Anorexiant-induced transient myopiaafter myopic laser in situ keratomileusis

Woojin Lee, MD, Jee Ho Chang, MD, Kyu Hwa Roh, MD, J.K. Chung, MD,Young Hoon Ohn, MD, PhD

We report a case of acute transient myopia associated with ciliochoroidal effusion induced by ano-rexiants. The patient had had myopic laser in situ keratomileusis 7 years earlier. Acute bilateralmyopia associated with anterior chamber shallowing, intraocular pressure elevation, diffuse cilio-choroidal effusion, and perimacular retinal folds was relieved 14 days after discontinuation ofanorexiant medications. Tropicamide and atropine were used to deepen the anterior chamber.Sympathomimetic drugs such as phendimetrazine and ephedrine are used as anorexiants andmay induce transient myopia associated with ciliochoroidal effusion, shallow anterior chamber,and acute angle-closure glaucoma.

J Cataract Refract Surg 2007; 33:746–749 Q 2007 ASCRS and ESCRS

CASE REPORT

Transient myopia associated with ciliochoroidal effu-sion has been reported after the use of several drugs;eg, sulfanilamides,1,2 hydrochlorothiazide,3 topira-mate,4,5 and acetazolamide.6,7 Chlorthalidone8 andtriamterene9 are suspected as the causative agents insimilar cases. The presumed pathogenetic mechanismis ciliochoroidal effusion, which causes anterior rota-tion of the entire ciliary body, resulting in the narrow-ing or, possibly, the disappearance of the ciliary sulcusand subsequent anterior shifting of the lens–irisdiaphragm.

Other etiologies that cause ciliochoroidal effusioninclude ocular inflammation,10,11 nanophthalmos,12

panretinal photocoagulation,13 scleral buckling,14

pars plana vitrectomy,15 trauma,16,17 and various sys-temic diseases.18,19 We present a patient with anorex-iant-induced transient myopia several years afteruneventful myopic laser in situ keratomileusis(LASIK).

Accepted for publication October 5, 2006.

From the Department of Ophthalmology, Soonchunhyang Univer-sity College of Medicine, Soonchunhyang University BucheonHospital, Bucheon, South Korea.

No author has a financial or proprietary interest in any material ormethod mentioned.

Corresponding author: Woojin Lee, MD, Department of Ophthal-mology, Soonchunhyang University College of Medicine, #1174Jung-dong, Wonmi-gu, Bucheon, Gyeonggi-do, 420-767, SouthKorea. E-mail: ethiot@hanmail.net.

Q 2007 ASCRS and ESCRS

Published by Elsevier Inc.

746

CASE REPORT

A28-year-oldwomandeveloped bilateral decreased visual acuity af-ter taking anorexiantmedications prescribedby an obesity clinic. Thesymptoms began abruptly the ninth day after she started taking themedications, which included phendimetrazine tartrate, a caffeine–ephedrine mixture, L-carnitine, and a compound drug composedof green tea extract and orthosiphon powder. The patient had un-eventful myopic LASIK surgery by another ophthalmologist 6 yearsearlier and had excellent uncorrected visual acuity (UCVA) prior tothe new symptoms. She had a history of sensitivity to sulfa drugs.

The initial examination revealed a visual acuity of 20/40 witha �8.0 diopter (D) myopic correction, a shallow anterior chamberdepth (ACD) (Figure 1), and an intraocular pressure (IOP) of 25 mmHgwith applanation tonometry in both eyes. No sign of ocular in-flammation other than mild conjunctival injection and chemosiswas observed by slitlamp biomicroscopy. Gonioscopic examinationshowed appositional angle closure of 360 degrees with opening ofthe angle with indentation (Figure 2). Despite the shallow ACDand IOP elevation, the pupils responded briskly to light. The patientwas started on a short-acting cycloplegic agent to deepen the ante-rior chamber. After 3 hours, the anterior chamber had deepenedand the IOP decreased to 16 mm Hg in both eyes. Bilateral retinalfolds were noted in the posterior polar areas in both eye on dilatedfundus examination (Figure 3). The initial B-scan ultrasonographydisclosed ciliochoroidal thickening (Figure 4). The central ACDwas 2.62 mm in the right eye and 2.50 mm in the left eye, and thelens thickness was 3.94 mm and 3.98 mm, respectively. Corneal to-pography revealed well-centered ablation patterns in both eyeswithout signs of corneal ectasia.

Atropine sulfate 1% was instilled once in both eyes, and the pa-tient was observed regularly at the outpatient clinic. In case of addi-tional IOP elevation, a combination eyedrop of timolol 0.5%with dorzolamide 2% (Cosopt) twice a day and oral acetazolamide250 mg 2 times a day were prescribed. The patient was also in-structed to discontinue all anorexiant medications, includingphendimetrazine and ephedrine.

On the visit 3 days later, the visual acuity was 20/20 in the righteye and 20/25 in the left eye with�0.75 D correction. The peripheral

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doi:10.1016/j.jcrs.2006.10.072

747CASE REPORT: ANOREXIANT-INDUCED TRANSIENT MYOPIA ASSOCIATED WITH CILIOCHOROIDAL EFFUSION

Figure 1. Initial biomicroscopicfinding. Central (A) and peripheral(B) anterior chamber shallowingare seen.

