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药物性青光眼:机制与管理

Drug-induced glaucomas: mechanism and management.

作者信息

Tripathi Ramesh C, Tripathi Brenda J, Haggerty Chris

机构信息

Departments of Ophthalmology, University of South Carolina School of Medicine, Columbia, South Carolina 29209, USA.

出版信息

Drug Saf. 2003;26(11):749-67. doi: 10.2165/00002018-200326110-00002.

Abstract

Glaucoma comprises a heterogeneous group of diseases that have in common a characteristic optic neuropathy and visual field defects, for which elevated intraocular pressure is the major risk factor. The level of intraocular pressure within the eye depends on the steady state of formation and drainage of the clear watery fluid, called the aqueous humour, in the anterior chamber of the eye. An obstruction in the circulatory pathway of aqueous humour causes an elevation in intraocular pressure. Because intraocular pressure is the most modifiable parameter, therapeutic measures (medical and surgical) are aimed at reducing the pressure to protect against optic nerve damage. Glaucomatous optic neuropathy results from degeneration of the axonal nerve fibres in the optic nerve and death of their cell bodies, the retinal ganglion cells. Clinical examination of the optic nerve head or disc and the peripapillary nerve fibre layer of the retina reveals specific changes, and the resulting visual field defects can be documented by perimetry. Glaucoma can be classified into four main groups: primary open-angle glaucoma; angle-closure glaucoma; secondary glaucoma; and developmental glaucoma. Drug-induced glaucoma should be considered as a form of secondary glaucoma because it is brought about by specific systemic or topical medications. Although there is a high prevalence of glaucoma worldwide, the incidence of drug-induced glaucoma is uncertain. Drugs that cause or exacerbate open-angle glaucoma are mostly glucocorticoids. Several classes of drugs, including adrenergic agonists, cholinergics, anticholinergics, sulpha-based drugs, selective serotonin reuptake inhibitors, tricyclic and tetracyclic antidepressants, anticoagulants and histamine H(1) and H(2) receptor antagonists, have been reported to induce or precipitate acute angle-closure glaucoma, especially in individuals predisposed with narrow angles of the anterior chamber. In some instances, bilateral involvement and even blindness have occurred. In this article, the mechanism and management of drug-induced glaucomatous disease of the eye are emphasised. Although the product package insert may mention glaucoma as a contraindication or as an adverse effect, the type of glaucoma is usually not specified. Clinicians should be mindful of the possibility of drug-induced glaucoma, whether or not it is listed as a contraindication and, if in doubt, consult an ophthalmologist.

摘要

青光眼是一组异质性疾病,其共同特征是具有典型的视神经病变和视野缺损,而眼内压升高是主要危险因素。眼内的眼内压水平取决于眼内前房内一种清澈水样液体(称为房水)生成与排出的稳态。房水循环途径受阻会导致眼内压升高。由于眼内压是最可调节的参数,治疗措施(药物和手术)旨在降低眼压以防止视神经损伤。青光眼性视神经病变是由视神经中的轴突神经纤维变性及其细胞体(视网膜神经节细胞)死亡所致。对视神经乳头或视盘以及视网膜乳头周围神经纤维层进行临床检查可发现特定变化,通过视野计可记录由此产生的视野缺损。青光眼可分为四大类:原发性开角型青光眼;闭角型青光眼;继发性青光眼;以及发育性青光眼。药物性青光眼应被视为继发性青光眼的一种形式,因为它是由特定的全身或局部药物引起的。尽管全球青光眼患病率很高,但药物性青光眼的发病率尚不确定。导致或加重开角型青光眼的药物大多是糖皮质激素。据报道,几类药物,包括肾上腺素能激动剂、胆碱能药物、抗胆碱能药物、磺胺类药物、选择性5-羟色胺再摄取抑制剂、三环和四环抗抑郁药、抗凝剂以及组胺H(1)和H(2)受体拮抗剂,可诱发或促使急性闭角型青光眼发作,尤其是在前房角狭窄的易感个体中。在某些情况下,会出现双侧受累甚至失明。本文着重介绍药物性青光眼眼病的发病机制和治疗。尽管药品说明书可能会提及青光眼是禁忌证或不良反应,但通常未明确青光眼的类型。临床医生应留意药物性青光眼的可能性,无论其是否列为禁忌证,如有疑问,应咨询眼科医生。

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