劉莉莉(綜述),黃敏麗(審校)

(1.柳州市工人醫(yī)院眼科,廣西 柳州 545005； 2.廣西醫(yī)科大學(xué)第一附屬醫(yī)院眼科，南寧 530021)

糖尿病黃斑水腫的治療現(xiàn)狀

劉莉莉1(綜述),黃敏麗2※(審校)

(1.柳州市工人醫(yī)院眼科,廣西 柳州 545005； 2.廣西醫(yī)科大學(xué)第一附屬醫(yī)院眼科，南寧 530021)

糖尿病黃斑水腫(diabetic macular edema，DME)嚴(yán)重?fù)p害糖尿病患者視力。其發(fā)病機(jī)制較為復(fù)雜，主要為黃斑區(qū)毛細(xì)血管周細(xì)胞和血管內(nèi)皮細(xì)胞損傷、血視網(wǎng)膜屏障破裂、毛細(xì)血管擴(kuò)張，液體和血漿成分自視網(wǎng)膜毛細(xì)血管內(nèi)皮細(xì)胞及異常滲漏血管瘤滲出，導(dǎo)致視網(wǎng)膜水腫增厚，硬性滲出形成[1]。糖尿病患者中有10%～25%出現(xiàn)黃斑水腫，而患嚴(yán)重視網(wǎng)膜病變者伴DME比例較高[2]。DME治療包括控制內(nèi)科基礎(chǔ)病及?？浦委煟杭す夤饽⑹中g(shù)治療、曲安奈德玻璃體腔注射、抗血管內(nèi)皮生長因子(vascular endothelial growth factor，VEGF)玻璃體腔注射?，F(xiàn)對(duì)DME的治療現(xiàn)狀予以綜述。

1內(nèi)科治療

DME病程越長，全身并發(fā)癥越重，預(yù)后越差，早期輕度的黃斑水腫可通過系統(tǒng)的內(nèi)科治療控制，進(jìn)展為彌漫性黃斑水腫時(shí)，視力損害較難恢復(fù)。Matsuda等[3]將接受抗VEGF治療的患者分成兩組，糖化血紅蛋白≤7%的患者經(jīng)治療后，最佳矯正視力有顯著提高，糖化血紅蛋白>7%的患者視力則無明顯提高，治療期間，血糖控制較好的患者黃斑中心凹厚度明顯降低。

2激光光凝

激光長期以來作為糖尿病黃斑水腫的標(biāo)準(zhǔn)治療，包括氬激光、紅寶石激光、氪激光、多波長激光、摻釹釔鋁石榴石(Neodymium-doped Yttrium Aluminium Garnet，ND:YAG)激光、閾下微脈沖半導(dǎo)體激光、帕斯卡(Pascal)激光器。激光治療主要通過凝固效應(yīng)也即是熱效應(yīng)，使缺血的區(qū)域成為瘢痕組織，新生血管因缺少充足的氧而消退，加強(qiáng)視網(wǎng)膜色素上皮細(xì)胞的交通作用，即激光破壞了感光細(xì)胞，從而減少了視網(wǎng)膜的耗氧量，減輕了內(nèi)層視網(wǎng)膜的缺氧狀態(tài)，引起視網(wǎng)膜小動(dòng)脈的收縮，靜脈壓減小從而減少細(xì)胞的水腫[3]。黃斑水腫的光凝分為局部光凝、黃斑部格柵光凝、改良的格柵光凝。根據(jù)激光波長不同，黃斑水腫激光首選黃激光，其次為綠激光。美國早期糖尿病視網(wǎng)膜病變治療研究組研究顯示，黃斑部格柵光凝使患者3年內(nèi)中度視力喪失風(fēng)險(xiǎn)減少50%[4]。黃斑部激光光凝對(duì)嚴(yán)重的彌漫性黃斑水腫效果欠佳，特別是合并大量硬性滲出，激光不能提高視力，短期內(nèi)會(huì)因血視網(wǎng)膜屏障破壞加重而使水腫加重，從而引起視力減退?，F(xiàn)不斷有新的激光種類，據(jù)Lavinsky等[5]、Vujosevic等[6]報(bào)道閾下微脈沖半導(dǎo)體激光，閾下微脈沖半導(dǎo)體激光光凝時(shí)溫度低于氬激光、氪激光，減輕脈絡(luò)膜損害，保存病變表面一部分視網(wǎng)膜功能；Muqit等[7]報(bào)道近年來美國OptiMedia公司推出的Pascal激光器，發(fā)出的短脈沖將激光損害局限在視網(wǎng)膜色素上皮質(zhì)。

