Colocalization of Tie2, angiopoietin 2 and vascular endothelial growth factor in fibrovascular membrane from patients with retinopathy of prematurity

PURPOSE: The tyrosine kinase receptor Tie2 and its ligands, the angiopoietins (Angs), play important roles in vascular integrity and neovascularization, modulating vascular endothelial growth factor (VEGF) activity. To elucidate the potential role of Angs and the Tie2 system in retinopathy of prematurity (ROP), we have investigated the expression of Angs, Tie2 and VEGF within fibroproliferative membranes in ROP. METHODS: Fibroproliferative membranes were obtained from 38 cases with stage 5 ROP at the time of vitrectomy. Membranes were fixed in formalin and embedded in paraffin. Each specimen was serially sectioned for immunohistochemistry. Polyclonal antibodies specific for Ang1, Ang2, Tie2 and VEGF were used for immunostaining. Immunoreactivity for von Willebrand factor (factor VIII) was also assessed to confirm the identity of vascular endothelial cells. RESULTS: Positive staining for Tie2 was observed in 23 of 38 specimens (60.5%). Tie2 was localized in vascularized regions of fibrovascular membranes and was co- expressed with VEGF and factor VIII. Ang2 stained positively in 18 of 38 (47.3%) serial sections where Tie2 was present, and was also co-expressed with VEGF and factor VIII. Ang1 was not generally observed in these specimens (3/38). CONCLUSIONS: VEGF and Ang2-Tie2 interactions may play an important role in the pathogenesis of ROP.     

Comparison of EphA receptor tyrosine kinases and ephrinA ligand expression to EphB-ephrinB in vascularized corneas

PURPOSE: Eph cell surface receptors and their ligands, ephrins, are involved in neuronal patterning and neovascularization. Our purpose is to compare and characterize the expression of ephrinA ligands and EphA receptors to ephrinB ligands and EphB receptors in excised mouse corneal tissue, in corneal epithelial and keratocyte cell lines, and during corneal angiogenesis. METHODS: Mouse corneal epithelial cells and keratocytes were immortalized using SV40T antigen viral infection of primary cultures. The immortalized epithelial cells and keratocytes were cloned and characterized using antibodies to keratin, vimentin, integrin alpha5beta1, and alpha-smooth muscle actin. Basic fibroblast growth factor pellets were implanted to induce corneal neovascularization. The eyes of wild-type, ephrinB2(tlacZ/+), and EphB4(tlacZ/+) heterozygous mice were harvested and sectioned 7 days after pellet implantation. Confocal immunohistochemistry was performed to compare the expression of the Eph/ephrinA family (EphA1-8, ephrinA1-5) and Eph/ephrinB family (EphB1-4, EphB6 ephrinB1-3). RESULTS: EphA1, EphA3, ephrinA1, ephrinA2, EphB1, EphB4, ephrinB1, and ephrinB2 were detected in wild-type mouse corneal epithelial cells and keratocytes. EphA2 was immunolocalized only in epithelial cells. Also, EphA3, ephrinA1, EphB1, EphB4, and ephrinB1 were immunolocalized to the corneal epithelium and stroma. In the vascularized corneas, ephrinB1 was immunolocalized mainly to the keratocytes around the vessels, and ephrinB2, EphB1, and EphB4 were colocalized mainly with CD31 to the vascular endothelial cells. CONCLUSIONS: The characterization of ephrin ligand and Eph receptor expression during cornea angiogensis in this study suggests that the Eph/ephrin family of receptor tyrosine kinases and their ligands may play a role in the regulation of corneal angiogenesis.     

Enzyme-assisted vitrectomy with bacterial collagenase. Pilot human studies

Clostridiopeptidase A, a bacterial collagenase, was used to assist vitrectomy with membrane stripping in six patients with dense intravitreal fibroproliferative tissue associated with retinopathy of prematurity, diabetic retinopathy, or proliferative vitreoretinopathy. When it was injected intra-operatively, allowed to incubate for 15 minutes, and then removed by irrigation/aspiration, no side effects of lens opacity, lens dislocation, or retinal hemorrhage were observed. Use of this enzyme may facilitate removal of fibroproliferative tissue in certain difficult vitrectomy cases.     

