Alcon Laboratories, Inc., Fort Worth, Texas, U.S.A.
J Glaucoma. 1995 Oct;4(5):354-69.
Glucocorticoids (GC) can regulate aqueous humor outflow and have often been associated with primary open angle glaucoma (POAG). The ocular or systemic administration of glucocorticoids can cause the elevation of intraocular pressure by increasing aqueous humor outflow resistance via morphological and biochemical changes in the trabecular meshwork (TM). The ability of glucocorticoids to induce ocular hypertension is dependent on individual responsiveness, the potency of the glucocorticoid, the route of administration, and the duration of treatment. Glucocorticoid-induced ocular hypertension occurs not only in humans, but also in rabbits, cats, dogs, and nonhuman primates. Glucocorticoids have a multitude of effects on trabecular meshwork cells causing changes in TM protein expression, cytoskeletal organization, extracellular matrix deposition, cell shape, and cell function. Many of these changes in the TM may be responsible for the generation of glucocorticoid-induced ocular hypertension. There have been several reports of increased cortisol levels, altered cortisol metabolism, and differential glucocorticoid responsiveness in patients with ocular hypertension and POAG. However, there is as yet no clear evidence for a causal role between glucocorticoids and primary open angle glaucoma. Finally, there is evidence that a variety of steroids of differing pharmacological steroid classes can lower the elevated intraocular pressure (IOP) in glucocorticoid-induced ocular hypertension and/ or in glaucoma patients. Continued research in the coming years should (a) identify the molecular mechanisms responsible for glucocorticoid-induced ocular hypertension and glaucoma, (b) determine whether glucocorticoids play a role in the pathogenesis of primary open angle glaucoma, and (c) determine the therapeutic utility of anti-glaucoma steroids.
糖皮质激素（GC）可以调节房水流出，并且常常与原发性开角型青光眼（POAG）有关。糖皮质激素的眼部或全身给药可通过小梁网（TM）的形态和生化变化增加房水流出阻力，从而引起眼压升高。糖皮质激素引起的眼压升高的能力取决于个体的反应性、糖皮质激素的效力、给药途径和治疗持续时间。糖皮质激素引起的眼压升高不仅发生在人类，还发生在兔子、猫、狗和非人类灵长类动物中。糖皮质激素对小梁网细胞有多种作用，导致 TM 蛋白表达、细胞骨架组织、细胞外基质沉积、细胞形状和细胞功能的变化。这些 TM 的许多变化可能是导致糖皮质激素引起的眼压升高的原因。有几篇报道称，眼压升高和 POAG 患者的皮质醇水平升高、皮质醇代谢改变和糖皮质激素反应性差异。然而，目前尚无明确证据表明糖皮质激素与原发性开角型青光眼之间存在因果关系。最后，有证据表明，各种具有不同药理学类固醇类别的类固醇可以降低糖皮质激素引起的眼压升高和/或青光眼患者的眼压升高。在未来几年的持续研究中，应（a）确定导致糖皮质激素引起的眼压升高和青光眼的分子机制，（b）确定糖皮质激素是否在原发性开角型青光眼的发病机制中起作用，以及（c）确定抗青光眼类固醇的治疗效果。
