Unraveling the relation between vitiligo, Interleukin 17, and serum amyloid A

There is debate concerning the precise etiopathogenesis of vitiligo. According to certain theories, a series of inflammatory responses that mediate the loss of melanocytes are caused by both cellular and humoral immune responses. It has also been demonstrated that Interleukin 17 (IL-17) promotes melanocyte death and inhibits melanogenesis through different mechanisms. Serum Amyloid A (SAA) levels are over-expressed in autoimmune diseases. Th17 cytokines are regulated by serum amyloid A proteins.

To measure serum levels of IL-17 and SAA in vitiligo patients aiming to explain their possible role in disease pathogenesis and the other aim is to correlate their levels with disease activity and severity.

This study included 60 vitiligo patients and 40 healthy age and sex controls. Enzyme-linked immunosorbent assay was used to measure serum levels of SAA and IL-17.

This study revealed significant increase in levels of serum IL-17 and SAA in patients than controls (p < 0.05). Both markers showed significant positive correlations with VASI score and duration of vitiligo; only IL-17 showed statistically significant positive correlation with VIDA scores. Patients with vitiligo showed a statistically significant positive connection between serum IL-17 levels and SAA (γ = 0.992, p-value <0.05).

Increased serum level of IL-17 and SAA in vitiligo patients together with their positive relation to vitiligo severity and the duration of the disease show that these two markers play a key role in the vitiligo development.