Attenuation of EphrinB2 Reverse Signaling Decreases Vascularized Area and Preretinal Vascular Tuft Formation in the Murine Model of Oxygen-Induced Retinopathy

Purpose. EphB4 and ephrinB2 are known key regulators of retinal vascular development, but due to their capacity for bidirectional signaling, delineation of their individual roles in this process remains unclear. To better dissect out individual contributions, a model of proliferative retinopathy in mice with attenuated ephrinB2 reverse signaling was studied. It was hypothesized that endothelial ephrinB2 reverse signaling regulates hypoxia-induced capillary sprouting, as well as the pathologic formation of neovascular tufts in postnatal retinal microvascular networks. Methods. Genetically manipulated mice with attenuated ephrinB2 reverse signaling (ephrinB2(lacZ/+)), along with wild-type (WT) controls, were exposed to oxygen-induced retinopathy (OIR), a postnatal model of proliferative retinopathy. At peak disease (postnatal day 18), microvascular networks were analyzed to examine intraretinal revascularization, capillary sprouting, and pathologic neovascularization responses. EphB4 and phosphorylated ephrinB protein expression patterns along retinal microvessels were also assessed. Results. EphrinB2(lacZ/+) mice exhibited reduced hypoxia-induced revascularization (P ≤ 0.04) and reduced formation of neovascular tufts (P < 0.001), as compared with WT controls. Corresponding to the observed inhibition of retinal angiogenesis, ephrinB2(lacZ/+) retinas displayed an increased number of blind-ended capillary sprout tips (P < 0.02) and endothelial filopodial processes (P = 0.001). In WT and ephrinB2(lacZ/+) OIR-exposed retinas, ephrinB was confined to endothelial cells, with expression detected along angiogenic vascular processes including neovascular tufts and blind-ended capillary sprouts. Conclusions. EphrinB2 reverse signaling is a regulator of key processes during retinal vascularization and controls pathologic retinal angiogenesis through direct effects on capillary sprouting and endothelial filopodia formation.     

睫状体平坦部四切口玻璃体手术治疗严重增生性糖尿病视网膜病变

目的探讨睫状体平坦部四切口玻璃体手术治疗有广泛纤维血管膜增生的糖尿病视网膜病变（PDR）的临床效果。方法为病例对照试验。回顾性选择27例（28只眼）有广泛纤维血管膜增生的PDR Ⅵ期患者作为试验组,采用睫状体平坦部四切口玻璃体手术,双手进行眼内操作,如膜分离与切除,视网膜复位,眼内光凝硅油充填。选择同期有广泛纤维血管膜增生的PDR Ⅵ期患者30例（30只眼）作为对照组,由同一术者完成睫状体平坦部三切口玻璃体手术。结果试验组28只眼均顺利完成膜分离与切除,1只眼出现2个医源性视网膜裂孔。随访7～54个月,术后视网膜均复位,多数患者视力有不同程度提高。对照组2只眼有部分膜残留,3只眼出现4个医源性视网膜裂孔,随访12个月视网膜均复位,3只眼发生新生血管性青光眼。结论四切口玻璃体手术采用双手操作眼内剥膜,可明显提高手术效率,减少组织损伤,是治疗有广泛纤维血管膜增生的严重PDR的较好方法。（中华眼科杂志,2008,44：17—19）     

