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| CASE REPORT |
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| Ahead of print publication |
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Latanoprost-associated cystoid macular edema in a patient with phakic eyes
Wei-Che Lin1, Jui-Wen Hsieh2, Shawn H Tsai3, Yu-Wen Lan4
1 Department of Ophthalmology, MacKay Memorial Hospital, Taipei City; Department of Medicine, MacKay Medical College, New Taipei City, Taiwan
2 Department of Ophthalmology, MacKay Memorial Hospital, Taipei City, Taiwan
3 Department of Ophthalmology, MacKay Memorial Hospital, Taipei City; Department of Medicine, MacKay Medical College, New Taipei City; Department of Optometry, MacKay Junior College of Medicine, Nursing, and Management, Taipei City, Taiwan
4 Department of Ophthalmology, MacKay Memorial Hospital, Taipei City; Department of Medicine, MacKay Medical College, New Taipei City; MacKay Junior College of Medicine, Nursing, and Management, Taipei City, Taiwan
| Date of Submission | 15-Feb-2022 |
| Date of Acceptance | 10-Mar-2022 |
| Date of Web Publication | 05-Aug-2022 |
Correspondence Address:
Yu-Wen Lan,
No. 92, Sec. 2, Zhongshan N. Rd., Taipei City 10449
Taiwan
 Source of Support: None, Conflict of Interest: None DOI: 10.4103/tjo.tjo_19_22
Here, we report a case of bilateral cystoid macular edema (CME) in a woman with phakic eyes after 22 years of latanoprost use. Optical coherence tomography revealed multiple intraretinal cysts, and fluorescein angiography revealed characteristic petaloid dye leakage from the perifoveal capillaries. A cause-effect relationship was suspected when CME resolved after switching from latanoprost to dorzolamide, as confirmed by positive rechallenge and dechallenge tests. Since prostaglandin analog-induced CME has only been reported in patients with pseudophakic, aphakic, or phakic eyes with retinal conditions predisposing to macular edema, this seems to be the first reported case of latanoprost-induced CME in a patient with phakic eyes without retinal risk factors.
Keywords: Case report, crystalline lens, cystoid macular edema, latanoprost
How to cite this URL:
Lin WC, Hsieh JW, Tsai SH, Lan YW. Latanoprost-associated cystoid macular edema in a patient with phakic eyes. Taiwan J Ophthalmol [Epub ahead of print] [cited 2023 Mar 23]. Available from: https://www.e-tjo.org/preprintarticle.asp?id=353452 |
| Introduction | |  |
Latanoprost is a 17-phenyl-substituted prostaglandin F2 α-isopropyl ester prodrug that enhances uveoscleral outflow as a physiological mechanism lowering intraocular pressure (IOP). Common adverse effects include hypertrichosis, eyelid hyperpigmentation, and conjunctival hyperemia, and rare side effects include cystoid macular edema (CME), particularly in patients with aphakic or pseudophakic eyes or known risk factors for macular edema.[1] Here, we report a case of bilateral (OU) CME after 22 years of latanoprost use in a patient without prior ocular surgery or CME-associated risk factors.
| Case Report | | |
A 53-year-old Asian woman presented with bilateral metamorphopsia for 2 weeks. She had a history of primary open-angle glaucoma for 28 years. She had received 0.25% timolol twice a day for 4 years and then switched to 0.005% latanoprost once before bedtime (QHS) for better IOP control.
On examination, her best-corrected visual acuity was 20/100 in the right eye (OD) and 20/50 in the left eye (OS), and IOP was 16.0 mmHg (OU). Slit-lamp examination revealed grade 2 nuclear cataract, with no evidence of intraocular inflammation (OU). Fundus examination showed cup–disc ratios of 0.5 OD and 0.4 OS, with a slight decrease in foveal reflectivity (OU). Optical coherence tomography (OCT) showed well-defined intraretinal cysts (OU) with the central macular thickness (CMT) of 319 μm OD and 326 μm OS [Figure 1]a and [Figure 1]b. Fluorescein angiography revealed petaloid leakage from the perifoveal retinal capillaries in the late phase, without staining of the optic disc (OU) [Figure 2]a and [Figure 2]b; thus, bilateral CME was diagnosed. Latanoprost was discontinued and replaced with 2% dorzolamide thrice a day (TID). After 1 month, the best-corrected visual acuity had been restored to 20/30 OD and 20/40 OS, and metamorphopsia had improved. OCT demonstrated subsided CME with CMT of 218 μm OD and 227 μm OS [Figure 3]a and [Figure 3]b. | Figure 1: Optical coherence tomography showing cystoid macula edema in the right (a) and left eye (b) after 22 years of latanoprost use
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 | Figure 2: Fluorescein angiography showing characteristics of cystoid macular edema with petaloid leakage from perifoveal retinal capillaries in the right (a) and left eye (b)
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 | Figure 3: Optical coherence tomography showing subsided cystoid macular edema in the right (a) and left eye (b) after switching from latanoprost to dorzolamide
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Because her IOP was not sufficiently low with 2% dorzolamide, a rechallenge test was performed 3 months after the discontinuation of latanoprost. She agreed to restart latanoprost QHS (OD) while on 2% dorzolamide TID (OS). After 1 month, OCT revealed recurrent CME (OD) with CMT of 316 μm, while OS remained normal [Figure 4]a and [Figure 4]b. For the dechallenge test, both eyes were switched to a combination of brimonidine and brinzolamide twice a day for better IOP control. One month later, OCT revealed no signs of CME [OU; [Figure 5]a and [Figure 5]b]. | Figure 4: After re-challenging the right eye with latanoprost, optical coherence tomography revealed recurrent cystoid macula (a). The left eye remained normal (b)
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 | Figure 5: The dechallenge test showed subsided cystoid macular edema in the right eye (a), while the left eye remained normal (b)
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| Discussion | | |
Here, we reported a case of CME (OU) in a patient 22 years after latanoprost initiation. The patient had phakic eyes with no ocular or systemic conditions increasing the risk of CME. CME was diagnosed based on the characteristic OCT and fluorescein angiography findings; however, no other possible causes of CME could be recognized. A cause-effect relationship was suspected because of the resolution of macular edema after latanoprost discontinuation, later confirmed by rechallenge and dechallenge tests.
