الفهرس 
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Abstract
Acne vulgaris is one of the common dermatological diseases frequently found in late childhood and adolescence. Sebaceous hyperplasia, follicular hyperkeratinization, and bacterial hypercolonization, as well as immune reactions and inflammations may lead to acne, which has a quite complex pathogenesis. Genetic predisposition The molecular mechanisms involved in acne vulgaris are believed to be due to the action of increased levels of proinflammatory factors including TNF-α and IL-8 play an important role in the pathogenesis of acne vulgaris, that is supported by several studies which showed increased incidence of acne vulgaris among relatives of affected patients and high rates of concordance for acne vulgaris among monozygotic twins when one is affected.
Interleukin-8 is a pro-inflammatory chemokine which chemo attracts and mediates proliferation and growth of many immune cells. TNF-α, is a multifunctional, pro inflammatory cytokine. It has been implicated as a key cytokine in the pathogenesis of acne vulgaris because of its ability, alone or in interactions with other mediators, to induce several cytokines and adhesion molecules involved in the development of acne lesions. It is proven that acne vulgaris had genetic basis as many inflammatory diseases. The clarification of which should permit a better understanding of disease etiology, allowing the improved classification, diagnosis, and treatment.
The present study aimed to evaluate the serum level of TNF- α and IL-8 and demonstrate genetic polymorphism of IL8- 251T/A and TNF-α 308G/A in acne patients.
This case-control study was conducted on 40 acne patients and 40 age and sex matched healthy volunteers as a control group. They were collected from the Dermatology Outpatient Clinic, Faculty of Medicine, Menoufia University Hospital during the period from September, 2015 to march, 2016. For all, ELISA and Real Time –PCR were used to evaluate IL-8 and TNF- α serum levels and to detect genetic polymorphism of IL-8- 251T/A and TNF-α 308 G/A genes respectively.
The result of the current study showed that: serum IL-8 levels demonstrated statistically significant higher mean values than that of control group (42.95±46.93 pg/ml vs 2.51±2.62 pg/ml) (p=0.000). Studying the relation between IL-8 serum levels and studied personal and clinical criteria of acne patients revealed non-significant correlations or associations except for acne severity (P=0.000).
No significant differences were observed regarding genotypes and alleles of IL-8-251T/A polymorphism among the studied groups. Studying the relation between IL-8-251T/A genotypes and the assessed personal and clinical criteria of acne patients revealed non-significant correlations or associations in acne patients except for site of acne (p=0.001) and its severity (p=<0.001).
There was significant association between IL-8 serum level and its studied genotypes, as AA genotype carriers recorded the highest values (190.02 ±43.93) followed by TA (43.83 ±40.46) and the lowest levels were observed in TT genotype carriers (11.69± 6.62) (p= 0.000).
In Acne patients, TNF-α serum levels mean value was significantly (P=0.000) higher than that of controls (3.94±3.38 pg/ml vs 0.84±0.52 pg/ml). Studying the relation between TNF- α serum levels and the assessed personal and clinical criteria of acne patients Summary revealed non-significant correlations or associations except for acne severity (p=0.006).
All control subjects were carriers of TNF- α 308 G/G (wild type), however, 30(75%) acne patients carried TNF- α 308 G/G genotype, 3 cases(7.5%) had TNF- α 308 A/A genotype and 7 patients (17.5%) carried TNF- α 308 G/A genotype, with a significant difference between both groups (p=0.003).
Studying the relation between TNF-α308G/A genotypes and the assessed personal and clinical criteria of acne patients revealed non-significant associations (p=>0.05 for all). Also, there were no significant differences in the serum levels of TNF-α regarding its genotypes.
There was a significant positive correlation between IL-8 and TNF- α serum levels among acne vulgaris patients (r= 0.29, p= 0.050).
Summary