激肽原1和类胰岛素生长因子结合蛋白6作为增生性玻璃体视网膜病变生物标志物的研究

目的 评估增生性玻璃体视网膜病变(PVR)特异性蛋白质激肽原l和类胰岛素生长因子结合蛋白6(GFBP-6)作为生物标志物的可能性.方法 对照试验研究.收集24例PVR手术前患者的玻璃体和血清,玻璃体样本分为轻度组(PVR-B级)和重度组(PVR-C、D级),以20名健康人血清和8只捐献眼球的玻璃体作为对照.同时收集15例玻璃体切除联合注气患者、8例玻璃体切除联合硅油填充术后6个月痊愈患者及8例巩膜环扎加压术后未愈患者的血清样本.应用免疫印迹法和酶联免疫吸附试验(ELISA)检测血清样本中激肽原1和IGFBP-6表达水平.对不同分级间的PVR患者玻璃体和血清中激肽原1和IGFBP-6含量比较,采用样本均数t检验;术前与术后6个月PVR患者血清中激肽原1和IGFBP-6含量比较,采用配对t检验;而巩膜环扎术后未愈、硅油填充眼患者与健康人血清激肽原1和IGFBP-6比较,采用单因素方差分析和进一步两两比较t检验.结果 免疫印迹法检测结果显示,24例PVR患者术前玻璃体样本均呈现激肽原1阳性条带,其中22例患者的IGFBP-6呈阳性,且术前血清中可检测到两种蛋白质;对照组的玻璃体和血清中均未检测出激肽原1和IGFBP-6.ELISA法检测玻璃体中蛋白激肽原1含量,显示轻度PVR患者为(237.5±32.1)μg/L,重度PVR患者为(281.0±63.0)μg/L,差异有统计学意义(t=5.44,P<0.05).ELISA法检测血清中蛋白激肽原1含量为(443.3±190.1)μg/L,高于其在玻璃体的含量,差异有统计学意义(t=5.27,P<0.05);15例玻璃体切除联合气体填充患者术后6个月血清中蛋白激肽原1含量为(81.9±18.6)μg/L,与术前(443.3±190.1)μg/L比较,差异有统计学意义(t=5.26,P<0.05);巩膜环扎术后未愈患者血清中激肽原1含量为(116.8±45.1)μg/L,健康人含量为(57.9±14.1)μg/L,硅油填充眼患者含量为(51.6±14.1)μg/L,三组间含量比较,差异有统计学意义(F=4.57,P<0.05);进一步两两比较,巩膜环扎术后未愈患者血清中激肽原1含量明显高于健康人组和硅油填充眼组,差异均有统计学意义(t=3.95,4.34;均P<0.05).ELISA法检测玻璃体中IGFBP-6含量,显示轻度PVR患者为(283.9±69.9)ng/L,重度PVR为(352.9±64.4)ng/L,差异有统计学意义(t=5.08,P<0.05);ELISA法检测血清中IGFBP-6含量为(185.3±34.9)ng/L,低于玻璃体内含量,差异有统计学意义(t=7.95,P<0.05);玻璃体切除联合气体填充术后6个月患者血清中IGFBP-6含量为(65.4±31.8)ng/L,较术前含量下降,差异有统计学意义(t=11.10,P<0.05);巩膜环扎术后未愈患者血清中IGFBP-6含量为(109.2±6.6)ng/L,硅油填充眼患者含量为(62.5±3.3)ng/L,健康人含量为(76.1±17.3)ng/L,三组间差异有统计学意义(F=4.68,P<0.05);进一步两两比较,差异也有统计学意义(t=3.16,2.77;均P<0.05).结论 PVR患者与健康人玻璃体和血清中激肽原1和IGFBP-6含量有较明显差别,且随PVR严重程度其表达水平有变化.激肽原1和IGFBP-6有可能作为PVR的生物标志物,但肯定性的结论有待于进一步的临床大样本验证.     

