BACKGROUND

Alopecia areata is a hair follicle disorder characterized by the development of multiple circular bald patches on the scalp, often accompanied by elevated cytokine production and immune cell infiltration around hair follicles. Our aspiration is to explore whether blood analysis can reveal additional factors that contribute to the disparities between individuals with alopecia areata and those who are healthy. Such research could potentially establish a robust foundation for the advancement of future therapeutic strategies.

METHODS

In Fujian, China, we have collected blood samples from a cohort of 28 alopecia areata patients and a control group of 28 healthy individuals for comparative analysis. A detailed assessment of cytokines, eosinophil counts, vitamin levels, and immunoglobulin profiles within these samples was conducted. Subsequently, statistical analysis was applied to elucidate the differences between the two groups.

RESULTS

While the blood analysis revealed higher average levels of IL-4, IL-10, and TNF-α in alopecia areata patients compared to healthy individuals, these differences were not statistically significant. Similarly, vitamin levels showed no significant variation between the patient and healthy groups. However, the Wilcoxon rank sum test identified a significant increase in IFN-γ and a significant decrease in immunoglobulin IgG4 levels among alopecia areata patients, pointing to a possible role in the disease's pathogenesis. Receiver operating characteristic (ROC) curve analysis had demonstrated that the area under the ROC curve (AUC) for IFN-γ and IgG4 was 0.656 and 0.704, respectively, suggesting that IFN-γ and IgG4 had a certain discrimination effect on alopecia areata. Utilizing the Youden index to optimize specificity, we propose that IgG4 levels below 824.85 mg/L and IFN-γ levels above 0.565 pg/mL could serve as biomarkers for assessing the risk of alopecia areata.

CONCLUSIONS

These findings highlight the need for further exploration of the link among alopecia areata, IgG4- and IFN-γ-related mechanisms, potentially uncovering novel therapeutic targets for managing this condition.