Expression of ephrinB1 and its receptor in glaucomatous optic neuropathy

OBJECTIVE: To determine ephrinB1, ephrinB2 and EphB1 expression in the optic nerve head (ONH) and retina of monkeys with glaucoma and in human ONH astrocytes. METHODS: Using immunohistochemistry, the localisation of ephrinB1, ephrinB2 and EphB1 was determined in the ONH and retina bilaterally in monkeys with monocular laser-induced glaucoma. RT-PCR, western blot and immunocytochemistry were used to study ephrinB1, ephrinB2 and EphB1 expression in cultured human ONH astrocytes from donors with and without glaucoma. RESULTS: There was an increase in ephrinB1 and EphB1 expression in mild to moderate glaucoma. In the ONH, both ephrinB1 and EphB1 were localised to astrocytes and EphB1 was also localised to lamina cribrosa cells and perivascular cells. In the retina, ephrinB1 localised to Muller cells and astrocytes, and EphB1 was found in retinal ganglion cells. In ONH astrocytes in humans with glaucoma, ephrinB1 and EphB1 were up-regulated but barely present in donors without glaucoma. CONCLUSIONS: Ephrins are activated in early and moderate glaucoma in the ONH and retina. We postulate that the up-regulation of Eph/ephrin pathway may play a protective role by limiting axonal damage and inflammatory cell invasion. Loss of ephrin signalling in advanced glaucoma may explain macrophage activation.     

玻璃体腔注射Bevacizumab对PDR患者增殖膜中CTGF及PEDF的影响

目的:研究增殖性糖尿病视网膜病变(PDR)玻璃体腔注射抗-VEGF药物bevacizumab后对增殖膜中结缔组织生长因子(CTGF)及色素上皮衍生因子(PEDF)的影响.方法:回顾2015-01/2016-12入本院行增殖性糖尿病视网膜病变治疗的患者117例126眼,采用病例对照的研究方法,将所选病例随机分为两组,分别为A组60例63眼和B组57例63眼.其中A组单纯进行玻璃体切割手术,B组患者在玻璃体切割术前玻璃体腔注射0.05mL/1.25mg bevacizumab.在手术中剥离取用两组患者的视网膜增殖膜进行染色,然后进行组织病理学观察,观察两组患者视网膜增殖膜中原始细胞和新生血管的变化,以及患者增殖膜中CTGF和PEDF因子的表达.结果:在对两组患者CTGF、PEDF因子表达进行观察发现,两组患者视网膜增殖膜中的CTGF和PEDF都在细胞质内表达.其中A组呈现出38眼阳性表达,阳性表达率为60.3%,相比于A组而言,B组的CTGF的阳性表达率92.1%明显更高,两组差异有统计学意义(P<0.05).而两组的PEDF阳性表达率分别为90.5%和95.2%,差异无统计学意义(P>0.05).结论:PDR患者在玻璃体腔注射抗VEGF药物bevacizumab后,视网膜的新生血管明显减少,有利于玻璃体切割手术的进行.且PDR患者玻璃体腔注射bevacizumab后,CTGF的阳性表达率明显增高,而PEDF因子在前膜上的表达则没有明显的变化.     

PDR玻璃体切除术后早期影响眼压的相关因素分析

目的:探讨增生性糖尿病视网膜病变(proliferative diabeticretinopathy,PDR)玻璃体切除术后早期引起眼压升高的可能原因。方法:选取行玻璃体切除术的72例100眼PDR患者进行回顾性分析,观察术后高眼压的发生率,并对引起术后高眼压的相关因素进行统计学分析。术后早期高眼压的诊断标准为:术后2wk内任何时间非接触性眼压计测眼压>25mmHg(1mmHg=0.133kPa)。结果:玻璃体切除术后27眼(27%)发生高眼压,其中男、女的发病率分别为27.27%和26.79%,两组比较差异无统计学意义(P>0.05)。眼内充填与平衡液充填组的发病率为30.95%和6.25%,两组比较差异有统计学意义(P<0.05)。硅油充填与C3F8充填组的发病率为34.28%和31.25%,两组比较差异无统计学意义(P>0.05)。术中行全视网膜光凝与补充视网膜光凝组的发病率为41%和20%,两组比较差异有统计学意义(P<0.05)。术前视网膜病变4期、5期、6期组的发病率分别为9.52%,23.81%,40.56%,各组比较差异有统计学意义(P<0.05)。术前未合并视网膜脱离与合并视网膜脱离组的发病率为19%和41%,两组比较差异有统计学意义(P<0.05)。术中联合晶状体切除术与术中未联合晶状体切除术组的发病率为34%和15%,两组比较差异有统计学意义(P<0.05)。经Logistic回归分析,术前合并视网膜脱离及术中眼内充填是引起玻璃体切除术后早期高眼压的独立危险因素。结论:PDR玻璃体切除术后眼压升高与术前合并视网膜脱离、术中联合晶状体切除、术中眼内充填、术中行全视网膜光凝相关,引起术后高眼压的独立危险因素为术前合并视网膜脱离、术中眼内充填。PDR玻璃体切除术后高眼压的发病率高,危害性大,早期发现并予个体化治疗可以增加玻璃体切除术的成功率,最大程度提高患者的视力。     

