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Abstract：
The idea of psoriatic disease continuum has been progressively prompted based on the advances of the knowledge about the pathogenic steps underpinning the occurrence of psoriasis (PSO) and psoriatic arthritis (PSA). To evaluate biomolecules (inflammatory cytokines, inflammatory chemokines, cell adhesion and cellular mediators) in naïve patients with PSO, PSA with PSO, and PSA sine PSO. To stratify the results considering the presence of psoriatic nail involvement, extensive skin disease and obesity evaluating all involved patients.
By multiplex technology, 20 serum biomolecules were assessed with the inclusion of pro-inflammatory cytokines (GM-CSF, IFN-γ, IL-1α, IL-1β, IL-6, IL-8, IL-12p70, IL-17A, IL-23, TNF), anti-inflammatory cytokines (IFN-α, IL-4, IL-10, IL-13), inflammatory chemokines (IP-10, MCP-1, MIP-1α, MIP-1β), cell adhesion and cellular mediators (ICAM-1, E-selectin, P-selectin). The assessment of possible statistical differences between the means of the three groups was performed by One-Way ANOVA. In addition, by non-parametric T-tests, we stratified the results according to selected clinical characteristics (psoriatic nail involvement, PASI ≥ 10, BMI ≥ 30).
In 80 assessed naïve patients, patients with PSO showed significant increases of E-selectin (p=0.021) and IL-8 (0.041) than other groups. In patients with PSA with PSO, significant higher levels of ICAM-1 were observed (p=0.009) than other groups. We did not observe further differences comparing pro-inflammatory and anti-inflammatory cytokines, inflammatory chemokines, and cell adhesion and cellular mediators in patients with PSO, PSA with PSO, and PSA sine PSO. Patients with psoriatic onychopathy showed significant increased levels of ICAM-1 (p=0.010) and IP-10 (0.030) than others. In patients with PASI ≥ 10, significantly enhanced values of IL-8 (p=0.004), TNF (p=0.013), E-selectin (p=0.004), MIP-1α (p=0.003), and MIP-1β (p=0.039). In patients with BMI ≥ 30, significantly higher levels of E-selectin were pointed out (p=0.035) than others.
Our findings may suggest that a similar cytokine profile may characterize naïve patients with PSO, PSA with PSO, and PSA sine PSO, reinforcing the concept of psoriatic disease continuum. However, some differences may be also shown, underlying possible pathogenic differences and leading to the clinical heterogeneity of these patients.
By multiplex technology, 20 serum biomolecules were assessed with the inclusion of pro-inflammatory cytokines (GM-CSF, IFN-γ, IL-1α, IL-1β, IL-6, IL-8, IL-12p70, IL-17A, IL-23, TNF), anti-inflammatory cytokines (IFN-α, IL-4, IL-10, IL-13), inflammatory chemokines (IP-10, MCP-1, MIP-1α, MIP-1β), cell adhesion and cellular mediators (ICAM-1, E-selectin, P-selectin). The assessment of possible statistical differences between the means of the three groups was performed by One-Way ANOVA. In addition, by non-parametric T-tests, we stratified the results according to selected clinical characteristics (psoriatic nail involvement, PASI ≥ 10, BMI ≥ 30).
In 80 assessed naïve patients, patients with PSO showed significant increases of E-selectin (p=0.021) and IL-8 (0.041) than other groups. In patients with PSA with PSO, significant higher levels of ICAM-1 were observed (p=0.009) than other groups. We did not observe further differences comparing pro-inflammatory and anti-inflammatory cytokines, inflammatory chemokines, and cell adhesion and cellular mediators in patients with PSO, PSA with PSO, and PSA sine PSO. Patients with psoriatic onychopathy showed significant increased levels of ICAM-1 (p=0.010) and IP-10 (0.030) than others. In patients with PASI ≥ 10, significantly enhanced values of IL-8 (p=0.004), TNF (p=0.013), E-selectin (p=0.004), MIP-1α (p=0.003), and MIP-1β (p=0.039). In patients with BMI ≥ 30, significantly higher levels of E-selectin were pointed out (p=0.035) than others.
