151 face injury. Considering the onset of corneal infiltration,
the cause of corneal infiltrate in this case appears to be de- layed type hypersensitivity (DTH) reaction. DTH reaction takes 2 to 3 days to develop, and foreign materials act as haptens that conjugate with proteins, the complex of which combines with T lymphocytes, leading to an inflammatory response [1,2]. A previous study showed that oxidized cooking oil enhanced DTH in mice [3]. Further experi- mental study is needed to reveal the maturation of dendrit- ic cells and to determine whether the DTH is triggered af- ter cooking oil exposure. Transient myopic changes were mostly induced from sclera-choroidal inflammation or changes in the lens-iris diaphragm [4]. An increase in K value occurred during corneal inflammation in this case.
When back-calculation was applied using the clinical his- tory method, the change in K value was well matched with the change in refraction of the corneal plane (Fig. 1C) [5].
Corneal thermal injury may cause collagen shrinkage and induce a transient steepening in the central cornea, as in conductive keratoplasty.
In conclusion, we described a rare case of delayed onset transient corneal infiltration and transient myopic shift fol- lowing a cooking oil burn. Clinicians should keep in mind delayed corneal changes though no ocular abnormalities are observed immediately after thermal ocular surface in- jury related with cooking oil.
Jong Ho Ahn, Dong Hyun Kim
Department of Ophthalmology, Gachon University Gil Medical Center, Incheon, Korea
E-mail (Dong Hyun Kim): [email protected]
Conflict of Interest
No potential conflict of interest relevant to this article was reported.
References
1. Krachmer JH, Mannis MJ, Holland EJ, editors. Cornea. St.
Louis: Elsevier Mosby; 2011. p. 1178-80.
2. Black CA. Delayed type hypersensitivity: current theories with an historic perspective. Dermatol Online J 1999;5:7.
3. Ogino H, Sakazaki F, Okuno T, et al. Oxidized dietary oils enhance immediate- and/or delayed-type allergic reactions in BALB/c mice. Allergol Int 2015;64:66-72.
4. Herbort CP, Papadia M, Neri P. Myopia and inflammation.
J Ophthalmic Vis Res 2011;6:270-83.
5. Hoffer KJ. Intraocular lens power calculation for eyes after refractive keratotomy. J Refract Surg 1995;11:490-3.
Early Retinal Changes in Hunter Syndrome According to Spectral Domain Optical Coherence Tomog- raphy
Dear Editor,
Mucopolysaccharidosis is an inheritable storage disease with deficiency of lysosomal enzymes that degrade glycos- aminoglycans [1]. Mucopolysaccharidosis type II, also known as Hunter syndrome, is an X-linked inherited defi- ciency of enzyme iduronate 2-sulfatase, resulting in pro- gressive accumulation of dermatan sulfate and heparin
sulfate [1]. In many mucopolysaccharidoses, glycosamino- glycans accumulate in the retinal pigment epithelial (RPE) cells, resulting in pronounced lysosomal distension [2].
Previous studies have revealed outer nuclear layer thinning and the absence of outer segments, as well as reduced in- ner segments from the anterior midperipheral retina [2,3].
However, structural changes of the retina determined by high-resolution spectral domain optical coherence tomog- raphy (SD-OCT; Spectralis, Heidelberg Engineering, Hei- delberg, Germany) in the early stage of Hunter syndrome with visual impairment have not been reported. With the introduction of SD-OCT, high-resolution images of the ret- ina and optic disc could reveal occult and early structural changes related to disease progression [4]. Herein, we re- port a patient with Hunter syndrome whose visual acuity decrease was associated with early outer retinal layer
Korean J Ophthalmol 2016;30(2):151-153 http://dx.doi.org/10.3341/kjo.2016.30.2.151
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Korean J Ophthalmol Vol.30, No.2, 2016
changes found on SD-OCT.