3糖皮質(zhì)激素治療

糖皮質(zhì)激素通過淋巴細(xì)胞、巨噬細(xì)胞、多形核白細(xì)胞、血管內(nèi)皮細(xì)胞、成纖維母細(xì)胞等發(fā)揮眼部抗炎作用，抑制磷脂釋放花生四烯酸，從而抑制由其轉(zhuǎn)化的炎性介質(zhì)：前列腺素、前列腺過氧化物、白三烯、血栓素等，下調(diào)VEGF的水平，降低血管通透性，促進(jìn)水腫液吸收，抑制上皮細(xì)胞的增生及新生血管的形成，從而改善血視網(wǎng)膜屏障，達(dá)到治療目的。

3.1曲安奈德玻璃體腔內(nèi)注射Gillis等[8]將69眼(41例)納入一項(xiàng)5年隨機(jī)對(duì)照試驗(yàn)研究，34眼接受曲安奈德玻璃體腔內(nèi)注射(intravitreous injection triamcinolone acetonide，IVTA),35眼接受安慰劑治療。IVTA組經(jīng)治療后42%患眼視力提高5行，相比之下安慰劑組只有32%患者眼有提高。激素眼內(nèi)應(yīng)用可引起高眼壓、加快白內(nèi)障進(jìn)展，玻璃體腔注藥可引起眼內(nèi)炎、玻璃體出血、視網(wǎng)膜脫離等。Beck等[9]及Elman 等[10-11]研究表明，彌漫性黃斑水腫患者經(jīng)激素治療后效果較好，眼壓升高和白內(nèi)障的進(jìn)展則較明顯。

3.2緩釋型玻璃體腔內(nèi)植入物為提高眼內(nèi)操作安全性，緩釋型玻璃體腔內(nèi)植入物成為新的給藥途徑。它可減少玻璃體內(nèi)腔注射次數(shù)，保持玻璃體腔內(nèi)的藥物濃度，減少玻璃體腔內(nèi)注射引起的術(shù)中、術(shù)后并發(fā)癥。

3.2.1緩釋型地塞米松植入物美國眼力健公司生產(chǎn)的緩釋型地塞米松植入物(地塞米松0.7 mg)作用時(shí)間可達(dá)6個(gè)月[12-13]。一項(xiàng)回顧性研究[14]顯示，9例持續(xù)黃斑水腫患者經(jīng)地塞米松植入物治療，最佳矯正視力(best corrected visual acuity，BCVA)均有提高；Boyer等[15]研究表明，地塞米松植入物治療對(duì)已行玻璃體切割術(shù)的DME患者同樣有效。優(yōu)點(diǎn)在于可自行眼內(nèi)降解，避免再次手術(shù)。

3.2.2氟輕松非生物降解型給藥系統(tǒng)由美國博士倫公司生產(chǎn)，用25號(hào)針頭植入玻璃體腔，可存留3年之久。局限性為不能眼內(nèi)降解，需手術(shù)取出。Campochiaro等[16-17]研究顯示，隨訪24個(gè)月及36個(gè)月時(shí)與假注射組相比，氟輕松治療組BCVA均有明顯提高，高眼壓和白內(nèi)障的進(jìn)展較假注射組明顯。

4抗VEGF

糖尿病患者眼內(nèi)視網(wǎng)膜內(nèi)VEGF水平明顯增加，促進(jìn)血管內(nèi)白細(xì)胞黏附，啟動(dòng)炎癥反應(yīng)，血管通透性增加，黃斑水腫?？筕EGF藥物有抗新生血管形成，減少滲出、減輕水腫，穩(wěn)定及提高視力作用。目前常用的抗VEGF藥物有哌加他尼納、蘭尼單抗、貝伐單抗，阿柏西普。

4.1哌加他尼納哌加他尼納是一種核糖核受體，其特異性結(jié)合到VEGF-A165異構(gòu)體(眼部主要的VEGF蛋白)，是最早運(yùn)用于DME治療的抗VEGF藥物。一項(xiàng)Macugen治療DME的隨機(jī)對(duì)照試驗(yàn)[18]中提示，低濃度的Macugen(0.3 mg)治療較安慰劑對(duì)照組在BCVA和黃斑中心厚度上均有顯著提高，高濃度(1 mg、3 mg)與低濃度相比差異無統(tǒng)計(jì)學(xué)意義。另一項(xiàng)隨機(jī)對(duì)照試驗(yàn)[19]中隨訪第54周，Macugen治療組患者視力提高較安慰劑組明顯，2年的隨訪期，Macugen治療組視力持續(xù)改善。其抗VEGF作用有限，價(jià)格高，目前應(yīng)用較少。

