Cutaneous and ocular toxicology · 2026
Investigating the role of serum human beta defensin-2 in psoriasis and psoriatic arthritis: a case-control study on hBD-2 and CRP, ESR.
СтатьяНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Kaya Necip Enis, Kurmuş Gökçe Işıl, Özdemirel Ali Erhan, Altunay Enes, Gönül Müzeyyen
Аннотация
INTRODUCTION: Human beta-defensin 2 (hBD-2) is an antimicrobial peptide upregulated by IL-17A and TNF-α, important in skin immunity and inflammation. While hBD-2 is elevated in psoriatic skin, its systemic expression and clinical significance remain unclear, particularly in psoriatic arthritis (PsA).
OBJECTIVES: To compare serum hBD-2 levels among patients with psoriasis vulgaris, PsA, and healthy controls, and to evaluate its correlation with disease severity and inflammatory markers.
METHODS: This case-control study included 66 patients with psoriasis, 30 with PsA, and 67 healthy controls. Serum hBD-2, C-reactive protein (CRP), and erythrocyte sedimentation rate (ESR) were measured. Psoriasis severity was assessed using the Psoriasis Area and Severity Index (PASI). A p value < 0.05 was considered statistically significant.
RESULTS: Median serum hBD-2 levels were significantly higher in psoriasis and PsA groups compared to controls (p < 0.001), but no significant difference was found between the two patient groups (p: 0.223). In the psoriasis group, hBD-2 showed no significant correlation with PASI (r: 0.218, p: 0.095), CRP (r: 0.158, p: 0.277), or ESR (r: 0.129, p: 0.369). CRP and ESR were significantly higher in the PsA group than in other groups (p < 0.001 and p: 0.002, respectively).
CONCLUSIONS: Although serum hBD-2 is elevated in psoriasis and PsA, it does not correlate with clinical or laboratory disease activity in psoriasis. These findings suggest that hBD-2 may reflect local cutaneous immune activation rather than systemic inflammation.
OBJECTIVES: To compare serum hBD-2 levels among patients with psoriasis vulgaris, PsA, and healthy controls, and to evaluate its correlation with disease severity and inflammatory markers.
METHODS: This case-control study included 66 patients with psoriasis, 30 with PsA, and 67 healthy controls. Serum hBD-2, C-reactive protein (CRP), and erythrocyte sedimentation rate (ESR) were measured. Psoriasis severity was assessed using the Psoriasis Area and Severity Index (PASI). A p value < 0.05 was considered statistically significant.
RESULTS: Median serum hBD-2 levels were significantly higher in psoriasis and PsA groups compared to controls (p < 0.001), but no significant difference was found between the two patient groups (p: 0.223). In the psoriasis group, hBD-2 showed no significant correlation with PASI (r: 0.218, p: 0.095), CRP (r: 0.158, p: 0.277), or ESR (r: 0.129, p: 0.369). CRP and ESR were significantly higher in the PsA group than in other groups (p < 0.001 and p: 0.002, respectively).
CONCLUSIONS: Although serum hBD-2 is elevated in psoriasis and PsA, it does not correlate with clinical or laboratory disease activity in psoriasis. These findings suggest that hBD-2 may reflect local cutaneous immune activation rather than systemic inflammation.