Çaytemel Ceyda, Türkoğlu Zafer, Ağırgöl Şenay, Ustaoğlu Eda, Demir Filiz T, Uzuner Esen G
Department of Dermatology and Venereology, Istanbul Haseki Training and Research Hospital, Istanbul, Turkey.
Department of Dermatology and Venereology, Istanbul Medipol University, School of Medicine, Istanbul, Turkey.
Indian J Dermatol. 2022 Mar-Apr;67(2):205. doi: 10.4103/ijd.ijd_694_21.
The etiopathogenesis and cold stimulation mechanism are not fully understood in cold urticaria (CU). Substance (SP) is released from skin neurons as a result of cold stimulation. It causes mast cell degranulation and therefore causes mast cell chymase (MCC) release. Angiotensin-converting enzyme (ACE) plays a role in removing SP from the environment. ACE also catalyses the conversion of angiotensin I (AT1) to angiotensin II (AT2), like MCC. This study aims to investigate the role of SP, ACE and MCC in the pathogenesis of CU.
Patients with acquired CU were included in the study. Two punch biopsies were taken from the urticaria plaque resulting from the stimulation and the intact skin without lesions. The samples were evaluated histopathologically. All samples were stained immunohistochemically with SP, ACE and MCC antibodies.
The number of patients included in the study was 21. In the plaque lesion, the presence of dermal neutrophil and eosinophil, neutrophil in the vascular lumen were found to be statistically significantly higher than intact tissue ( = 0.046, = 0.014, = 0.014). Strong positive staining was detected in the full thickness of the epidermis, vascular endothelial cells, eccrine and sebaceous glands with ACE. MCC was statistically significantly higher in lesional skin than lesion-free skin samples ( < 0.001).
Mast cell maintains its central role in CU pathogenesis. SP, which causes neurogenic inflammation, may not be detected due to its rapid destruction in the tissue. Strong staining of ACE, which takes part in the local renin-angiotensin-aldosterone (RAS) system in the skin, should be documented quantitatively.
寒冷性荨麻疹（CU）的发病机制和冷刺激机制尚未完全明确。冷刺激可使皮肤神经元释放P物质（SP）。它会导致肥大细胞脱颗粒，进而引起肥大细胞糜蛋白酶（MCC）释放。血管紧张素转换酶（ACE）在从环境中清除SP方面发挥作用。ACE还像MCC一样催化血管紧张素I（AT1）转化为血管紧张素II（AT2）。本研究旨在探讨SP、ACE和MCC在CU发病机制中的作用。
纳入获得性CU患者进行研究。从刺激引起的荨麻疹斑块及无病变的完整皮肤处各取两块打孔活检组织。对样本进行组织病理学评估。所有样本均用SP、ACE和MCC抗体进行免疫组织化学染色。
纳入研究的患者有21例。在斑块病变中，真皮层中性粒细胞和嗜酸性粒细胞的数量以及血管腔内中性粒细胞数量在统计学上显著高于完整组织（P = 0.046，P = 0.014，P = 0.014）。ACE在表皮全层、血管内皮细胞、汗腺和皮脂腺中检测到强阳性染色。MCC在皮损处皮肤中的含量在统计学上显著高于无皮损皮肤样本（P < 0.001）。
肥大细胞在CU发病机制中维持其核心作用。引起神经源性炎症的SP可能因其在组织中迅速被破坏而未被检测到。应定量记录参与皮肤局部肾素 - 血管紧张素 - 醛固酮（RAS）系统的ACE的强染色情况。