EphrinB2 and EphB4 expression in pterygia: new insights and preliminary results

Objective: Pterygium is a growth of fibrovascular tissue onto the cornea, in which the mechanisms of cell proliferation and vascularization are unknown. The ephrin-Eph system, especially ephrinB2 and its receptor EphB4, has been shown to play an important role in tumor angiogenesis. EphrinB2 and EphB4 have also been reportedly involved in the pathogenesis of ocular angiogenesis. This study was designed to investigate the expression of ephrinB2 and its receptor EphB4 in pterygia.Design: Experimental study of the expression of ephrinB2 and its receptor EphB4 in pterygia.Participants: Twenty-three primary pterygia, 5 recurrent pterygia, and 11 normal conjunctiva were studied.Methods: Immunohistochemistry studies were used to assess ephrinB2 and EphB4 protein expression levels and the tissue distribution in the samples.Results: EphrinB2 and EphB4 staining was present at a dense level in the total epithelium of the head portions of both primary and recurrent pterygial specimens, although just in the basal and parabasal layer of the epithelium of most of the normal conjunctivae.Conclusions: EphrinB2 and EphB4 appear to be overexpressed in pterygium, and they may play important roles in its development.     

玻璃体腔注射抗血管内皮生长因子单克隆抗体bevacizumab对增生型糖尿病视网膜病变纤维血管膜中整合素链接激酶表达的影响

目的 观察玻璃体腔注射抗血管内皮生长因子单克隆抗体bevacizumab(商品名Avastin)对增生型糖尿病视网膜病变(PDR)纤维血管膜中整合素链接激酶(ILK)表达及视网膜血管内皮细胞数量的影响.方法 玻璃体切割手术中取出的24例PDR患者的视网膜前纤维血管膜,其中12例患者手术前1周玻璃体腔单次注射bevaei...     

三种视网膜病视网膜前膜中基质金属蛋白酶及其天然抑制分子的表达

目的 研究增殖性糖尿病视网膜病变(proliferative diabetic retinopathy,PDR)、增殖性玻璃体视网膜疾病(proliferative vitreoretinopathy,PVR)和急性视网膜坏死(acute retinalnecrosis,ARN)患者视网膜前膜中基质金属蛋白酶(matrixmetalloproteinases:MMPs)及其天然抑制物(tissueinhibitorsofmetalloproteinages,TIMPs)的表达情况.方法 玻璃体手术中剥取PVR、PDR和ARN患者的视网膜前膜,同供体眼视网膜作为正常对照,冰冻切片后进行免疫组织化学染色,包括:MMP-1,MMP-2,MMP-3,MMP-7,MMP-9,TIMP-1和TIMP-2.结果 正常视网膜中能够观察到MMP-1,MMP-3,TIMP-1和TIMP-2的表达,在PVR、PDR和ARN患者标本中各种分子的表达都增强,尤以MMP-2,MMP-3和MMP-7明显.结论 正常视网膜中存在MMPs和TIMPs分子维持着细胞外基质动态的平衡,在PVR,PDR和ARN患者中MMP-2,MMP-3和MMP-7等MMPs分子表达增强,在其病变过程中可能起重要作用.     

