2000
DOI: 10.1054/plef.2000.0208
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Keloids in rural black South Africans Part 2: dietary fatty acid intake and total phospholipid fatty acid profile in the blood of keloid patients

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Cited by 25 publications
(26 citation statements)
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“…Based on nutritional deficiencies in FAs, identified in keloids and in keloid patients (Louw et al, 1997a,b;Louw and Dannhauser, 2000;Louw, 2000b), an immunonutritional approach with FAs (Louw, 2003) and phytochemical dietary compounds (Phan et al, 2003a) for keloid management has emerged. Modulation of human immune and inflammatory responses by dietary FAs is now commonly known (Kelley, 2001;Yaqoob, 2004).…”
Section: Immunonutritional Disordermentioning
confidence: 99%
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“…Based on nutritional deficiencies in FAs, identified in keloids and in keloid patients (Louw et al, 1997a,b;Louw and Dannhauser, 2000;Louw, 2000b), an immunonutritional approach with FAs (Louw, 2003) and phytochemical dietary compounds (Phan et al, 2003a) for keloid management has emerged. Modulation of human immune and inflammatory responses by dietary FAs is now commonly known (Kelley, 2001;Yaqoob, 2004).…”
Section: Immunonutritional Disordermentioning
confidence: 99%
“…Despite sufficient dietary FA intake and metabolism in keloid patients (Louw and Dannhauser, 2000), and sufficient FA circulation via microvasculature to fibroblasts and wound healing cells in the interface and peripheral keloid areas, prolonged inflammatory and cytokine mediated reactions are believed to be responsible for continuous depletion of membrane antiinflammatory FA sources and likely deregulation of signaling pathways (Louw et al, 1997a,b). In the central areas of the keloids, deprivation of FA sources through microvessel occlusion contributes to FA deficient fibroblasts compared with those in the peripheral areas (Louw et al, 1997b), decreased fibroblast proliferation, and hypoxic conditions under which fibroblasts express a greater number of binding sites for TGF-b (Kischer, 1992;Bettinger et al, 1996;Appleton et al, 1996).…”
Section: Angiogenesis and Hypoxiamentioning
confidence: 99%
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“…This may reflect changes in the mechanisms that cause these esters to accumulate in the skin, namely their transfer from the dermis, adipose tissue and serum, their synthesis in the epidermis, and their modification by bacterial enzymes [11,12]. In relation to this, patients with keloids have been found to consume higher levels of dietary linoleic acid (LA) and arachidonic acid (AA) than recommended (7–11 g/d), and they also consume α-linolenic acid (ALA), eicosapentaenoic acid (EPA), and docosahexaenoic acid (DHA) at levels below the recommended 1.1–1.5 g/d [9]. Moreover, keloids bear higher levels of AA than the skin of keloid-prone and non-keloid-prone patients [10].…”
Section: Introductionmentioning
confidence: 99%