That the observed biochemical deficit plays a causative role in the manifestations of atopy was indicated by the fact that in a double-blind, placebo-controlled crossover trial, gamma-linolenic acid in the form of evening primrose oil (Efamol), partially corrected both the biochemical abnormalities and the clinical state.
在一组50名患有特应性皮炎的年轻成年人的血浆磷脂中，顺式亚油酸升高，同时γ-亚麻酸以及前列腺素前体二高γ-亚麻酸和花生四烯酸缺乏。这表明特应性个体中负责将亚油酸转化为γ-亚麻酸的δ-6-去饱和酶功能存在缺陷。囊性纤维化患者往往具有特应性表型，这支持了之前的观点，即纯合子囊性纤维化患者的关键缺陷可能在于δ-6-去饱和酶。特应性患者可能对非甾体抗炎药的副作用异常敏感。他们在皮肤涂抹烟酸化合物后不会出现潮红反应，而这种反应是由前列腺素介导的。前列腺素前体的缺乏可以解释这两种现象。在一项双盲、安慰剂对照的交叉试验中，月见草油（Efamol）形式的γ-亚麻酸部分纠正了生化异常和临床症状，这一事实表明所观察到的生化缺陷在特应性表现中起因果作用。