增殖性玻璃体视网膜病变细胞凋亡的信号传导途径研究

目的 :探讨增殖性玻璃体视网膜疾病细胞凋亡的信号传导途径 ,以寻求新的药物治疗途径。方法 :2 3例增殖性玻璃体视网膜病变 (PVR) ,增殖性糖尿病性视网膜病变 (PDR) ,黄斑裂孔 (MH)及黄斑前膜 (MP)的视网膜前膜 (epiretinalmem brane,ERM )由玻璃体切割术中取得。细胞凋亡的情况由terminaldeoxynucleotidyltransfrase dUTP nickendlabeling(TUNEL法 )进行评估。Caspase 3及PARP的表达由特异性抗体抗活性Caspase 3和抗P 85片段的PARP检测。Cytokeratin与抗活性的Caspase 3双染色法进行凋亡细胞类型的鉴别。结果 :大多数发生凋亡的细胞为RPE细胞 ,而凋亡细胞与抗活性Caspase 3和抗P 85片段的PARP表达增加相关。细胞凋亡的数目与发生慢性视网膜脱离 (>2个月 )的病例有关 ,但凋亡系数 (apopto sisindex ,AI)在两组间无显著性差异 (1 4 4 2 9vs 3 2 2 86 ,P =0 1877)。PVR ,PDR ,MP各组的凋亡系数分别为 2 32 5 % ,3 4 2 % ,5 5 % ,P值分别为PPVR&PDR>0 1(0 16 85 ) ,PPDR&MP>0 1(0 5 380 ) ,PPVR&MP>0 1(0 8333)。结论 :此项研究发现细胞凋亡在PVR、PDR、MH及MP发病中的重要调节作用。诱导Caspase 3活性表达可作为一种治疗增殖性视网膜疾病的新的尝试     

Vitreous levels of angiopoietin 2 and vascular endothelial growth factor in patients with proliferative diabetic retinopathy

PURPOSE: To investigate the levels of angiopoietin-2 (Ang2) and vascular endothelial growth factor (VEGF) in the vitreous fluids of patients with proliferative diabetic retinopathy (PDR) and to ascertain their involvement, if any, in angiogenesis of PDR. DESIGN: Retrospective case-control study. METHODS: Forty-one eyes of 41 patients with proliferative diabetic retinopathy and 18 eyes of 18 patients with nondiabetic ocular diseases (control group). Nondiabetic control eyes included 11 with idiopathic macular hole and 7 with idiopathic epiretinal membrane. Vitreous fluid samples were obtained at vitrectomy, and the levels of Ang2 and VEGF were measured by enzyme-linked immunosorbent assay. RESULTS: Vitreous level (mean +/- SD) of Ang2 was significantly higher in patients with PDR (1,753 +/- 3,213 pg/ml) than in control patients (112 +/- 113 pg/ml) (P < .0001). The vitreous concentration of VEGF was also significantly higher in patients with PDR (812 +/- 1,108 pg/ml) than in control patients (1.7 +/- 4.4 pg/ml) (P < .0001). Both Ang2 and VEGF levels in eyes with active PDR were significantly higher than in those with inactive PDR. The vitreous concentration of Ang2 correlated significantly with that of VEGF in eyes with proliferative diabetic retinopathy ([correlation coefficient] rho = 0.497, P = .001). CONCLUSIONS: These data demonstrate an increase of Ang2 in the vitreous fluid of patients with PDR and suggest an association of Ang2 and VEGF with angiogenic activity in PDR.     

