Abstract

Background & Introduction: Insulin-Like Growth Factor-1 (IGF-1) belongs to the growth factor family, structurally resembling pro-insulin, enabling it to bind to insulin receptors. It plays an important role in many tissues including skin, particularly acne pathogenesis by stimulating sebum production and affecting androgen levels. Studies comparing IGF-1 levels in acne patients and controls have found statistically significant differences, proving acne as a sign of insulin resistance. However, no such study has been carried out in Pakistan. Methodology: After approval from the institutional ethical board and informed consent, a case-control study was carried out with 270 acne patients and 80 age and gender- matched controls. Patients belonged to either gender and aged between 15 – 35 years were divided into mild, moderate and severe categories. IGF-1 levels were noted after exclusion of any condition interfering with IGF-1 level and correlated with acne severity and with levels of testosterone, dihydrotestosterone (DHT) and dehydroepiandrosterone sulphate (DHEAS). Quantitative variables were expressed as median and percentiles. Comparisons were done by Mann-WShitney test and correlations by Spearman correlation. A p value of < 0.05 was considered statistically significant. Results: Out of 350 cases and controls, There were 142 (41%) males and 208 (59%) females. In cases, there were 155 females and 115 males, whereas in controls, there were 54 females and 26 males. Median age of the patients was 20 years. Ninety-Seven patients had mild, 108 moderate and 65 had severe disease. Median levels of IGF-1 were 292 ng/m in cases. IGF-1 levels were significantly different between cases and controls and between mild and severe acne, but not between mild and moderate acne. IGF-1 levels were strongly correlated with the levels of androgenic hormones. Conclusion: Increase of IGF-1 levels in acne point to the role of insulin resistance and diet in acne. Future treatments may be targeted to treat IGF-1 levels by dietary interventions reducing glycemic load.

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