The Role of Long Pentraxin 3 and Nuclear Factor Kappa Beta in Vitiligo Occurrence and Disease Severity

Objectives. To reveal the role of long pentraxin 3 (PTX3) and nuclear factor kappa beta (NF-kB) in vitiligo and their relationship with disease severity. Materials and Methods. The study groups consisted of a total of 54 patients, including 27 patients diagnosed with vitiligo and 27 healthy controls without any cutaneous disease. Patients with amelanotic, sharply demarcated, and chalk-white macular lesions were defined as vitiligo. The diagnosis of vitiligo was confirmed by Wood’s lamp examination. No biopsies were taken from the lesions, and no additional laboratory testing was performed. Skin and hair pigmentations in lesions other than hands and feet were evaluated. Vitiligo grading was done using the largest macules overall. Spreading rates were evaluated in selected lesions with Wood’s lamp. The long pentraxin 3 and NF-kB levels in serum samples of participants were measured by the ELISA method. Results. According to the Vitiligo European Task Force consensus 16 of 27, vitiligo patients were in the slow progressive phase, and 11 patients were in the active progressive phase. The serum PTX3 levels of the patients in the vitiligo group were found to be significantly higher than those of the control group (8.21 ± 2.11 ng/ml vs. 6.76 ± 1.90 ng/ml, $p$ < 0.03). Similarly, the serum NF-kB levels of the patients in the vitiligo group were significantly higher than those of the patients in the control group (15.03 ± 3.45 ng/ml vs. 12.19 ± 4.20 ng/ml, $p$ < 0.01). A positive and significant correlation was found between serum NF-kB and PTX3 (r = 0.677 and $p$ < 0.01). PTX3 and NF-kB levels were significantly higher in patients in the active progressive phase than in patients in the slow progressive phase. PTX3 and NF-kB values in the active progressive phase tended to be higher than those detected when the disease was in the slow progressive phase. Conclusions. High serum PTX3 and NF-kB levels in vitiligo are evidence of impaired proinflammatory activity and innate and adaptive immunity.