4.2蘭尼單抗蘭尼單抗于2006年在美國上市。它是人源化的重組抗體片段(Fab，或結(jié)合抗體片段)，可對(duì)抗所有VEGF亞型[20]。Massin等[21]研究中，第12個(gè)月時(shí)蘭尼單抗治療組BCVA明顯高于安慰劑組；Nguyen等[22-23]和Do等[24]的研究中蘭尼單抗組BCVA改善較激光組明顯，與聯(lián)合治療組相比差異無統(tǒng)計(jì)學(xué)意義。

4.3貝伐單抗貝伐單抗為全長的重組人源化重組抗體，對(duì)VEGF A亞型有效。在眼科新生血管性疾病如濕性年齡相關(guān)黃斑病變，中心性滲出性脈絡(luò)膜視網(wǎng)膜病變、變性近視黃斑區(qū)視網(wǎng)膜所形成的脈絡(luò)膜新生血管、新生血管性青光眼等方面應(yīng)用越來越廣泛。Kook等[25]一個(gè)回顧性研究中，對(duì)慢性彌漫性黃斑水腫患者經(jīng)24個(gè)月反復(fù)玻璃體腔內(nèi)注射貝伐單抗后，水腫明顯改善，對(duì)慢性缺血性黃斑水腫患者亦有效。貝伐單抗有增加心血管風(fēng)險(xiǎn)，對(duì)于危重患者慎用。

4.4阿柏西普阿柏西普與VEGF-A亞型有更強(qiáng)親和力。眼內(nèi)半衰期長。阿柏西普在治療年齡相關(guān)性黃斑病變時(shí)和蘭尼單抗療效相同[26]。一項(xiàng)雙盲隨機(jī)對(duì)照試驗(yàn)Ⅱ期臨床試驗(yàn)[27-28]中，將4種不同劑量、不同給藥次數(shù)的阿柏西普組和激光組做比較，24周時(shí)阿柏西普組的BCVA均有提高，52周時(shí)阿柏西普組BCVA仍有提高。

5手術(shù)治療

5.1玻璃體切除術(shù)學(xué)者認(rèn)為由于玻璃體的機(jī)械作用和生理作用，增加血管的通透性，導(dǎo)致DME的發(fā)生、發(fā)展[29]。伴有玻璃體后脫離患者中DME的發(fā)生率低于無后脫離患者[30]，自發(fā)玻璃體后脫離可使DME好轉(zhuǎn)[30-31]。玻璃體切除術(shù)解除玻璃體機(jī)械性牽引，視網(wǎng)膜通過玻璃體腔向缺血無灌注區(qū)運(yùn)氧能力增強(qiáng)，提高含氧量，促進(jìn)微血管收縮，減輕了水腫。手術(shù)適應(yīng)證為玻璃體積血，增殖膜形成、彌漫性黃斑水腫，無法行視網(wǎng)膜光凝者； Kadonosono等[32]稱玻璃體切除術(shù)后增加黃斑中心凹毛細(xì)血管血流量。此外，去除玻璃體有助于減少眼內(nèi)有毒物質(zhì)及細(xì)胞因子，如組胺、自由基清除劑和VEGF[33]。

5.2視網(wǎng)膜內(nèi)界膜剝離術(shù)糖尿病眼內(nèi)界膜中的纖維連接蛋白、層粘連蛋白、膠原蛋白水平提高[34-35],視網(wǎng)膜內(nèi)界膜剝離術(shù)作為一種治療黃斑裂孔新興方法，適用于玻璃體積血、光學(xué)相干斷層掃描或術(shù)中發(fā)現(xiàn)黃斑水腫的患者。玻璃體切除術(shù)聯(lián)合視網(wǎng)膜內(nèi)界膜術(shù)療效顯著。一項(xiàng)研究報(bào)道玻璃體切割術(shù)并發(fā)癥：視網(wǎng)膜裂孔(9.6%)，視網(wǎng)膜裂孔(9.6%)，視網(wǎng)膜前膜(9%)，視網(wǎng)膜脫離，新生血管性青光眼和虹膜紅變(各1.9%)[36]。

6聯(lián)合治療

聯(lián)合治療成為學(xué)者研究的方向。玻璃體腔內(nèi)注射藥物聯(lián)合激光，可以有效減輕黃斑水腫，亦可減輕玻璃體腔內(nèi)注射的風(fēng)險(xiǎn)。