A 5-year-old boy with Hunter syndrome was referred to our clinic for evaluation of ocular involvement. At initial presentation, his best corrected visual acuities were 20 / 25 in both eyes (OU). Cycloplegic refractive errors were +4.50 Dsph = -3.00 Dcyl × axis 180 in the right eye (OD) and +4.50 Dsph = -3.75 Dcyl × axis 180 in the left eye (OS). Slit lamp biomicroscopy showed clear corneas OU. Fundus- copic examination was unremarkable.
At the age of 9, he complained of visual acuity decrease OU. On ophthalmic examination, best corrected visual acuities were 20 / 30 OD and 20 / 50 OS. Cycloplegic re- fractive errors were +4.00 Dsph = -3.50 Dcyl × axis 180 OD and +4.00 Dsph = -4.25 Dcyl × axis 180 OS. Slit lamp biomicroscopy showed clear corneas OU (Fig. 1A and 1B).
There was no relative afferent papillary defect. Optic disc
margins showed mild blurring. However, lumbar spinal tapping revealed normal intracranial pressure. Visual field testing with Goldmann kinetic perimetry were normal OU.
On funduscopic examination, the retina looked grossly in- tact, but standard electroretinography revealed a reduction of scotopic responses, consistent with rod cell degenera- tion. Reduced b-wave amplitudes in the maximal responses and reduced oscillatory potentials were also observed OU.
SD-OCT showed thickening of the external limiting membrane at the central macula, especially near the fovea (Fig. 1C and 1D). The ellipsoid line formerly known as the inner and outer segment photoreceptor junction appeared normal in thickness and contour, well distinguished from the RPE layer underneath. The peripapillary circular scan images showed a mild increase in bilateral peripapillary retinal nerve fiber layer thickness.
Our study demonstrates the structural changes of the retina determined by high-resolution SD-OCT in the early stage of Hunter syndrome. Previously, Yoon et al. [3] re- ported high-speed, ultrahigh-resolution OCT findings of the retina in Hunter syndrome. Stratus OCT revealed a loss of photoreceptors outside the fovea and cystoid spaces within the inner nuclear layer, ganglion cell layer, and out- er nuclear layer [3]. Our patient only showed thickening of the external limiting membrane with no other abnormal findings in the RPE, suggesting that changes of the outer nuclear and photoreceptor layers precede RPE abnormali- ties. In contrast to our study, the previous case experienced more variable ocular symptoms typical of Hunter syn- drome, such as exophthalmos, hypertelorism, and bilateral visual field loss with a ring scotoma pattern, which were not found in our patient.
The external limiting membrane, between photoreceptor inner segments and Müller cell apical processes, is filled with the interphotoreceptor matrix, which contains a het- erogeneous collection of glycoproteins, enzymes, and gly- cosaminoglycans [5]. Our SD-OCT findings correlate well with previous histopathological findings in the early stage of Hunter syndrome. The typical histopathological find- ings reported previously, such as a total loss of RPE, an overall loss of rods and cones, and reduced outer nuclear layer with atrophic bipolar cells, are usually shown as the disease progresses [2].
In conclusion, SD-OCT can be used as a diagnostic mo- dality to monitor patients with Hunter syndrome and to de- tect subclinical progression of the disease in the early stages.
Fig. 1. Slit lamp biomicroscopy showed clear corneas in the right (A) and left (B) eyes. (C,D) Comparison of spectral domain optical coherence tomography (SD-OCT; Spectralis, Heidelberg Engineering, Heidelberg, Germany) scans of the macula in early stage Hunter syndrome and normal control. (C) Vertical scan im- ages with SD-OCT of the patient’s right eye. There was marked thickening of the external limiting membrane (ELM). The ellip- soid zone (EZ) formerly known as the inner and outer segment photoreceptor junction appeared normal in thickness and con- tour, well distinguished from the retinal pigment epithelial layer underneath. The photoreceptor layer and retinal pigment epitheli- um-Bruch’s membrane complex (RPE/Bruch’s complex) showed no thinning or other abnormal change. (D) SD-OCT of the nor- mal eye from a control subject showed four distinct high-signal bands in the outer retinal layer without foveal thickening of the ELM.