类胰岛素生长因子结合蛋白-6作为PVR血清分子标志物的验证

目的验证类胰岛素生长因子结合蛋白-6（IGFBP-6）是否可以作为增生性玻璃体视网膜病变（PVR）的血清分子标志物。方法收集PVRA、B、C、D级玻璃体（n=8）及术前术后6个月血清样本（n=20），PVRC级以上为严重PVR。正常供体眼玻璃体样本（n=8）和健康体检者血清（n=20）作为正常对照，对玻璃体和相应的血清样本分别进行IGFBP-6的免疫印迹分析和酶联免疫吸附试验（ELISA）。环扎术后未愈者（n=8）和硅油眼（n=8）患者的血清样本进行ELISA分析。在临床研究中的个体使用方面符合赫尔辛基宣言，参与试验者签署知情同意书。结果22例PVR患者（总体24例）玻璃体和血清中可检测到IGFBP-6，而供体眼玻璃体和正常人的血清中未测到。PVRC级、D级中IGFBP-6条带明显强于PVRB级。ELISA结果显示严重PVR患者玻璃体和血清中IGFBP-6质量浓度明显高于轻度PVR（F=3．34，P=0．04）。PVR患者术后6个月血清中IGFBP-6由（185．3±34．9）pg／mL明显下降至（65．4±31．8）pg／mL（t=11．10，P=0．015），与玻璃体术后硅油眼和正常对照组的血清中的质量浓度接近（t=0．08，P=0．989；t=1．59，P=0．131），但明显低于环扎术后未愈组（t=3．16，P=0．009）。结论IGFBP-6是PVR患者玻璃体和血清的特异蛋白质，与PVR的严重程度和预后评估相关，可作为PVR血清分子标志物。     

血清Leptin和TNF-α与2型糖尿病视网膜病变的相关关系研究

目的 探讨血清中瘦素(Leptin)、肿瘤坏死因子α(tumor necrosis factor-α,TNF-α)的水平与2型糖尿病视网膜病变发生发展之间的关系.方法 对88例2型糖尿病患者(按照糖尿病视网膜病变分级标准,再将其分为3个亚组)及30例健康对照者,采用放射免疫法测定血清中Leptin和TNF-α,免疫抑制比浊法测定糖化血红蛋白,记录相关的临床和生化指标.结果 2型糖尿病视网膜病变组患者血清Leptin水平(10.57±1.84)μg·L-1显著高于无视网膜病变组的(7.90±1.58)μg·L-1(P<0.01);增生性糖尿病视网膜病变组血清Leptin水平(11.66±1.21)μg·L-1显著高于非增生性糖尿病视网膜病变组的(9.56±1.75)μg·L-1(P<0.01)及无视网膜病变组的(7.90±1.58)μg·L-1(P<0.01).2型糖尿病视网膜病变组患者血清TNF-α水平(60.45±13.33)pmol·L-1显著高于无视网膜病变组的(39.97±8.38)pmol·L-1(P<0.01);增生性糖尿病视网膜病变组血清TNF-α水平(69.93±10.86)pmol·L-1显著高于非增生性糖尿病视网膜病变组的(51.60±8.47)pmol·L-1(P<0.01)及无视网膜病变组(39.97±8.38)pmol·L-1(P<0.01).血清Leptin水平与病程、糖化血红蛋白、体质量指数成正相关(r=0.639,P<0.01;r=0.260,P<0.05;r=0.468,P<0.01);血清TNF-α与病程、空腹血糖、体质量指数成正相关(r=0.680、0.355、0.299,P<0.01),与收缩压、舒张压成正相关(r=0.281、0.234,P<0.05),与高密度脂蛋白胆固醇成负相关(r=-0.423,P<0.01).血清Leptin、TNF-α水平成正相关(r=0.660,P<0.05).结论 2型糖尿病合并糖尿病视网膜病变患者血清Leptin、TNF-α水平增高;随着糖尿病视网膜病变程度的加重,血清中的Leptin、TNF-α水平也逐渐升高,提示其与糖尿病视网膜病变,特别是糖尿病视网膜痛变的严重程度相关.     

