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特应性皮炎和皮肤 T 细胞淋巴瘤患者血液中的血清淀粉样蛋白 A 水平。

Serum amyloid A levels in the blood of patients with atopic dermatitis and cutaneous T-cell lymphoma.

机构信息

Department of Dermatology, University of Tokyo Graduate School of Medicine, Tokyo, Japan.

Department of Dermatology, International University of Health and Welfare, Chiba, Japan.

出版信息

J Dermatol. 2018 Dec;45(12):1440-1443. doi: 10.1111/1346-8138.14665. Epub 2018 Oct 5.

Abstract

Serum amyloid A (SAA) is an acute phase protein, which activates immune cells and induces cytokines and chemokine. SAA levels in blood have been reported to be elevated in case of inflammation, infections, neoplasia and tissue injury. In this study, we examined SAA levels in the blood of patients with atopic dermatitis (AD) and cutaneous T-cell lymphoma (CTCL). SAA levels in sera of AD patients, those of CTCL patients and those of healthy controls were not significantly different. When AD or CTCL patients were classified by disease severity, there was still no difference in SAA levels. In AD patients, however, SAA levels positively correlated with the number of eosinophils in peripheral blood and serum soluble interleukin-2 receptor (sIL-2R) levels. There were significant correlations between SAA levels in blood and the number of white blood cells in peripheral blood and serum sIL-2R levels in CTCL patients. AD patients without topical steroid treatment and CTCL patients without narrowband ultraviolet B therapy showed increased levels of SAA, which suggested that SAA levels may easily fluctuate with treatment. These results imply a possible contribution of SAA in development of AD and CTCL.

摘要

血清淀粉样蛋白 A(SAA)是一种急性相蛋白,可激活免疫细胞并诱导细胞因子和趋化因子。据报道,血液中的 SAA 水平在炎症、感染、肿瘤和组织损伤时升高。在这项研究中,我们检查了特应性皮炎(AD)和皮肤 T 细胞淋巴瘤(CTCL)患者血液中的 SAA 水平。AD 患者、CTCL 患者和健康对照者血清中的 SAA 水平无显著差异。当按疾病严重程度对 AD 或 CTCL 患者进行分类时,SAA 水平仍无差异。然而,在 AD 患者中,SAA 水平与外周血嗜酸性粒细胞数和血清可溶性白细胞介素-2 受体(sIL-2R)水平呈正相关。CTCL 患者血液中的 SAA 水平与外周血白细胞数和血清 sIL-2R 水平之间存在显著相关性。未接受局部皮质类固醇治疗的 AD 患者和未接受窄带紫外线 B 治疗的 CTCL 患者 SAA 水平升高,这表明 SAA 水平可能随治疗而容易波动。这些结果提示 SAA 可能在 AD 和 CTCL 的发病机制中起作用。

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