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色素播散综合征和色素性青光眼的病理生理学

Pathophysiology of pigment dispersion syndrome and pigmentary glaucoma.

作者信息

Campbell D G, Schertzer R M

出版信息

Curr Opin Ophthalmol. 1995 Apr;6(2):96-101. doi: 10.1097/00055735-199504000-00015.

Abstract

Pigmentary glaucoma results from zonular-pigment dispersion, primarily in young, myopic, white individuals. The concavity of the midperipheral iris allows iridozonular contact. Released pigment is carried to the trabecular meshwork where it resides: (1) benignly, not affecting the intraocular pressure, as in pigment dispersion syndrome; or (2) malignantly, elevating the intraocular pressure, as in pigmentary glaucoma. Small amounts of pigment are quickly phagocytized. If the particulate load is heavy, the cells migrate further along the outflow pathway. The flattening of the iris in pigmentary glaucoma patients receiving iridotomies, along with the backward flow of pigment observed during treatment, demonstrates a greater pressure in the anterior than the posterior chamber. This reverse pupillary block may be due to temporary ocular deformations caused by blinking, as small aqueous aliquots are forced into the anterior chamber. Flattening of the concave iris is the key to current and future management of these patients.

摘要

色素性青光眼由晶状体悬韧带色素播散引起,主要见于年轻、近视的白人个体。周边虹膜的凹陷使得虹膜与晶状体悬韧带接触。释放的色素被带到小梁网并在那里停留:(1)呈良性,不影响眼压,如色素播散综合征;或(2)呈恶性,升高眼压,如色素性青光眼。少量色素会迅速被吞噬。如果颗粒负荷较重,细胞会沿着流出通道进一步迁移。接受虹膜切开术的色素性青光眼患者的虹膜变平,以及治疗期间观察到的色素逆流,表明前房压力高于后房。这种反向瞳孔阻滞可能是由于眨眼引起的暂时性眼部变形,因为少量房水被挤入前房。凹陷虹膜变平是这些患者当前和未来治疗的关键。

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