The mystery of angiographically silent macular oedema due to taxanes

被引:37
作者
Kuznetcova T.I. [1 ,2 ]
Cech P. [3 ]
Herbort C.P. [1 ,4 ]
机构
[1] Centre for Ophthalmic Specialised Care (COS), 1003 Lausanne
[2] Ophthalmology Department, I.P. Pavlov State Medical University, Saint-Petersburg
[3] Centre de Chimiothérapie Anti-Cancéreuse (CCAC), Lausanne
[4] University of Lausanne, Lausanne
关键词
Cystoid macular oedema; Fluorescein angiography; Indocynine green angiography; Optical coherence tomography; Paclitaxel; Taxane drugs;
D O I
10.1007/s10792-012-9558-9
中图分类号
学科分类号
摘要
Taxanes are widely used anticancer agents, produced from the plants of the genus Taxus (yews). One of the rare side-effects caused by taxanes is a bilateral cystoid macular oedema (CMO). The particularity of this type of CMO is that it is angiographically silent showing no leakage or pooling on fluorescein angiography (FA). To date, the mechanism of this oedema has not been clearly understood and existing theories do not explain this phenomenon very well. Our aimwas to report a case of paclitaxel-inducedCMOand put forward a putative explanation for this occurrence.A 64-year-oldwoman presentedwith a 7-month history of progressively decreasing bilateral visual acuity with an apparently normal fundus. At entry her best-corrected visual acuity (BCVA) was 0.4 for far and near OD and 0.5 for far and near OS. Optical coherence tomography (OCT) revealed a CMO with a central thickness of 561 lm OD and 488 lm OS; there were no signs of intraocular inflammation. FA showed no capillary leakage and quasi absent late hyperfluorescence OU. Indocyanine green angiography was within normal limits. Classical CMO treatment was ineffective and only discontinuation of paclitaxel resulted in recovery of a normal macular structure after 4 weeks with an increase of BCVA to 0.9 OD and 1.0 OS. In order to understand the properties of taxane drug-induced cystoid macular oedema (TDICMO) we compared the spectral OCT findings of our case to an inflammationinduced CMO of equal thickness and to a case of multifocal choroiditis. The plane of separation of TDICMO was above the external limiting membrane in both cases. In contrast to inflammation-inducedCMO where the four external bandswerewell identified, there was attenuation of these bands in TDICMO but no disruption of the layers as seen inmultifocal choroiditis, indicating that the fluid inTDICMOhad a high viscosity producing a shadow underneath. TDICMO most probably originates from retinal pigment epithelium dysfunction by their effect onmicrotubule functions and not from vascular leakage. The content of the CMO seems to bemade up of viscous fluid. As the origin of the CMO is not inflammatory, classical CMO treatments have no effect and only discontinuation of the taxane drug allows reversal of the CMO. © Springer Science+Business Media B.V. 2012.
引用
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页码:299 / 304
页数:5
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