Prostaglandins are metabolic products of arachidonic acid that play an important role in inducing inflammation and edema in systemic tissue, including the eye.[2] Considering that glaucoma medications are usually applied topically, the effect of exogenous prostaglandins on the posterior segment of the eye is debatable. A study by Bito and Baroody [3H]-labeled prostaglandin F2α esters showed evidence of corneal penetration in phakic rabbit eyes. Further, prostaglandin levels were remarkably high in the ciliary body and also detected in the retina and choroid.[3] Therefore, topical latanoprost could exert a biological effect on the posterior segment and induce CME.
The mechanism underlying the development of CME from latanoprost use is not fully understood. However, for patients with pseudophakic or aphakic eyes, latanoprost use has been hypothesized to disrupt the blood-aqueous barrier, which is associated with the development of CME.[4] Another study supports the role of inflammatory mediators, such as prostaglandins, in blood-retinal barrier disruption, with evidence that anti-inflammatory agents may prevent or aid the recovery of CME caused by prostaglandin analogs.[5]
Although several studies have reported that latanoprost induces CME, all of those patients had ocular or systemic conditions increasing the risk of CME, such as a history of CME or anterior uveitis, epiretinal membrane, vein occlusion, diabetes mellitus, and complicated or uneventful cataract surgery.[6],[7] In a study by Warwar et al., 2.1% of the 94 patients developed CME while being treated with latanoprost, but all of them had pseudophakic eyes.[8] In a review by Hu et al., 47 of 48 eyes with prostaglandin-induced CME were pseudophakic, aphakic, or had a subluxated intraocular lens. One patient with a surgery-naïve phakic eye had a history of epiretinal membrane, branch retinal vein occlusion, and CME. This study also suggests that latanoprost is associated with a higher frequency of CME development compared to bimatoprost (0.19% and 0.00%, respectively).[9]
Our patient developed bilateral CME after 22 years of latanoprost use, which is significantly longer than that reported for eyes with CME risk factors. In a study by Warwar et al., the patients with pseudophakic eyes developed CME after 2–8 months of latanoprost use.[8] In a systemic review by Hu et al., the median time of onset of CME was 30 days (range: 7–365 days).[9] Cataract surgery may induce changes in the lens epithelial cells and aid the endogenous production of proinflammatory molecules.[10] The altered lens barrier and induced inflammation could render the eye more susceptible to prostaglandin-associated CME.[11] By acting as a barrier between the anterior and posterior segments, an intact lens may greatly reduce, though not entirely eliminate, the risk of developing CME.
| Conclusion | | |
In conclusion, this seems to be the first reported case of CME resulting from latanoprost use in a patient with phakic eyes without coexisting risk factors. The cause-effect relationship was strongly established via repeated challenge and dechallenge tests. Latanoprost and other prostaglandin analogs should be used with caution, particularly considering the numerous alternative ocular hypotensive agents available today. Patients receiving such therapy should be closely monitored for symptoms consistent with CME.
Declaration of patient consent
The authors certify that they have obtained all appropriate patient consent forms. In the form, the patient has given her consent for her images and other clinical information to be reported in the journal. The patient understands that her name and initials will not be published and due efforts will be made to conceal her identity, but anonymity cannot be guaranteed.
Acknowledgment
The patient consent to publish images and other clinical information.
Financial support and sponsorship
Nil.
Conflicts of interest
The authors declare that there are no conflicts of interests of this paper.
| References | | |
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| 3. | Bito LZ, Baroody RA. The ocular pharmacokinetics of eicosanoids and their derivatives. 1. Comparison of ocular eicosanoid penetration and distribution following the topical application of PGF2 alpha, PGF2 alpha-1-methyl ester, and PGF2 alpha-1-isopropyl ester. Exp Eye Res 1987;44:217-26. |
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[Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5]
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