Klin Monbl Augenheilkd 2013; 230(7): 692-696
DOI: 10.1055/s-0032-1328472
Übersicht
Georg Thieme Verlag KG Stuttgart · New York

Klinik und Therapie des Steroidglaukoms

Symptoms and Therapy for Steroid Glaucoma
F. Rüfer
Augenheilkunde, Augenklinik Bellevue, Kiel
,
D. Uthoff
Augenheilkunde, Augenklinik Bellevue, Kiel
› Author Affiliations
Further Information

Publication History

eingereicht 15 January 2013

akzeptiert 04 February 2013

Publication Date:
06 June 2013 (online)

Zusammenfassung

Bei einer Steroidresponse kommt es nach topischer oder systemischer Anwendung von Steroiden zu einer Vermehrung von extrazellulärer Matrix im Trabekelmaschenwerk und dadurch zu einer Erhöhung des Kammerwasserabflusswiderstands. 30–40 % der Normalbevölkerung sind Steroidresponder. Etwa 5 % entwickeln Anstiege des intraokularen Druckes (IOD) von > 15 mmHg. Diese Patienten werden als „High Responder“ bezeichnet. Bei Patienten mit primärem Offenwinkelglaukom (POWG) liegt der Anteil der Steroidresponder bei etwa 90 %. Das Ausmaß der Steroidresponse ist abhängig von Art und Dauer der Anwendung eines Steroids. Die höchste IOD-steigernde Potenz hat Dexamethason. Mögliche Differenzialdiagnosen sind POWG, okuläre Hypertension, Normaldruckglaukom, Pseudoexfoliationsglaukom und Sekundärglaukome anderer Genese. Für die Diagnosestellung ist eine detaillierte Anamnese wichtig. Beweisend ist ein Rückgang des IOD nach Absetzen der Steroide. Die Therapie eines Steroidglaukoms umfasst neben der topischen Anwendung von Antiglaukomatosa unter anderem fistulierende Eingriffe, Trabekulotomie und Lasereingriffe. Bisher sind jedoch für das Steroidglaukom wenig vergleichende Studien zu unterschiedlichen operativen Verfahren publiziert worden. Nach Anwendung von intravitreal oder subkonjunktival applizierten Steroiden kommt bei therapieresistenter IOD-Steigerung auch eine operative Entfernung der Steroide aus dem Auge in Betracht. Eine Gentherapie des Steroidglaukoms wird derzeit noch erforscht.

Abstract

In steroid responders, topical or systemic application of steroids leads to extracellular deposits in the trabecular meshwork which increase trabecular meshwork outflow resistance. 30–40 % of the normal population are steroid responders. About 5 % develop an intraocular pressure (IOP) rise of > 15 mmHg. These patients are termed “high responders”. In patients with primary open angle glaucoma (POAG), the proportion of steroid responders sums up to 90 %. The extent of steroid response depends on the kind of steroid used and on the duration of its administration. Dexamethasone has the highest IOP increasing potency. Differential diagnoses are POAG, ocular hypertension, normal tension glaucoma, pseudoexfoliation glaucoma and secondary glaucoma due to different reasons. To make the diagnosis, a detailed anamnesis is crucial. A recompensated IOP after the end of steroid use proves the diagnosis. The treatment of steroid glaucoma includes topical antiglaucoma medications, glaucoma filtration surgery, trabeculotomy, and laser surgery. So far, only few comparative studies on different treatment options have been published on steroid glaucoma. In some cases of therapy-resistant IOP increases following intravitreal or subconjunctival steroid administration, operative removal of the steroids can be considered. A gene therapy treatment of steroid glaucoma is still a topic of research.

 
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