血清sICAM-1及透明质酸与糖皮质激素治疗TAO敏感性关系的研究

目的探讨血清可溶性细胞间黏附分子-1(soluble intercellular adhesion molecule1,sICAM-1)及透明质酸(hyaluronic acid,HA)与甲状腺相关眼病(thyroid-associated ophthalmopathy,TAO)糖皮质激素治疗敏感性的关系。方法 41例(74眼)活动期TAO患者给予糖皮质激素治疗,根据疗效将患者分为治疗有效组和无效组,观察治疗前后血清sICAM-1及HA的水平变化。结果治疗有效组58眼,治疗前患者血清sICAM-1及HA平均含量分别为(1136.2±162.5)μg·L-1、(124.8±61.4)μg·L-1,治疗后两者的含量分别为(829.7±94.6)μg·L、(81.5±33.9)μg·L-1,均较治疗前显著下降(P=0.000、P=0.001)。治疗无效组16眼,血清sICAM-1水平治疗后(1209.1±136.2)μg·L-1较治疗前(1078.6±120.3)μg·L-1有所上升(P=0.046),HA的水平治疗后(112.7±51.4)μg·L-1较治疗前(126.5±63.8)μg·L-1变化较小(P=0.623)。有效组治疗后血清sICAM-1、HA水平均低于无效组(P=0.000、P=0.037);治疗前两组水平差异均无统计学意义(P=0.338、P=0.841)。结论 TAO患者血清sICAM-1及HA水平的变化与糖皮质激素治疗的敏感性密切相关,可作为评价糖皮质激素治疗效果的指标。     

静脉注射后环丙沙星在眼内炎及眼球穿通伤患者眼内的药物水平

目的 研究静脉注射后环丙沙星在眼内炎及眼球穿通伤患者眼内的药物水平.方法 老年性白内障对照组25例25眼、眼球穿通伤组21例21眼、眼内炎组12例12眼分别在白内障手术、玻璃体切割手术前1 h静脉注射环丙沙星,术中取房水或(和)玻璃体,双缩脲法测定房水蛋白含量,反向高效液相色谱法测定房水及玻璃体环丙沙星的浓度.结果 老年性白内障对照组、眼球穿通伤组及眼内炎组房水蛋白含量分别为(0.09±0.05)g·L-1、(2.31±1.71)g·L-1和(7.78±5.34)g·L-1,3组间比较差异均有显著统计学意义(P均<0.01);3组房水环丙沙星浓度分别为(0.18±0.07)mg·L-1、(0.19±0.08)mg·L-1和(0.52±0.18)mg·L-1,眼内炎组明显高于其他2组(P均<0.01),其他2组比较差异无统计学意义(P>0.05);玻璃体环丙沙星浓度眼内炎组为(0.50±0.38)mg·L-1,较眼球穿通伤组的(0.06±0.03)mg·L-1高(P均<0.01);眼内炎组房水和玻璃体中环丙沙星浓度与房水蛋白含量呈正相关(r=0.889和rs=0.841,P均<0.05).结论 眼内炎患者血-眼屏障通透性增高,静脉注射环丙沙星眼内渗透性增加,房水及玻璃体药物浓度可达大部分眼内致病菌最小抑菌浓度,可作为细菌性眼内炎治疗性用药.     

增生性玻璃体视网膜病变玻璃体中的Ⅲ型前胶原

目的:检测增生性玻璃体视网膜病变(PVR)患者血清及玻璃体中Ⅲ型前胶原(Procollagen Ⅲ,PC Ⅲ)的含量,探讨其在PVR发病中的作用。方法:用放射免疫测定法测定5例正常人玻璃体,20例正常人血清及29例孔源性视网膜脱离合并PVR患者玻璃体及血清中的PC Ⅲ。用Logistic回归模型分析PVR患者发病时间、手术史、增生膜及PVR分级与PC Ⅲ含量的相关性。结果:PVR患者血清和对照组血清PC Ⅲ含量分别为83.76±18.52和85.02±17.50μg/L(P>0.05)。正常对照玻璃体PC Ⅲ含量低于最小可测值(40 μg/L)。PVR患者组中有12例未检测到,其余17例玻璃体中PC Ⅲ含量明显升高,平均268.69±176.07μg/L(P<0.05)。玻璃体PC Ⅲ水平与病史长短和PVR级别相关,发病时间延长,其玻璃体PC Ⅲ含量大于40μg/L的概率是小于40 μg/L的5.2655倍;PVR级别增加,其玻璃体PC Ⅲ含量大于40 μg/L的概率是小于40 μg/L的2.7978倍。结论:多数PVR患者玻璃体内可测得PC Ⅲ含量增加,并与PVR分级及发病时间长短相关。PC Ⅲ合成活跃属眼内的局部反应。提示PC Ⅲ及Ⅲ型胶原在PVR发展中起一定的作用。眼科学报1998;14:76—79。     

