【摘要】 目的：研究低浓度丝裂霉素在翼状胬肉治疗中的有效性和安全性。方法：前瞻、随机、对照临床试验，将确诊为翼状胬肉的400例患者550眼随机分为4组—第一组：100例患者的130眼，不使用丝裂霉素;第二组：100例患者的140眼，使用0.2g/L丝裂霉素;第三组：100例患者的150眼，使用0.3g/L丝裂霉素;第四组：100例患者的130眼，使用0.4g/L丝裂霉素。每组接受暴露巩膜的原发性翼状胬肉切除术。入选当天以及术后2wk;2,6mo;1a分别记录患者的视力、眼压、眼球运动、虹睫炎、疤痕、症状(流泪、畏光、异物感)和体征(结膜充血、角巩膜溃疡和巩膜穿孔)。 结果：第三组和第四组的翼状胬肉术后复发率明显低于第一组和第二组(P<0.01)。术后第四组的眼压升高、虹睫炎、症状和体征的发生明显高于第一、二、三组。结论：低浓度丝裂霉素在预防翼状胬肉术后复发的治疗中是有效的。它的有效性随着浓度的增加而增加，同时，它的安全性随着浓度的增加而下降。
【关键词】 低浓度;丝裂霉素;翼状胬肉;复发
A letter from Prof. Nimet nay GNDOAN， MD in Turkey
Dear Prof. XiuWen Hu, MD.
I have just received a complementary copy of the latest issue of IJO which included our article with the reference:
Gündoan N, Yazc AC, �瘙塁im�瘙塂ek A. “A study on dominant eye measurement”. International Journal of Ophthalmology, 2008;8(10):19801986
As I expressed our feelings before that we are very proud and happy that our manuscript has been published in so important scientific journal which have very serious and reliable editorial policy.
Thank you very much for your generous gift and kind cooperation.
With warmest regards,
Prof. Nimet nay GNDOAN MD.
Ba�瘙塂kent University Faculty of Medicine
Chairman of Physiology Department
Eski�瘙塂ehir Yolu 20. Km Balca Kampüsü
06815 EtimesgutANKARA
Email: [email protected]
·Brief report·
Bilateral idiopathic cystoid macular edema: report of four cases
Seyed Ali Tabatabaee, Mohammad Soleimani, Mohammad Taher Rajabi, Mohammad Yaser
Kiarudi
Department of Ophthalmology, School of Medicine, Medical Sciences/Tehran University, Tehran, Iran
AbstractWe report clinical manifestations, angiographic, and optical coherence tomography (OCT) findings of four cases with bilateral idiopathic cystoid macular edema (CME). All were male with age between 30 and 52 years. All of them had compliant of bilateral visual loss during the last week. Fundus examination of their eyes showed macular edema in the posterior pole bilaterally. Fluorescein angiography revealed no specific finding in one of them and “typical petaloid pattern” in others. OCT showed subretinal fluid in all of them. All patients were managed with diagnosis of idiopathic CME, and after 6 weeks they had improved visual acuity.
KEYWORDS: cystoid macular edema (CME);bilateral; idiopathic; fluorescein angiography (FA); optical coherence tomography (OCT)
Tabatabaee SA, Soleimani M, Rajabi MT, Kiarudi MY. Bilateral idiopathic cystoid macular edema: report of four cases. Int J Ophthalmol
(Guoji Yanke Zazhi)2008;8(11):21822184
INTRODUCTION
Cystoid macular edema (CME) is a major cause of visual loss especially in uveitis. At present, one of the most widely used investigations for confirming the presence of CME is fundus fluorescein angiography (FA). FA shows the source of edema to be abnormal perifoveal retinal capillary permeability, seen as multiple small focal fluorescein leaks and late pooling of the dye in cystoid spaces [1,2] . Optical coherence tomography(OCT) shows subretinal fluid in CME [3].
CME can be associated with such conditions: diabetic retinopathy, central and branch retinal vein occlusion, any type of uveitis (particularly pars planitis), retinitis pigmentosa, cataract extraction, retinal detachment surgery, vitrectomy, glaucoma procedures, photocoagulation, and cryopexy. However, in rare cases CME can occur as an idiopathic disease [4]. In very rare cases, CME can be bilateral [5]. Herein, we report clinical manifestations, angiographic and OCT findings of 4 cases of idiopathic bilateral CME. In fact we did a case series.
Our study was reviewed and was performed in accordance with the ethical standards laid down in the 1964 Declaration of Helsinki. Written informed consent was obtained from all patients.
CASE REPORT
An alert, healthy 30yearold man was presented with bilateral visual loss from one week ago. Best corrected visual acuity (BCVA) was 3/10 in both eyes. Slit lamp examination was normal. Fundus examination showed macular edema in the posterior pole of both eyes. FA was normal. OCT was performed and showed subretinal fluid in macular area .ERG was normal. Systemic work up did not show any specific finding and he did not mention any history of trauma to his eyes. The patient was treated with a topical NSAID and systemic acetazolamide 250mg for 3 weeks and systemic prednisone 1mg/kg in one week. Final BCVA was 7/10 in right eye and 8/10 in left eye after six weeks with minimal findings of macular edema in the posterior pole and OCT bilaterally.