ACD was estimated to be less than one half the corneal thickness,and the central ACDwas approximately 5 corneal thicknesses. Intra-ocular pressure normalized, and no further medications wereprescribed.

Two weeks after the anorexiant medications were discontinued,the UCVA was 20/20 in both eyes, with a spherical equivalent of�0.25 D. The IOP normalized to 12 mm Hg in the right eye and 10mm Hg in the left eye, and slitlamp biomicroscopic findings werenormal. A-scan measurements showed an ACD of 3.87 mm and3.79 mm, respectively, and lens thickness decreased to 3.67 mm inboth eyes. Follow-up B-scan (Figure 5) and fundoscopy showedthe ciliochoroidal thickening and perimacular retinal folds haddisappeared.

DISCUSSION

Phendimetrazine and ephedrine are sympathomi-metic drugs that have been used as anorexiants. Bothdrugs release norepinephrine from presynaptic neu-rons. Phendimetrazine is a U.S. Food and DrugAdministration–approved drug, although it is recom-mended that the drug be used for only a fewweeks, 12weeks being the maximum.20

Sympathomimetic drugs may cause pupillary my-driasis by an anticholinergic effect, resulting in

Figure 2. Initial gonioscopic finding. Appositional angle closure isnoted along with opening of the angle with indentation (arrow).

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pupillary block glaucoma, especially in patients whohave a predisposition for angle closure, but have notbeen known to cause ciliochoroidal effusion. In thiscase, it seems that the mechanism for angle closure isnot related to pupillary block, evidenced by the ab-sence of mid-dilated and nonreactive pupils. Also,the age of the patient and the pre-LASIK myopia donot fall into the common risk factors for angle-closureglaucoma.

The pathogenetic mechanism responsible for the id-iosyncratic event in this case seems to be ciliochoroidaleffusion, evidenced by the ultrasonographic resultsand perimacular retinal folds. Ciliochoroidal effusionresults in anterior rotation of the entire ciliary bodyand anterior shifting of the lens–iris diaphragm,thereby obstructing the trabecular outflow. The annu-lar ciliochoroidal effusion also causes thickening of thecrystalline lens and leads to a further forward shift ofthe lens. This series of events results in myopic shiftand IOP elevation.

Ikeda et al.17 termed this clinical entity ciliochoroi-dal effusion syndrome. They advocate that irrespec-tive of the primary disease, once the ciliochoroidaleffusion with ciliary body edema occurs, the iris, cili-ary body, and lens undergo identical changes. Theexact pathophysiologic mechanism of ciliary bodyswelling induced by drugs is unknown. Some authorsadvocate an allergic reaction for the mechanism; how-ever, Krieg and Schipper8 do not agreewith this theorybased on their observation that rechallenging with thesame medication failed to produce an identical event.They speculate that drug-induced prostaglandin ele-vation contributes to ciliary body edema.

Many studies document that adrenergic agonistsstimulate the synthesis of prostaglandins and othereicosanoids.21,22 In this case, sympathomimetic drugssuch as phendimetrazine and ephedrine are thoughtto stimulate the E-prostanoid2 (EP2) receptors by syn-thesis of prostaglandins E2 (PGE2). Increased intraocu-lar levels of PGE2 cause vasodilation and increase thevascular permeability of the ciliary body.23 The EP2 re-ceptors, along with EP1 and EP4 receptors, are widely

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748 CASE REPORT: ANOREXIANT-INDUCED TRANSIENT MYOPIA ASSOCIATED WITH CILIOCHOROIDAL EFFUSION

Figure 3. Initial fundoscopic find-ing showing perimacular folds.

Figure 4. Initial ultrasonographicfinding. Diffuse ciliochoroidal thick-ening (marked between the blackand white arrowheads) is noted.

Figure 5. Follow-up ultrasono-graphic findings 2 weeks afterdiscontinuation of anorexiant med-ications. Previously observed dif-fuse ciliochoroidal thickeningdisappeared, with restoration ofnormal B-scan findings.

distributed in the human iris, ciliary muscle, and ante-rior chamber angle.24

The essential part of the treatment for suspectedcases of drug-induced ciliochoroidal effusion may in-clude early recognition of this relatively rare adversereaction and discontinuation of the causative agent.Also, reassurance of the anxious patient, especiallythose who have had LASIK or other ocular surgeries,constitutes an important aspect of the treatment. Be-cause the suggested mechanism of angle closure

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does not involve pupillary block, pilocarpine and pe-ripheral laser iridotomy seem to be ineffective.

Acute angle-closure glaucoma and associated myo-pic shift after hyperopic LASIK have been reported,but the report did not mention drug relevance.25 Toour knowledge, there has been no documentation ofdrug-induced myopia and angle-closure glaucoma ineyes aftermyopic LASIK. Althoughmyopic regressionand corneal ectasia are common causes of myopic shiftin patients who have had laser refractive correction,

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749CASE REPORT: ANOREXIANT-INDUCED TRANSIENT MYOPIA ASSOCIATED WITH CILIOCHOROIDAL EFFUSION

intake of anorexiants should be ruled out, especially inpatients presenting with acute myopic shifts.

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First author:Woojin Lee, MD

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