特发性眼眶炎性假瘤患者血清细胞间黏附分子-1水平及其临床意义

目的探讨特发性眼眶炎性假瘤(idiopathic orbital inflammatory pseudotumor,IOIP)患者血清细胞间黏附分子-1(intercellular adhesion molecule 1,ICAM-1)水平与IOIP的发生发展的关系。方法应用酶联免疫双抗体夹心法(ELISA法)测定60例IOIP患者(病例组)和30例正常健康者的血清ICAM-1水平。所有IOIP患者均经过病理组织学检查证实。采用SPSS 17.0软件比较IOIP组和对照组之间血清ICAM-1水平的差异,并分析IOIP组血清ICAM-1水平与病例及眼别的关系。结果 IOIP患者血清ICAM-1水平为(251.68±76.16)μg·L-1,比正常对照组(176.56±29.80)μg·L-1明显增高(P<0.05);随着IOIP病程的延长,ICAM-1的表达呈明显上升趋势,病程>12个月患者(326.60±38.71)μg·L-1与病程6~12个月患者(264.53±34.90)μg·L-1及病程<6个月患者血清ICAM-1水平(184.04±53.05)μg·L-1两两比较差异均有统计学意义(均为P<0.05),双眼发病者血清ICAM-1水平(293.30±69.34)μg·L-1明显高于单眼发病者(240.17±74.56)μg·L-1(P<0.05)。结论IOIP患者血清ICAM-1水平可反映病程长短和严重程度,检测血清ICAM-1水平在评估疾病的严重性、病程长短等方面具有一定的参考价值。     

增生性糖尿病视网膜病变玻璃体中结缔组织生长因子的定量分析

目的 定量测定结缔组织生长因子(connective tissue growth factor,CTGF)在增生性糖尿病视网膜病变(proliferative di-abetic retinopathy,PDR)患者玻璃体中的浓度,探讨其在PDR发病机制中的作用.方法 采用双抗体夹心酶联免疫吸附测定法定量检测27眼PDR、5眼非增生性糖尿病视网膜病变及5眼正常对照组玻璃体中CTGF的浓度.结果 PDR组玻璃体中CTGF浓度(567.09±181.15)ng·L-1明显大于对照组(128.06±57.28)ng·L-1及非增生性糖尿病视网膜病变组(150.70±52.39)ng·L-1(P均<0.01).PDR组中Ⅵ期患者玻璃体中CTGF浓度(706.17±88.78)ng·L-1大于Ⅳ期(349.20±110.60)ng·L-1及Ⅴ期(526.70±122.50)ng·L-1(P均<0.01).结论 PDR患者玻璃体中CTGF浓度升高可能与视网膜新生血管纤维膜的形成有关,CTGF在PDR发展过程中起着一定作用.     