The second, third, and fourth cases were alert, healthy 45,47 and 52yearold men who were presented with compliant of bilateral visual loss . BCVA was 3/10, 4/10 in both eyes of 2 cases and 2/10 at right eye and F.C. at 3m at left eye in the last case. Slit lamp examination was within normal limits bilaterally. Fundus examination of them showed macular edema in the posterior pole. ERG was normal.
FA showed multiple small focal fluorescein leaks and late pooling of the dye in cystoid spaces in all 3 cases (Figure 1). OCT was performed and showed cystoid spaces in macular area (Figure 2). Systemic work up did not show any specific findings and they did not mention any history of trauma to their eyes. We treat them with a topical NSAID and systemic acetazolamide 250 mg for 3 weeks and systemic prednisone 1mg/kg for one week. Final BCVA after six weeks was 6/10, 8/10, and 7/10 at right eyes and 7/10, 6/10, and 7/10 at the left eyes, respectively, with minimal findings of macular edema in the posterior pole and OCT, bilaterally.
DISCUSSION
The pathogenesis of CME may be due to abnormal permeability of the perifoveal retinal capillaries that occurs in different conditions such as diabetic retinopathy, central and branch retinal vein occlusion, any type of uveitis (particularly pars planitis), retinitis pigmentosa, cataract extraction, retinal detachment surgery, vitrectomy, glaucoma procedures, photocoagulation, cryopexy, and in rare cases it can occur as an idiopathic disease [4,6] .
Figure 1Flourscein angiography of the case 2 showing focal fluorescein leaks and late pooling of the dye in cystoid spaces
Figure 2OCT finding of the case 2 showing multiple cystoid spaces in macular area
Because of Henles fiber layer, pooling of leakage classically forms a flowerpetal pattern as macular edema occurs. FA identifies breakdown of the bloodretinal barrier. Barrier breakdown precedes fluidrelated thickening at focal sites and it shows multiple small focal fluorescein leaks and late pooling of the dye in cystoid spaces[7,8]. Central foveal thickness analysis by sequential OCT enable us to monitor macular edema more accurately than by slitlamp biomicroscopy [3].
Chong et al [9] reported a 48yearold man with polyneuropathy, organomegaly, endocrinopathy, monoclonal gammopathy, and skin changes (POEMS) syndrome that had bilateral CME and optic disc edema. Telander et al [10] reported a patient with bilateral vision loss due to CME associated with docetaxel (an anticancer agent) therapy. Ozdek et al [11]reported a unique case of retinitis pigmentosa (RP) associated with bilateral disc edema and unilateral macular hole perhaps related to CME. Bilateral CME can be associated with orbital pseudotumor, neurosyphilis, tubulointerstitial nephritis, Crohns disease, and electric current strike [1216]. Also, bilateral CME can be associated with successful HAART(highly active antiretroviral therapy) treatment and with nicotinic acid treatment[17,18]. Dominant cystoid macular dystrophy (DCMD) is characterized by a prolonged course of bilateral macular cystoid change associated with leakage on FA, progressive loss of central vision, peripheral retinal pigmentary disturbances, and subnormal electrooculogram. The pigmentary changes and the electrooculographic findings suggest dysfunction of the retinal pigment epithelium. Mednivil reported a 21yearold woman with bilateral CME affected by this dystrophy[5].
Here we report four cases of bilateral idiopathic CME that one was associated with no leakage in FA. Bressler believe that CME from niacin typically is not accompanied by fluorescein leakage on angiography[19]. Jampol has speculated on the aetiology of the cystic changes in niacin retinopathy and has proposed two possibilities. The first is subclinical leakage in the extracellular space stimulated by the release of prostaglandins by niacin. This would require fluorophotometry of the vitreous to verify the subclinical leakage. The other possibility is a toxicity to Muller cells with subsequent swelling that was not sufficient to disrupt the bloodretina barrier[20]. Teitelbaum and Tresley also describe a 53yearold Asian female with cystic maculopathy associated with normal capillary permeability secondary to docetaxel that did not have any leakage on FA[21].
OCT can detect subretinal fluid in CME and in some cases with no specific findings in FA can be performed[22]. OCT is a new method for highresolution crosssectional imaging of the retina and macular area. It is noninvasive and safe and can be repeated. It can be ideally suited to repeated measurement of CME. Antcliff et al reported five cases from one hundred twentyone eyes that subretinal fluid was missed by FA but was detected by OCT[ 8].
Schilling et al[23] reported that during longterm followup, lowdose acetazolamide can be a useful therapeutic option for chronic CME in uveitis. The effect was better in patients with quiescence of uveitis than in those with chronically active uveitis. According to the study of Thurau, corticosteroid therapy is an effective treatment for CME[24]. Peterson et al[25] addressed the use of topical indomethacin eye drops for chronic CME. However, we treated cases with a topical NSAID and systemic acetazolamide 250mg for 3 weeks and systemic prednisone 1mg/kg for one week; and there was an acceptable final vision.
To our knowledge, idiopathic bilateral CME is reported rarely,however this can be related to any cause that we could not find them and if our knowledge progress more and more; perhaps we can find some reasons. One of these cases did not have any specific finding in FA, this was another rare finding[8,20,21]. Treatment for them was very successful, although we can not describe a guideline for treatment of these cases as we can not describe a guideline for diagnosis of CME. This needs further study .
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