6.1曲安奈德和激光的聯(lián)用Chung等[37]研究表明，相比單用IVTA治療，IVTA+黃斑部格柵光凝治療，極大地改善難治性黃斑水腫患者的視力，且并發(fā)癥更少。Aydin等[38]研究顯示，IVTA先或與黃斑部格柵光凝同時(shí)治療彌漫性黃斑水腫均較單獨(dú)黃斑部格柵光凝療效明顯。

6.2激光和抗VEGF藥物聯(lián)用Maia等[39]將激光和IVTA 聯(lián)合應(yīng)用治療非增殖期糖尿病和彌漫性黃斑水腫，最佳矯正視力的提高和中心凹厚度、黃斑容積降低較單用光凝治療明顯。Gillies等[40]研究表明，聯(lián)合治療組患眼視力提高較單獨(dú)激光治療組明顯，但高眼壓及白內(nèi)障進(jìn)展較單獨(dú)激光組高。目前IVTA應(yīng)用于人工晶體眼及曾行玻璃體切割術(shù)眼時(shí)，易引起眼壓的升高。Mitchell等[41]研究表明，IVR及激光的聯(lián)合組最佳矯正視力改善優(yōu)于單用激光組。在之前Nguyen等[22-23]和Do等[24]研究顯示，IVTA組合與聯(lián)合組提高最佳矯正視力的差異無統(tǒng)計(jì)學(xué)意義，但聯(lián)合治療組最佳矯正視力及黃斑水腫均有改善，同時(shí)亦減少頻繁眼內(nèi)注藥。

7結(jié)語

DME治療方法中，基礎(chǔ)病治療尤為重要。激光長期以來作為DME治療標(biāo)準(zhǔn)，近年來隨著對(duì)DME發(fā)病機(jī)制的研究進(jìn)展，新的治療方法不斷出現(xiàn)，如玻璃體腔內(nèi)注射糖皮質(zhì)激素和抗VEGF治療，藥物的聯(lián)合治療或是激光和藥物的聯(lián)合治療，玻璃體切除術(shù)，這些方法各有優(yōu)缺點(diǎn)。我國已進(jìn)入老齡化社會(huì)，糖尿病患者日漸增多，需采取安全、經(jīng)濟(jì)、有效方法預(yù)防和治療DME。

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摘要：糖尿病黃斑水腫是由于高血糖所引起的眼部并發(fā)癥，是造成糖尿病患者視力嚴(yán)重?fù)p害的原因之一。DME是一種多因素引起的復(fù)雜的病理過程，傳統(tǒng)的治療方法主要是黃斑部激光治療。早期糖尿病視網(wǎng)膜病變研究組認(rèn)為激光治療對(duì)于臨床有意義的黃斑水腫是有效的。近年來，DME治療方法有了迅速進(jìn)展，如手術(shù)治療、眼內(nèi)注射藥物治療。其中新型的眼內(nèi)注射藥物已成為伴有中心視力下降的DME一線治療。

關(guān)鍵詞：糖尿病; 糖尿病黃斑水腫; 激光治療; 藥物治療; 手術(shù)

The Treatment of Diabetic Macular EdemaLIULi-li1,HUANGMin-li2. (1.DepartmentofOphthalmology,LiuzhouWorker′sHospital,Liuzhou545005,China; 2.DepartmentofOphthalmology,theFirstAffiliatedHospital,GuangxiMedicalUniversity,Nanning530021,China)

Abstract:Diabetic macular edema(DME),a serious eye complication caused by hyperglycemia,is one of the main causes of visual impairment in diabetic patients.DME is a complex pathological process caused by multiple factors.Conventional treatment is mainly based on laser photocoagulation.The study on early treatment for diabetic retinopathy showed that macular laser photocoagulation was beneficial for eyes with clinically significant macular edema.The treatment for DME is rapidly evolving in recent years,such as surgical treatment,intraocular pharmacotherapy.New drugs,given by intraocular injection,have become first line treatment for DME with loss of vision.

Key words:Diabetes; Diabetic macular edema; Laser photocoagulation; Drug therapy; Surgery

收稿日期：2014-10-18修回日期：2014-12-28編輯：相丹峰

doi：10.3969/j.issn.1006-2084.2015.15.036

中圖分類號(hào)：R774.5； R587.2

文獻(xiàn)標(biāo)識(shí)碼：A

文章編號(hào)：1006-2084(2015)15-2786-04