The association of acne vulgaris and disease severity with serum amyloid a1 and insulin levels

Abstract

Background: Acne vulgaris is a chronic inflammatory disease involving multiple factors such as increased sebum production, follicular hyperkeratinization, microbial colonization, and inflammation. Serum amyloid A1 (SAA1), an acute phase protein, and insulin, a hormone linked to metabolic and inflammatory pathways, may play significant roles in acne pathogenesis. Objective: This study aimed to evaluate SAA1 and insulin levels in patients with acne vulgaris and to investigate their relationship with disease severity and scar formation. Methods: A total of 72 acne vulgaris patients [13 males, 59 females; median age 22 (19–34) years] and 66 age-similar healthy controls [27 males, 39 females; median age 22 (18–38) years] were included. Acne severity was assessed using the Global Acne Grading System (GAGS), and scar severity was evaluated by the Global Scale for Acne Scar Severity. SAA1 and insulin levels were measured via ELISA from fasting blood samples. Additionally, anthropometric measurements and biochemical parameters were recorded. Results: A total of 138 participants were included, with 72 acne vulgaris patients and 66 healthy controls. The groups were age-similar, though a higher female proportion was observed in the acne group. SAA1 levels were significantly higher in acne patients (p=0.045), whereas insulin levels did not differ significantly (p=0.902). LDL, triglycerides, and total cholesterol were significantly lower in the acne group (p=0.003, p=0.045, p=0.023, respectively). SAA1 levels did not significantly correlate with acne severity (p=0.052) or scar severity (p=0.09). However, LDL and total cholesterol showed weak negative correlations with both acne severity and scar severity. Conclusion: Elevated SAA1 in acne vulgaris patients suggests that SAA1 may serve as a novel biomarker for assessing inflammation in acne. Further large-scale studies are needed to explore therapeutic implications targeting inflammation.