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Editor,—I read with interest the article by Koller and co-workers,1 in which the authors investigated causes and risk factors for membrane formation in the anterior chamber after argon laser trabeculoplasty (ALT). In their discussion the authors conclude that ALT and especially repeated ALT represent a risk for late membrane formation over the trabecular meshwork, which leads to late failure of ALT. They suggest that both late membrane formation and immediate intraocular pressure (IOP) spikes after ALT are induced by the same mechanism—that is, laser induced inflammation.
I agree with the authors that laser induced inflammation is a possible factor for subacute and late membrane formation over the trabecular meshwork. In a retrospective study2 in which the duration of success (IOP <22 mm Hg after treatment) was investigated we found that the length of success was significantly shorter in eyes which received no topical anti-inflammatory medication after ALT compared with the eyes which received such a treatment for 5 days following the same procedure. Is the risk for membrane formation similar after laser trabeculoplasties using different lasers? The authors did not discuss this question; however, this is a point of practical importance. In a prospective, comparative clinical and morphological study3one randomly selected eye of the patients underwent a conventional ALT, and the contralateral eye received a similar treatment but with a very low energy level of a pulsed Nd:YAG laser. In this study, which I performed several years before selective laser trabeculoplasty was developed, both eyes of the participants had identical type of open angle glaucoma in a very similar stage before treatment. The clinical efficacy of both types of laser trabeculoplasty was similar. The most important difference I found in the eyes requiring trabeculectomy was the presence of a membrane over the trabecular meshwork after ALT and the absence of this membrane after Nd:YAG laser trabeculoplasty in the same patients. These findings suggest that the type of laser or its thermal effect are also important factors when the causes of late failure are discussed.
In contrast with the authors' opinion I do not think that immediate IOP spikes 1 or 2 hours after ALT are caused by prostaglandins or inflammation. In clinical studies it was clearly shown that either topical corticosteroid or non-steroid pretreatments failed to reduce the early IOP spike though both types of treatments did reduce the inflammation after ALT.4-7 This clearly shows that late and acute IOP elevations are caused by different mechanisms. Recently it was shown8 that the trabecular meshwork contains contractile elements which are contracted by endothelin-1 (ET-1). The contraction causes a decrease of the outflow and a resulting IOP elevation. Lower ET-1 concentration, however, may induce relaxation via endothelin B receptors. In experimental studies9 exogenous ET-1 injected into the anterior chamber caused the typical biphasic IOP alterations we experience after ALT in clinical praxis: an immediate spike is followed by a prolonged (10–15 days) pressure decrease. Long term IOP decrease after ALT is caused by the biochemical alterations of the trabecular meshwork, and appear only after some weeks following the laser treatment. To investigate the potential role of ET-1 in the development of IOP spikes after ALT we performed ALT in rabbits.10-12 Very high ET-1 concentrations were found in the aqueous humour already 30 minutes after treatment, which persisted for 4 hours, but disappeared within 24 hours, and was not found in the sham treated contralateral eyes. This ET-1 release from the uveal tissue (which is known to be rich of endothelins) was associated with acute pressure elevation and later decrease on the treated but not on the sham treated eyes of the same animals. These findings suggest that the acute pressure spike after ALT is caused by a mechanism different from that of the long term pressure elevation: the latter is promoted by inflammation while the former maybe caused by acute endothelin release from the damaged uveal tissue.