Expression of thrombospondin‐2 as a marker in proliferative diabetic retinopathy

Purpose: To determine the expression of the endogenous anti‐angiogenic and pro‐fibrotic matricellular protein thrombospondin (TSP)‐2 and its receptors CD36 and CD47 in proliferative diabetic retinopathy (PDR). In addition, we examined the expression of TSP‐2 in the retinas of diabetic rats. Methods: Epiretinal membranes from 14 patients with PDR and nine patients with proliferative vitreoretinopathy were studied by immunohistochemistry. Vitreous samples from 30 PDR and 25 nondiabetic patients were studied by enzyme‐linked immunosorbent assay. Vitreous samples and retinas of rats were examined by Western blotting. Results: In epiretinal membranes, vascular endothelial cells and myofibroblasts expressed TSP‐2, CD36 and CD47. In PDR membranes, significant correlations were observed between numbers of blood vessels expressing the panendothelial cell marker CD34 and numbers of blood vessels and stromal cells expressing TSP‐2, CD36 and CD47. The numbers of blood vessels and stromal cells expressing CD34, TSP‐2, CD36 and CD47 were significantly higher in membranes with active neovascularization when compared with those with quiescent disease. Thrombospondin‐2 levels in vitreous samples from PDR patients were significantly higher than those in control patients without diabetes (p < 0.001). Western blot analysis revealed a significant increase in the expression of intact and cleaved TSP‐2 in vitreous samples from PDR patients and in the retinas of diabetic rats compared to nondiabetic controls. Conclusions: Upregulation of TSP‐2 may be a protective mechanism against inflammation and angiogenesis associated with PDR.     

严重增殖性糖尿病视网膜病变玻璃体切除术后视功能评价

目的：：探讨玻璃体切除术治疗严重增殖性糖尿病视网膜病变( proliferative diabetic retinopathy,PDR)Ⅵ期患者术后视功能的改善情况及影响视功能预后的因素,并用多焦视网膜电图( multifocal electroretinography,mfERG)评价视功能的改变。方法：回顾性分析PDR Ⅵ期患者113例130眼经标准的玻璃体视网膜手术治疗后的临床资料,并根据术前OCT检查及术中所见,分为牵拉性视网膜脱离合并显著黄斑病变组(99例113眼)及未合并黄斑病变组(14例17眼)两组。行OCT及mfERG检查,对手术前后视力、mfERG P1波振幅密度、OCT形态学改变、手术并发症及预后等进行重点分析。结果：术后视力改善率63.1%(82/130),视力在0.05以上者从术前19眼(14.6%)提高到术后61眼(46.9%),其中56眼视力>0.1。牵拉性视网膜脱离未合并黄斑病变组术后视力改善率(88.2%)及术后视力>0.1所占比例(94.1%)均高于合并显著黄斑病变组(59.3%和35.4%),差异有统计学意义( P<0.05)。术后mfERG各环P1波反应密度较术前增加,并随着时间延长,改善更加明显(P<0.05),牵拉性视网膜脱离未合并黄斑病变组术后mfERG(1+2)环P1波反应密度高于合并显著黄斑病变组(P<0.05)。结论：PDRⅥ期患者玻璃体切除术后视功能改善;mfERG一阶反应的后极部各环P1波反应密度增加,且随时间延长,改善更加明显;未合并黄斑病变组术后视功能改善优于合并显著黄斑病变组。     

糖尿病患者玻璃体积血病因分析

目的:分析糖尿病患者玻璃体出血的原因,为相关疾病的诊治提供资料。方法:对2004-04/2007-06我科收治的126例(142眼)玻璃体积血的糖尿病患者情况进行回顾性分析。结果:增殖性糖尿病视网膜病变(proliferative diabetic reti-nopathy,PDR)122眼(85.9%),视网膜静脉阻塞(retinal vein occlusion,RVO)10眼(7.0%),视网膜裂孔(retinal hole,RH)6眼(4.2%),玻璃体后脱离(posterior vitreous detachment,PVD)4眼(2.8%);PDR组患者对侧眼糖尿病视网膜病变显著重于其余各组。结论:增殖性糖尿病视网膜病变是糖尿病患者玻璃体出血的主要原因,此外,视网膜静脉阻塞、视网膜裂孔和玻璃体后脱离也占有一定比例;通过对侧眼情况的评估,有助于玻璃体出血原因的判断。     

