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炎症标志物的变化是由于自身免疫病的疾病激活导致的 自免疫病的突发性疾病
Gokhan Sahin1, Esra Pancar Yuksel, Fatma Aydin
1Assistant Prof. Gokhan Sahin, MD, PhD, Ondokuz Mayis University Medical Faculty Department of Dermatology, Samsun, Turkey; sgokhan55@hotmail.com.
Acta dermatovenerologica Croatica : ADC
|November 25, 2023
概括
炎症标志物如乙氨基和平均血小板体积 (MPV) 在自身免疫性突发性疾病的缓解期间下降,表明它们在疾病活性和发病过程中的作用.
科学领域:
- 皮肤病学 皮肤病学
- 免疫学 免疫学 免疫学
- 自身免疫性疾病的发病因子
背景情况:
- 自身免疫性突发性疾病涉及对皮肤结构的自身炎症.
- 炎症细胞在这些疾病的发病过程中发挥着关键作用.
研究的目的:
- 为了确定与自身免疫性突发性疾病中的疾病活性相关的炎症标记物的变化.
- 讨论这些标记物对疾病发病的贡献.
主要方法:
- 追溯分析了191名虫病 (PV) 和46名虫病 (BP) 患者.
- 在治疗前和治疗后检查的平均血小板体积 (MPV),血小板,乙素,基素数,ESR和CRP水平.
- 缓解被定义为自身免疫性皮肤突发性疾病强度评分 (ABSIS) ≥75%的下降.
主要成果:
- 在PV患者中,在缓解期间,MPV,乙素,基素计数,ESR和CRP显著下降.
- 在高血压患者中,在缓解期间,MPV,乙氨基酸计数和ESR显著下降.
- 血小板计数显示PV没有显著变化;血小板和基细胞计数显示血压没有显著变化.
结论:
- 乙素,基素和血栓细胞有助于PV病原发生.
- 乙氨基和血栓细胞可能会导致BP的病原性.
- 在急性阶段的反应剂水平在活跃疾病期间比缓解期更高.
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