Keloids in rural black South Africans. Part 1: general overview and essential fatty acid hypotheses for keloid formation and prevention

Louw, Louise

doi:10.1054/plef.2000.0207

Cited by 43 publications

(44 citation statements)

References 88 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…A number of hypotheses such as high skin tension [6,8], hypoxia [16], endocrine dysfunction [15], fatty acid [17], autoimmune [13,25] and genetic hypotheses [3,30] have been proposed to explain the keloid phenomenon. In recent years, more attention has been paid to the genetics exploring the genetics of keloids.…”

Section: Discussionmentioning

confidence: 99%

Clinical and epidemiological analysis of keloids in Chinese patients

Zheng

Xiuhua

et al. 2014

Arch Dermatol Res

View full text Add to dashboard Cite

Keloids are common abnormally raised fibroproliferative lesions that can occur following even minor cutaneous trauma. There are limited data on Chinese patients with keloids, and the purpose of our study was to investigate the clinical and epidemiological features of keloids in Chinese patients. Assessment was performed by unified, designed questionnaires. A total of 715 patients were enrolled and statistical analysis and heritability were performed using EPI INFO 6.0, SPSS13.0 and Falconer's method. Keloids occurred typically between the ages of 10 and 30 years, and the mean age of initial onset was 21.14 ± 13.45 years in females and 22.55 ± 11.36 years in males. The difference in the mean age of onset was not significant between males and females (p > 0.05). A greater severity of keloids was observed in the positive history family group than in the negative history family group, and this difference was statistically significant (χ (2) = 10.889, p < 0.05). The formation of keloids in multiple anatomical sites was found to be significant in the positive family history group. This difference was statistically significant (χ (2) = 15.47, p < 0.001). The prevalence of keloids in first-, second- and third-degree relatives of the proband with keloids was 7.62, 0.38 and 0.035 %, respectively. These results were higher than those in controls and the difference of the prevalence rates of first- and second-degree relatives between probands and controls was significant (χ (2) = 224.63 and 12.078, respectively, p < 0.001). The heritability of keloids in first-, second- and third-degree relatives was 72.45, 40.55 and 17.07 %, respectively. Our findings revealed that the most severe forms of keloids were observed in the probands with positive family history, and the heritability in first-degree relatives of probands was 72.45 %. It is certain, therefore, that genetic factors play a role in the hereditary composition of keloids.

show abstract

Section: Discussionmentioning

confidence: 99%

Clinical and epidemiological analysis of keloids in Chinese patients

Zheng

Xiuhua

et al. 2014

Arch Dermatol Res

View full text Add to dashboard Cite

show abstract

“…Several clinical and epidemiological studies support the notion that hypertension may participate in pathological scar development. First, African Americans have higher rates of keloids than Caucasians, and the same pattern is observed for hypertension morbidity . Second, a study of 100 keloid patients in Nippon Medical School showed that patients with multiple (>3) or large keloids (>10 cm 2 ) are more likely to have hypertension than those with mild keloids (<2 in number or <10 cm 2 in size) (Figure ) .…”

mentioning

confidence: 81%

The link between hypertension and pathological scarring: Does hypertension cause or promote keloid and hypertrophic scar pathogenesis?

Huang

Ogawa

2014

Wound Repair Regeneration

View full text Add to dashboard Cite

Pathological scars, namely, keloids and hypertrophic scars (HSs), are caused by excessive cutaneous wound healing that is characterized by histological extracellular matrix (ECM) accumulation, clinically relevant irritating symptoms, and frequent recurrence after surgical excision. To date, there are few effective and specific treatments. This partly reflects the poor understanding of the etiology of these scars and the lack of a suitable animal model. Systemic hypertension has been suggested to participate in pathological scarring. The evidence that supports this hypothesis is reviewed here. Thus, hypertension associates with changes that resemble the aberrant cutaneous wound-healing phases that characterize pathological scar development. It also associates with profibrotic functional changes in the cells that constitute keloids and HSs (endothelial cells, pericytes/myofibroblasts, dermal fibroblasts, and mast cells) and profibrotic ECM remodeling. These hypertension-associated changes are mediated to some extent by inflammation, hypoxia, and the angiotensin/renin-angiotensin-aldosterone system. Thus, hypertension may be an aggravating/risk factor for keloids and HSs. This will help to identify patients who are prone to heavy scars after surgery or postsurgical recurrence. Moreover, pharmacological agents for the prophylaxis and treatment of hypertension-induced fibrosis in other organs may also be useful for keloids/HSs.

show abstract

“…For example, Africans and African-Americans often develop scalp keloids because their tightly braided hair styles result in increased skin tension. 45 In addition, the characteristic shapes of keloid scars, namely, the butterfly, crab’s claw, and dumbbell shapes, are largely determined by the direction of the local mechanical forces on the skin. 46 Our previous review has described the potential molecular signaling pathways behind this phenomenon.…”

Section: Hypotheses On the Etiology Of Pathological Scarringmentioning

confidence: 99%

Keloids and Hypertrophic Scars

Huang

Murphy

Akaishi

et al. 2013

Plastic and Reconstructive Surgery Global Open

122

View full text Add to dashboard Cite

Summary:The development of cutaneous pathological scars, namely, hypertrophic scars (HSs) and keloids, involves complex pathways, and the exact mechanisms by which they are initiated, evolved, and regulated remain to be fully elucidated. The generally held concepts that keloids and HSs represent “aberrant wound healing” or that they are “characterized by hyalinized collagen bundles” have done little to promote their accurate clinicopathological classification or to stimulate research into the specific causes of these scars and effective preventative therapies. To overcome this barrier, we review here the most recent findings regarding the pathology and pathogenesis of keloids and HSs. The aberrations of HSs and keloids in terms of the inflammation, proliferation, and remodeling phases of the wound healing process are described. In particular, the significant roles that the extracellular matrix and the epidermal and dermal layers of skin play in scar pathogenesis are examined. Finally, the current hypotheses of pathological scar etiology that should be tested by basic and clinical investigators are detailed. Therapies that have been found to be effective are described, including several that evolved directly from the aforementioned etiology hypotheses. A better understanding of pathological scar etiology and manifestations will improve the clinical and histopathological classification and treatment of these important lesions.

show abstract

Keloids in rural black South Africans. Part 1: general overview and essential fatty acid hypotheses for keloid formation and prevention

Cited by 43 publications

References 88 publications

Clinical and epidemiological analysis of keloids in Chinese patients

Clinical and epidemiological analysis of keloids in Chinese patients

The link between hypertension and pathological scarring: Does hypertension cause or promote keloid and hypertrophic scar pathogenesis?

Keloids and Hypertrophic Scars

Contact Info

Product

Resources

About