血浆ET-1、NO和vWF与2型糖尿病视网膜病变相关关系

目的探讨反映血管内皮功能的标志物血浆内皮素1(endothelin1,ET-1)、一氧化氮(nitric oxide,NO)、血管性假血友病因子(von Willebrand factor,vWF)与2型糖尿病视网膜病变(diabetic retinopathy,DR)严重程度的关系。方法依据WHO标准选择2型糖尿病患者(diabetic mellitus,DM)伴有或不伴有DR85例和健康对照组30人,采用酶联免疫吸附双抗体夹心法和硝酸还原法测定血浆ET-1、vWF和NO,离子交换层析分光光度法测定糖化血红蛋白(hemoglobin A1C,HbA1C),记录相关临床和生化指标。结果2型糖尿病并发DR患者血浆ET-1、vWF水平(分别为3·04μg·L-1±1.27μg·L-1、136.18%±33.64%)显著高于无DR患者组(分别为1.48μg·L-1±1.16μg·L-1、66.68%±19.30%,P<0.01),但血浆NO水平(82.34μg·L-1±17·42μmol·L-1)低于无DR患者组(98·12μg·L-1±33.30μmol·L-1,P<0.05);血浆ET-1水平与收缩压,舒张压和病程呈正相关(r=0.431,0.382和0·450,P<0.05),与空腹血糖、HbA1C、vWF水平呈显著正相关(r=0·561,0.478和0.544,P<0.01);血浆NO与病程、vWF呈负相关(r=-0.431和-0.412,P<0.05);血浆vWF与ET-1、病程、FBG、HbA1C呈正相关(r=0.544,0.313,0.425和0·380,P<0.05),与NO水平呈负相关(r=-0.412,P<0·05)。结论血浆ET-1、NO、vWF水平的检测反映血管内皮功能受损程度可能与DR发生、发展有关,对DR的早期诊断和治疗具有一定意义。     

SDF-1在增生性糖尿病视网膜病变中的表达及意义

目的 观察基质细胞衍生因子(stromal cell derivedfactor-1,SDF-1)在糖尿病视网膜新生血管膜和玻璃体中的表达水平,并探讨其与增生性糖尿病视网膜病变(proliferativedibetic retinopathy,PDR)程度的相关性.方法 采用免疫组织化学法,对12例PDR患者视网膜新生血管膜上的SDF-1表达情况进行检测.采用双夹心酶联免疫吸附测定法对PDR组20例、PDR引起的新生血管性视网膜病变组10例、增生性玻璃体视网膜病变(proliferative vitreoretinopathy,PVR)组20例和正常人组10例的玻璃体中SDF-1浓度进行检测.结果 在12例新生血管膜的标本中10例有SDF-1的阳性表达.PDR组玻璃体中,SDF-l浓度为(351.31±120.30)ng·L-1,PDR引起的新生血管性视网膜病变组为(1 161.49±103.43)ng·L-1,PVR组为(72.59±8.78)ng·L-1,正常人组<62.5 ng·L-1;PDR组与PDR引起的新生血管性视网膜病变组、PVR组SDF-1含量相比,差异均有统计学意义(t=-18.17、10.31,P<0.001).结论 SDF-1参与了糖尿病视网膜新生血管的形成;玻璃体中的SDF-1浓度与PDR程度呈正相关.     

实验性增殖性玻璃体视网膜病变玻璃体内Ⅲ型前胶原的放射免疫测定

目的:检测巨噬细胞诱发的增殖性玻璃体视网膜病变（proliferative vitreoretinopathy，PVR）模型玻璃体内Ⅲ型胶原的合成活性。方法:用放射免疫法测量14只兔PVR眼及14只对照眼玻璃体中Ⅲ型前胶原（procollagenⅢ，PCⅢ）含量。结果:巨噬细胞注入7天时玻璃体中PCⅢ平均含量是257.58μg/L（236.04～266.88μg/L；n＝4），14天以后明显增加，28天时平均为912.23μg/L（881.36～943.10μg/L；n＝2）.14只对照眼未能检出。结论:实验性PVR玻璃体中可测得较高水平的PCⅢ，且含量随病程明显增加，与PVR的瘢痕化过程和牵拉性视网膜脱离（traction retinal de tachment，TRD）发生在时相上明显一致。(中华眼底病杂志,1998,14:43-44)     

