Winsz-Szczotka Katarzyna, Komosińska-Vassev Katarzyna, Olczyk Krystyna
Zakład Chemii Klinicznej i Diagnostyki Laboratoryjnej Slaskiej Akademii Medycznej, Sosnowiec.
Postepy Hig Med Dosw (Online). 2006;60:184-91.
Glycosaminoglycans (GAGs), which include chondroitin sulfate (CS), dermatan sulfates (DS), heparan sulfate (HS), heparin (H), keratan sulfate (KS), and hyaluronic acid (HA), are a group of linear, polyanionic heteropolysaccharides. The GAGs chains, except for those of hyaluronic acid, are covalently attached to core proteins, forming proteoglycans (PGs). PGs/GAGs are present at the cellular level as elements of the cell membrane and intracellular granules. They are also components of the ground substance of the extracellular matrix. These macromolecules are involved in cell adhesion, migration, and proliferation. Alterations in GAGs metabolism may influence the pathogenesis of many disorders, including Graves' disease. Graves' disease is an autoimmune thyroid pathology characterized by hyperthyroidism, thyroid hyperplasia, as well as ophthalmopathy and/or pretibial myxedema. The pathogenesis of these extrathyroidal manifestations involves fibroblast activation and increased glycosaminoglycan synthesis and accumulation. Disturbances in GAGs metabolism in tissue are associated with qualitative and quantitative GAGs alterations in Graves' patients' serum and urine. Although the mechanisms leading to the development of orbital and/or skin complications in the course of Graves' disease have not been fully elucidated, it is postulated that they depend on both immunological disturbances and the hyperthyroid state.
The alterations in GAGs metabolism connected with Graves' disease could lead to systemic changes in the proprieties of the extracellular matrix.
糖胺聚糖（GAGs）包括硫酸软骨素（CS）、硫酸皮肤素（DS）、硫酸乙酰肝素（HS）、肝素（H）、硫酸角质素（KS）和透明质酸（HA），是一组线性的、聚阴离子杂多糖。除透明质酸的糖胺聚糖链外，其他糖胺聚糖链均共价连接至核心蛋白，形成蛋白聚糖（PGs）。蛋白聚糖/糖胺聚糖在细胞水平作为细胞膜和细胞内颗粒的成分存在。它们也是细胞外基质基质的组成部分。这些大分子参与细胞黏附、迁移和增殖。糖胺聚糖代谢的改变可能影响包括格雷夫斯病在内的许多疾病的发病机制。格雷夫斯病是一种自身免疫性甲状腺疾病，其特征为甲状腺功能亢进、甲状腺增生以及眼病和/或胫前黏液性水肿。这些甲状腺外表现的发病机制涉及成纤维细胞活化以及糖胺聚糖合成和积累增加。组织中糖胺聚糖代谢紊乱与格雷夫斯病患者血清和尿液中糖胺聚糖的定性和定量改变有关。尽管格雷夫斯病过程中导致眼眶和/或皮肤并发症发生的机制尚未完全阐明，但据推测它们既取决于免疫紊乱，也取决于甲状腺功能亢进状态。
与格雷夫斯病相关的糖胺聚糖代谢改变可能导致细胞外基质特性的全身变化。
