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Study of visfatin expression in acne patients in tissue and serum

1 Department of Dermatology, Faculty of Medicine, Cairo University, Cairo, Egypt
2 Department of Biochemistry, Faculty of Medicine, Cairo University, Cairo, Egypt

Correspondence Address:
Suzan Shalaby,
6 Street 25 Takseem Elnasr Lelsayarat, Wadi Hof, Cairo
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/ijdvl.IJDVL_856_18

PMID: 32242871

Background: Acne is a chronic inflammatory disease of the pilosebaceous units, of multifactorial pathogenesis, one of which could be an adipokine such as visfatin. Aim: The aim of this study was to study visfatin expression both in lesional skin and serum, of acne patients versus healthy controls. The secondary aim was to study the relationship of visfatin levels with dyslipidemia/metabolic syndrome. Methods: This study included 30 patients with moderate and severe acne vulgaris and 30 age- and sex-matched healthy controls. Serum and tissue visfatin were estimated by enzyme-linked immune-sorbent assay. Clinical and laboratory examinations were done to assess the anthropometric data and various criteria of metabolic syndrome. Results: Tissue and serum visfatin levels were significantly higher in patients as compared to healthy controls. Tissue visfatin levels were significantly higher than its serum levels in both patients and controls. Serum visfatin was significantly higher in overweight individuals. No correlations were found between tissue and serum visfatin levels in both patients and controls. Moreover, serum and tissue visfatin levels did not correlate to any of the lipid profile parameters or criteria of metabolic syndrome in acne patients. Limitations: The study had a small sample size and did not localize the exact source of tissue visfatin. Polycystic ovary syndrome PCOS was not evaluated. Conclusion: Visfatin is an important proinflammatory adipokine, with significantly higher expression in acne patients. Tissue rather than serum visfatin might play a key role in acne.

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Online since 15th March '04
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