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自身免疫性干眼的眼表损伤。显微镜下病变的严重程度与干眼症状的严重程度平行。

Ocular surface injuries in autoimmune dry eye. The severity of microscopical disturbances goes parallel with the severity of symptoms of dryness.

作者信息

Cejková J, Ardan T, Cejka C, Malec J, Jirsová K, Filipec M, Ruzicková E, Dotrelová D, Brunová B

机构信息

Department of Eye Histochemistry and Pharmacology, Institute of Experimental Medicine, Academy of Sciences of the Czech Republic, Prague, Czech Republic.

出版信息

Histol Histopathol. 2009 Oct;24(10):1357-65. doi: 10.14670/HH-24.1357.

DOI:10.14670/HH-24.1357
PMID:19688700
Abstract

Autoimmune dry eye (Sjögren's syndrome, SS) is a chronic systemic disease characterized by salivary and lacrimal gland inflammation and tissue damage leading to keratoconjunctivitis sicca and xerostomia. In this review attention has been devoted to the cause of the development of oxidative injuries of the ocular surface of patients suffering from SS. It was shown that lacrimal glands and diseased conjunctival epithelium reveal increased expression of pro-inflammatory cytokines which are released into the tear fluid. A high amount of pro-inflammatory cytokines highly induce the elevated expression and activity of enzymatic systems that generate reactive oxygen and nitrogen species. An abundant amount of these toxic products leads to a decrease in antioxidants and to the formation of cytotoxic related oxidants, such as peroxynitrite. All these factors, together with reactive oxygen species from polymorphonuclear leukocytes, contribute to the development of oxidative injuries at the ocular surface. From the clinical point of view it is important that the level of severity of the above described microscopical disturbances found in conjunctival epithelial cells goes parallel with the level of severity of dry eye symptoms.

摘要

自身免疫性干眼(干燥综合征,SS)是一种慢性全身性疾病,其特征是唾液腺和泪腺炎症以及组织损伤,导致角结膜干燥症和口干症。在本综述中,我们关注了干燥综合征患者眼表氧化损伤发生的原因。研究表明,泪腺和患病的结膜上皮中促炎细胞因子的表达增加,这些因子会释放到泪液中。大量的促炎细胞因子会高度诱导产生活性氧和氮物种的酶系统的表达和活性升高。这些大量的有毒产物会导致抗氧化剂减少,并形成细胞毒性相关的氧化剂,如过氧亚硝酸盐。所有这些因素,连同多形核白细胞产生的活性氧,都促成了眼表氧化损伤的发生。从临床角度来看,结膜上皮细胞中上述微观干扰的严重程度与干眼症状的严重程度平行,这一点很重要。

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