A
C
D
B
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Seonghwan Kim, Yung Ju Yoo, Se Joon Woo, Hee Kyung Yang
Department of Ophthalmology, Seoul National University Bundang Hospital, Seoul National University College of Medicine, Seongnam, Korea
E-mail (Hee Kyung Yang): [email protected]
Conflict of Interest
No potential conflict of interest relevant to this article was reported.
References
1. Ashworth JL, Biswas S, Wraith E, Lloyd IC. Mucopolysac- charidoses and the eye. Surv Ophthalmol 2006;51:1-17.
2. McDonnell JM, Green WR, Maumenee IH. Ocular histo- pathology of systemic mucopolysaccharidosis, type II-A (Hunter syndrome, severe). Ophthalmology 1985;92:1772-9.
3. Yoon MK, Chen RW, Hedges TR 3rd, et al. High-speed, ul- trahigh resolution optical coherence tomography of the ret- ina in Hunter syndrome. Ophthalmic Surg Lasers Imaging 2007;38:423-8.
4. Chen TC, Cense B, Pierce MC, et al. Spectral domain opti- cal coherence tomography: ultra-high speed, ultra-high resolution ophthalmic imaging. Arch Ophthalmol 2005;
123:1715-20.
5. Bunt-Milam AH, Saari JC, Klock IB, Garwin GG. Zonulae adherentes pore size in the external limiting membrane of the rabbit retina. Invest Ophthalmol Vis Sci 1985;26:1377- 80.
Macular Edema after Gabapentin
Dear Editor,
Gabapentin is an anticonvulsant and has been used to manage neuropathic pain. It was originally developed as an antiepileptic agent; however, it is now recommended as a drug of choice for the treatment of neuropathic pain.
There is strong evidence that gabapentin is also effective in diabetic neuropathy and postherpetic neuralgia [1].
To the best of our knowledge, macular edema after use of gabapentin has not been reported to date. Therefore, we report a case of macular edema after gabapentin.
A 71-year-old man presented with a 1 day history of vi- sual disturbance and metamorphosis in both eyes. The pa- tient had taken oral gabapentin (Neurontin; Pfizer, New York, NY, USA) and oral methylprednisolone (Methylon;
Alvogen, Seoul, Korea) for 8 days for treatment of posth- erpetic neuralgia. He had no other significant medical his- tory, except hypertension controlled by oral medication.
Best-corrected visual acuity (Snellen) was 0.4 (right eye) and 0.2 (left eye), and the intraocular pressure was 9
mmHg (right eye), 11 mmHg (left eye), as determined by non-contact tonometry. Both eyes had moderate cataract.
Ophthalmic examination of the anterior segments revealed no other abnormal findings. Dilated fundus examination and spectral domain optical coherence tomography re- vealed macular edema and serous retinal detachment of macula in both eyes (Fig. 1A-1D). Fluorescence angiogra- phy revealed fluorescein dye pooling on the macula and multiple leakages in both eyes (Fig. 1E and 1F). The patient was advised to discontinue gabapentin, and the use of the drug was stopped.
Four weeks after the initial visit, best corrected visual acuity improved to 0.9 (both eye). Fundus exam and spec- tral domain optical coherence tomography revealed mark- edly improved macular edema and serous detachment in both eyes (Fig. 1G-1J).
Gabapentin is an amino acid initially designed as a cyclic gamma-aminobutyric acid analogue with action as a gamma-aminobutyric acid agonist [2]. It also acts on different brain receptors by an as-yet unknown mecha- nism.
Common adverse effects of gabapentin include dizzi- ness, fatigue, drowsiness, sexual dysfunction, weight gain, and peripheral edema [3]. Uncommonly, gabapentin causes blurred vision and diplopia [4]. Steinhoff et al. [5] reported
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