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The concept that EFAs are involved in the development of the atopic state preceded the discovery of PGs and the emergence of contemporary ideas about membrane structure application note and function. It came from Hansen's observation that the skin of EFA-deficient animals bears application note some resemblance to the dry, scaly skin of patients with atopic eczema. Hansen [12] determined application note that EFA levels in pooled plasma from eczematous children were lower than those of normal children. He advocated dietary EFA supplementation for treatment of childhood eczema. Results of clinical trials were variable [13-19], and dietary treatment of eczema was eclipsed by treatment with adrenal corticosteroids. Even today, with the art of clinical observation being undervalued in medical education, knowledgeable dermatologists know that allergic individuals often have dry skin and follicular keratoses, another manifestation of human EFA deficiency [20]. EFA METABOLISM IN ATOPIC ECZEMA Brown and Hansen [21] had found a higher than normal ratio of linoleate to arachidonate in plasma of children with eczema.
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