The investigation of the amounts and expressions of epidermal growth factor, epidermal growth factor receptor, and epidermal growth factor receptor gene polymorphisms in acne vulgaris

• Published in: Journal of cosmetic dermatology Vol. 20; no. 1; pp. 346 - 351
• Main Authors: Aydingoz, Ikbal Esen, Tukenmez Demirci, Gulsen, Agirbasli, Deniz, Oz‐Arslan, Devrim, Yenmis, Guven
• Format: Journal Article
• Language: English
• Published: England 01-01-2021
• Subjects: acne vulgaris; Acne Vulgaris - drug therapy; Acne Vulgaris - genetics; epidermal growth factor; Epidermal Growth Factor - genetics; epidermal growth factor receptor; ErbB Receptors - genetics; etiology; gene expression; Genes, erbB-1; Humans; Polymorphism, Genetic; acne vulgaris; epidermal growth factor; epidermal growth factor receptor; gene expression; etiology
• ISSN: 1473-2130; 1473-2165
• DOI: 10.1111/jocd.13498

Background
Epidermal growth factor receptor inhibitors (EGFRI) used in cancer chemotherapy cause acneiform folliculitis in 70%‐100% of patients in a dose‐dependent manner. Acneiform folliculitis is considered to be caused by an inflammatory process due to follicular hyperkeratosis and subsequently a set of changes both in epidermis and hair follicles as a result of epidermal growth factor receptor (EGFR) blockade. Both acne vulgaris and acneiform folliculitis due to EGFRIs show similar changes in the pilosebaceous unit. Furthermore, in both groups of patients, topical application of recombinant human epidermal growth factor (EGF) has been reported to improve the disease.
Aims
In this study, it was aimed to investigate the role of EGF and EGFR amount, expression, and EGFR gene polymorphisms in the etiopathogenesis of acne vulgaris.
Patients/Methods
156 acne vulgaris patients, within 18‐25 years of age, who had 15 or more inflammatory acne lesions on dermatologic evaluation were included in this study. The absence of any known systemic or genetic disease or cancer and any systemic or topical treatment for the last 1 month were prerequisites. In the control group, 154 volunteers in the same age range who were examined at the outpatient clinic with diagnoses of melanocytic nevus, ephelid, cherry angioma, and callus and who had no more than 3 inflammatory acne lesions were recruited. The amounts of EGF and EGFR were determined by sandwich ELISA, expressions of EGF and EGFR by reverse transcriptase polymerase chain reaction; EGFR polymorphisms were examined by restriction enzyme digestion, Sanger, and high‐resolution melting methods.
Results
The patient and control groups were compared in terms of EGFR gene polymorphisms in addition to the amount and expressions of EGF and EGFR. The amount of EGF in the serum was found to be significantly higher in the acne group. (P = .0012). There was no significant difference in other parameters studied.
Conclusion
The results of our study showed a significant increase in the amount of EGF in the acne group. Though EGF may be incriminated in the etiopathogenesis of AV, the most likely explanation about its role may be controlling inflammation from the very first stage.