الفهرس 
IntroductionOnly 14 pages are availabe for public view
Abstract
Acne vulgaris is one of the most common dermatological diseases worldwide. Several pathogenic mechanisms were evaluated for its role in the pathogenesis of acne. Psychological stress, hormonal imbalance, disturbed serum lipid profile and genetic factors were all implicated in acne development. Involvement of immune system and novel adipokines were recently linked to acne vulgaris pathogenesis.
Serum visfatin, also known as Nicotinamide phosphoribosyl transferase, is an adipokine that participates in several biologic process as inflammation and apoptosis. Moreover, visfatin possess a pivotal role in various inflammatory diseases either systemic or dermatological. Visfatin exerts several roles in the pathogenesis of insulin resistance, obesity and therefore was linked to development of inflammatory acne vulgaris.
High-glycemic-index diet induces hyperinsulinemia, which subsequently elicits endocrine responses and enhances androgen synthesis, ultimately affecting the development of acne through mediators such as androgens, insulin-like growth factor (IGF)-1, and IGF binding protein (IGFBP)-3. The current study aimed to evaluate serum visfatin levels in inflammatory acne vulgaris patients and also to assess the relation between visfatin and insulin resistance assessed by fasting insulin and HOMA-IR in acne patients.
The current study included 30 patients suffering from inflammatory acne vulgaris and 30 healthy control subjects. The patients were recruited from the outpatient clinic of dermatology of Ain Shams University Hospitals. Patients of both sexes, patients with moderate and severe acne were included. We excluded pregnant and lactating female patients. Patients with systemic disease as DM and morbid obesity. Patients with other dermatological diseases or receiving hormonal or acne treatments were also excluded.
We recorded the BMI and GAGS score for included patients. Also, we measured serum visfatin, fasting insulin, fasting glucose and calculated HOMA-IR.
We included 30 acne vulgaris patients (7 males and 23 females) with mean age of 22.7 ± 4 years. Mean value of BMI was 24.2 ± 4.8 Kg/m2. GAGS score was 27. tients expressing severe acne.
Acne patient shad significantly higher levels of fasting insulin and HOMA-IR compared to control subjects. This finding revealed the pivotal role of Insulin resistance in acne patients.
Included patients had statistically significant higher levels of visfatin (p=0.001) compared to control subjects. Serum visfatin revealed excellent discriminative power in acne patients with sensitivity 96.7% and specificity 100%. Therefore, serum visfatin showed a significant role in the pathogenesis of AV.
However, no significant correlation was detected between serum visfatin and either of fasting insulin or HOMA-IR. Therefore, significant association of serum visfatin with development of Insulin resistance can’t be established in the current study. Moreover, there was no association between serum visfatin levels and acne severity.
In conclusion, serum visfatin showed significant higher values in inflammatory AV potentiating the potential role of serum visfatin in the pathogenesis of AV. Moreover, the current study demonstrated the significant association of IR in AV patients. However, we couldn’t find any significant association between visfatin levels and Insulin resistance ,and therefore we assume that elevated serum visfatin levels in acne patients are related to the role of visfatin in inflammation and its relation to inflammatory acne.