Our findings may suggest that a similar cytokine profile may characterize naïve patients with PSO, PSA with PSO, and PSA sine PSO, reinforcing the concept of psoriatic disease continuum. However, some differences may be also shown, underlying possible pathogenic differences and leading to the clinical heterogeneity of these patients.
摘要：
■基于有关银屑病（PSO）和银屑病关节炎（PSA）发生的致病步骤的知识的进步，已经逐步提出了银屑病疾病连续体的概念。评估生物分子(炎性细胞因子，炎性趋化因子，幼稚PSO患者的细胞粘附和细胞介质），带PSO的PSA,和PSA正弦PSO。考虑到牛皮癣指甲受累的存在，对结果进行分层，广泛的皮肤病和肥胖评估所有涉及的患者。
■通过多路复用技术，20血清生物分子被评估与促炎细胞因子（GM-CSF，IFN-γ，IL-1α,IL-1β,IL-6,IL-8,IL-12p70,IL-17A,IL-23，TNF），抗炎细胞因子(IFN-α，IL-4,IL-10,IL-13),炎性趋化因子(IP-10，MCP-1，MIP-1α，MIP-1β），细胞粘附和细胞介质(ICAM-1，E-选择素，P-选择素）。通过单向ANOVA评估三组的均值之间可能的统计学差异。此外,通过非参数T检验，我们根据选定的临床特征(银屑病指甲受累，PASI≥10，BMI≥30）。
■在80名未评估的患者中，与其他组相比,PSO患者E-选择素(p=0.021)和IL-8(0.041)显著升高.在患有PSO的PSA患者中，ICAM-1水平显著高于其他组(p=0.009).我们没有观察到比较促炎和抗炎细胞因子的进一步差异，炎性趋化因子，以及PSO患者的细胞粘附和细胞介质，带PSO的PSA,和PSA正弦PSO。银屑病甲癣患者的ICAM-1（p=0.010）和IP-10（0.030）水平显着升高。在PASI≥10的患者中，IL-8值显着增强（p=0.004），TNF（p=0.013），E-选择素（p=0.004），MIP-1α（p=0.003），和MIP-1β(p=0.039)。在BMI≥30的患者中，E-选择素的水平明显高于其他患者（p=0.035）。
■我们的发现可能表明，类似的细胞因子谱可能是PSO患者的特征，带PSO的PSA,和PSA正弦PSO，加强银屑病疾病连续体的概念。然而,也可能显示出一些差异，潜在的致病差异，并导致这些患者的临床异质性。
■通过多路复用技术，20血清生物分子被评估与促炎细胞因子（GM-CSF，IFN-γ，IL-1α,IL-1β,IL-6,IL-8,IL-12p70,IL-17A,IL-23，TNF），抗炎细胞因子(IFN-α，IL-4,IL-10,IL-13),炎性趋化因子(IP-10，MCP-1，MIP-1α，MIP-1β），细胞粘附和细胞介质(ICAM-1，E-选择素，P-选择素）。通过单向ANOVA评估三组的均值之间可能的统计学差异。此外,通过非参数T检验，我们根据选定的临床特征(银屑病指甲受累，PASI≥10，BMI≥30）。
■在80名未评估的患者中，与其他组相比,PSO患者E-选择素(p=0.021)和IL-8(0.041)显著升高.在患有PSO的PSA患者中，ICAM-1水平显著高于其他组(p=0.009).我们没有观察到比较促炎和抗炎细胞因子的进一步差异，炎性趋化因子，以及PSO患者的细胞粘附和细胞介质，带PSO的PSA,和PSA正弦PSO。银屑病甲癣患者的ICAM-1（p=0.010）和IP-10（0.030）水平显着升高。在PASI≥10的患者中，IL-8值显着增强（p=0.004），TNF（p=0.013），E-选择素（p=0.004），MIP-1α（p=0.003），和MIP-1β(p=0.039)。在BMI≥30的患者中，E-选择素的水平明显高于其他患者（p=0.035）。
■我们的发现可能表明，类似的细胞因子谱可能是PSO患者的特征，带PSO的PSA,和PSA正弦PSO，加强银屑病疾病连续体的概念。然而,也可能显示出一些差异，潜在的致病差异，并导致这些患者的临床异质性。