磷酸果糖激酶-2/果糖-2，6-二磷酸酶3在增生型糖尿病性视网膜病变患者玻璃体和血清中的表达及其相关性分析

目的　定量检测增生型糖尿病性视网膜病变（proliferative diabetic retinopathy,PDR）患者玻璃体和血清中磷酸果糖激酶-2/果糖-2,6-二磷酸酶3（phospofructokinase-2/fructose-2,6-bisphosphatase 3,PFKFB3）和血管内皮细胞生长因子（vascular endothelial growth factor,VEGF）的表达水平,探讨PFKFB3在PDR患者中可能的作用机制。方法　纳入确诊为PDR拟行单眼玻璃体切割术的患者42例（42眼）作为试验组,并根据术前是否行玻璃体内注射抗VEGF药物进一步将试验组分为非注药组和注药组,纳入同期诊断为全层黄斑裂孔（full thickness macular hole,FTMH）及黄斑前膜（preretinal membrane of the macula,PRMM）的20例（20眼）患者作为对照组。收集各组患者的玻璃体和血清标本,定量检测各组标本中的PFKFB3和VEGF表达水平,并进行统计学分析。结果　试验组患者玻璃体中PFKFB3水平为（463.17±381.28）ng·L^-1,明显高于对照组［（158.43±86.88）ng·L^-1］（t=4.919,P＜0.001）,试验组血清中PFKFB3水平为（153.45±83.78）ng·L^-1,明显高于对照组［（92.72±32.42）ng·L^-1］（t=4.098,P＜0.001）。非注药组患者玻璃体中PFKFB3水平为（797.29±387.44）ng·L^-1,明显高于注药组［（257.56±181.49）ng·L^-1］（t=5.230,P＜0.001）,而非注药组血清中PFKFB3水平与注药组差异无统计学意义（t=0.679,P=0.501）。非注药、注药组和对照组患者玻璃体与血清中的PFKFB3水平无相关性（非注药组:r=0.194,P=0.471;注药组:r=0.071,P=0.731;对照组:r=0.254,P=0.279）。试验组患者玻璃体中VEGF水平为（1713.50±1386.90）ng·L^-1,明显高于对照组［（205.52±92.93）ng·L^-1］（t=7.014,P＜0.001）;试验组血清中VEGF水平为（224.98±168.08）ng·L^-1,明显高于对照组［（86.80±36.51）ng·L^-1］（t=5.082,P＜0.001）。非注药组患者玻璃体中VEGF水平为（3399.72±510.06）ng·L^-1,明显高于注药组［（675.82±242.57）ng·L^-1］（t=20.014,P＜0.001）,非注药组血清中VEGF水平为（373.40±174.23）ng·L^-1,明显高于注药组［（133.65±73.10）ng·L^-1］（t=5.228,P＜0.001）。非注药、注药组和对照组患者玻璃体与血清中的VEGF水平均存在正相关关系（非注药组:r=0.952,P＜0.001;注药组:r=0.423,P=0.031;对照组:r=0.776,P＜0.001）。非注药组、注药组和对照组患者玻璃体中PFKFB3与VEGF水平均存在正相关关系（非注药组:r=0.865,P＜0.001;注药组:r=0.587,P=0.002;对照组:r=0.807,P＜0.001）,而在血清中仅注药组的PFKFB3与VEGF水平存在正相关关系（r=0.444,P=0.023）。结论　PFKFB3可能参与了PDR的发生发展过程;VEGF可能通过上调PFKFB3的表达而参与PDR的发生发展。     

The development of severe proliferative vitreoretinopathy after retinal detachment surgery

A prospective clinical study was conducted to determine wether preoperative proliferative vitreoretinopathy (PVR), grade B, was a significant risk factor in the development of severe PVR after surgery for retinal detachment repair. Two series of consecutive retinal detachments associated with horseshoe retinal tears were compared. The first series included 40 eyes of 40 patients with preoperative PVR, grade O - A. The second series included 30 eyes of 27 patients with preoperative PVR, grade B. All eyes were operated on with conventional microsurgical techniques. At the first operation, no vitrectomies were carried out in any eyes. The incidence of postoperative PVR, grades C and D, was 20% (6/30 eyes) after a single operation in the series of eyes with preoperative PVR, grade B as compared to 0% in the series of eyes with preoperative PVR, grade O - A. The difference between the two groups was statistically significant (P = 0.01). It was also found that the incidence of postoperative proliferative PVR was significantly higher in eyes with preoperative vitreous hemorrhage (30.7%) as compared to eyes with no preoperative vitreous hemorrhage (0%;P = 0.02). Incomplete posterior vitreous detachment without collapse of the vitreous gel occurred significantly more frequently in eyes with preoperative proliferative vitreoretinopathy, grade B (68.4%, than in eyes with preoperative proliferative vitreoretinopathy, grade O - A(27.5%;P = 0.02).     