中国北部地区严重玻璃体积血的病因及其影响因素分析

目的:探讨中国北部地区严重玻璃体积血的病因及其影响因素.方法:对2011-01/2014-01在中国人民解放军火箭军总医院、北京市健宫医院及西安市第四医院因玻璃体积血(玻血)行玻璃体切割手术的患者进行回顾性分析.结果:1275例患者(1335眼)被纳入此研究.其中糖尿病视网膜病变(PDR)、视网膜静脉阻塞(RVO)、视网膜脱离/视网膜裂孔(RD/RH)、外伤、Eales病、老年性黄斑变性或息肉样脉络膜血管病变(AMD/PCV)所致玻璃体积血的总占比高达90%以上.年轻患者最常见玻璃体积血原因为外伤(40%)、PDR(19.5%)和Eales病(19.1%);中年患者最常见玻璃体积血原因为PDR(34.4%)、RVO(30.8%)及RD/RH(12.2%);RVO(35.7%)、PDR(26.6%)、RD/RH(14.6%)及AMD/PCV(8%)则是老年患者玻璃体积血的主要原因.结论:糖尿病视网膜病变、静脉阻塞及外伤是玻璃体积血最常见原因.不同年龄段中导致玻璃体积血发生的原因各有不同.PDR及RVO易出现复发性玻璃体积血,再次手术可能性大.     

激活T淋巴细胞与增生性糖尿病性视网膜病变关系的研究

目的:研究免疫介导过程对增生性糖尿病性视网膜病变(proliferative diabetic retinopathy PDR)的发生发展的潜在作用。方法:应用特异性的抗辅助T淋巴细胞(CD4)、抗白细胞介素-2(interleukin-2 IL-2)及其受体的单克隆抗体(interleukin-2 receptor IL-2R),对经扁平部玻璃体切割术获得的15例PDR视网膜前膜标本进行了研究。结果:在15例标本中,12例(80%)呈CD4阳性;12例(80%)发现有IL-2,且其中11例也呈CD4阳性;10例(67%)发现有IL-2R,其中9例呈CD4阳性并有释放的IL-2。大多数IL-2R阳性的前膜都来自Ⅰ型糖尿病患者,其中40%的患者小于40岁。结论:研究证实了半数以上的糖尿病视网膜前膜中有激活的免疫细胞和释放的淋巴因子,揭示了免疫反应过程和淋巴因子的生物效应对PDR视网膜前膜的形成起重要作用,尤其在青年患者和Ⅰ型糖尿病患者。眼科学报1999;15:229-232。     

增生型糖尿病视网膜病变玻璃体切除手术后再出血病因及治疗

目的 分析增生型糖尿病视网膜病变(PDR)玻璃体切割手术后再出血病因，观察再治疗效果。 方法 回顾分析302例PDR患者315只患眼接受玻璃体切割手术治疗后32只眼再出血并再次治疗后随访3~48个月（平均随访时间12个月）的临床资料。 结果 PDR玻璃体切割手术后再出血发生率为10%，再出血发生时间为手术后1～210 d，平均时间为51 d。再出血的主要原因中，28%为巩膜切口纤维血管向内生长，19%为视盘表面残存新生血管膜或血管残端处理不当，22%为视网膜激光光凝不足，9%为视网膜表面新生血管膜剥除不彻底，6%为视网膜静脉阻塞，16%为外力作用。通过冷凝巩膜切口处纤维血管、剥离视盘和视网膜表面残存新生血管膜并电凝视盘表面血管残端、补充视网膜激光光凝、 包扎双眼等治疗，再出血眼视力提高者占91%，视力下降者占9%。再次手术后并发症主要包括再次出血、虹膜后粘连、晶状体混浊加重、角膜上皮愈合延迟等。 结论 PDR玻璃体切割手术治疗后再出血的主要原因是巩膜切口纤维血管向内生长、视盘表面和（或）视网膜表面新生血管膜剥除不彻底、血管残端处理不当、视网膜激光光凝不足和外力作用。处理好巩膜切口、彻底剥离视盘和视网膜表面新生血管膜、电凝血管残端以及足够的视网膜激光光凝是预防和治疗PDR玻璃体切割手术后再出血的有效方法。(中华眼底病杂志,2007,23:238-240) 