Soluble TNF receptors in vitreoretinal proliferative disease

PURPOSE: To measure vitreous levels of soluble TNF-receptors (sTNF-Rs) types I and II in eyes with rhegmatogenous retinal detachment (RRD), uncomplicated or complicated with proliferative vitreoretinopathy (PVR), and in eyes with proliferative diabetic retinopathy (PDR). To examine whether there is any relationship between vitreous levels of sTNF-Rs and clinical features of these conditions and between vitreous sTNF-Rs and TNFalpha levels and serum levels of sTNF-RS: METHODS: Vitreous levels of sTNF-Rs and TNFalpha were measured by enzyme-linked immunosorbent assay in 30 eyes with PVR, 30 eyes with uncomplicated RRD, and 29 eyes with PDR. Vitreous from eyes of 10 deceased donors and 9 eyes with macular holes served as control specimens. Serum levels of sTNF-Rs were measured in 17 patients with PDR and 21 patients with PVR. RESULTS: Vitreous levels of sTNF-Rs I and II were increased in eyes with PVR, RRD, and PDR when compared with control eyes (P < 0.002). However, vitreous levels of sTNF-Rs I and II were higher in eyes with PVR than in eyes with RRD (P < 0.01) or PDR (P < 0.03). This contrasted with the findings that serum sTNF-Rs were higher in PDR than in PVR (P < 0.016) and that vitreous levels of TNFalpha were higher in eyes with PDR than in eyes with PVR (P < 0.0005). In PVR, vitreous sTNF-Rs levels were associated with the duration of retinal detachment, number of previous external operations, and grade of severity, whereas in PDR these levels were not related to the type or duration of diabetes or its complication with traction retinal detachment. CONCLUSIONS: These observations suggest the existence of TNF inhibitory mechanisms within the eye during retinal processes of inflammation and angiogenesis. That high vitreous levels of sTNF-Rs relate to severity of retinopathy suggests that these molecules may constitute reactive products of inflammation. Effective control of TNFalpha activity by sTNF-Rs within the retinal microenvironment may determine the outcome and severity of retinal proliferative conditions.     

Vitreous levels of intercellular adhesion molecule 1 (ICAM-1) as a risk indicator of proliferative vitreoretinopathy

AIM: To investigate whether high vitreous levels of the soluble intercellular adhesion molecule 1 (sICAM-1) may be related to clinical risk factors of proliferative vitreoretinopathy (PVR) and whether their measurement may serve as an additional risk indicator of this complication in eyes with rhegmatogenous retinal detachment (RRD). METHODS: Levels of sICAM-1 were measured by enzyme linked immunosorbent assays (ELISA) in vitreous from 36 eyes with RRD clinically considered to be at high risk of developing PVR (large retinal breaks, vitreous haemorrhage, long standing RRD, and previous vitreoretinal surgery). Levels of sICAM-1 in this group were compared with those in vitreous from 31 eyes with RRD without clinical risk factors for PVR, 32 eyes with established PVR and 10 eyes with macular holes. RESULTS: Vitreous from eyes with RRD at high risk of developing PVR contained significantly higher levels of sICAM-1 (range 6.1-97.7 ng/ml; Mann-Whitney test, p=0.0002) than those from eyes with RRD at low risk of developing this complication (range 4.8-17.7 ng/ml). Vitreous sICAM-1 levels in eyes with RRD at high risk of developing PVR were significantly lower than in eyes with established PVR (p=0.037), but higher than in eyes with macular holes (p <0.0001). Levels of sICAM-1 >/=15 ng/ml (3 x median of the levels present in control eyes) provide a useful cut off point for a highly specific test (96.7%) with high positive (91.6%) and negative (96.7%) predictive values, despite a relatively low sensitivity (30. 5%). CONCLUSIONS: The present findings suggest that laboratory measurement of sICAM-1 levels in vitreous from eyes with RRD may constitute an additional factor for identifying patients at high risk of PVR. Hence, determination of sICAM-1 levels may aid in the monitoring of patients likely to develop this complication and in the identification of patients who may benefit from adjuvant anti-inflammatory therapy.