Soluble cellular adhesion molecules in proliferative vitreoretinopathy and proliferative diabetic retinopathy.

PURPOSE. To measure vitreous levels of soluble intercellular adhesion molecule-1 (sICAM-1) and soluble vascular cellular adhesion molecule-1 (sVCAM-1) in the eyes of patients with retinal detachment (RD) due to proliferative diabetic retinopathy (PDR) or proliferative vitreoretinopathy (PVR) and to determine whether the levels of these mediators correlated with clinical parameters of disease. METHODS. Undiluted vitreous specimens were collected from 50 eyes of 48 patients undergoing vitrectomy for traction RD due to PDR (21 specimens) and recurrent RD due to PVR (19 specimens). Control vitreous specimens were obtained from patients undergoing macular hole repair (10 specimens). The levels of sICAM-1 and sVCAM-1 were measured in each sample by specific enzyme-linked immunoadsorbent assays. RESULTS. Vitreous levels of sICAM-1 were significantly increased in vitreous specimens from both PVR (median +/- SD; 12.0 +/- 76.3 ng/ml; P < 0.01) and PDR (8.4 +/- 24.0 ng/ml; P < 0.01) when compared to vitreous from eyes with macular holes (0. 3 +/- 4.2 ng/ml). Vitreous levels of sVCAM-1 were significantly increased in both PVR (36.5 +/- 255.2 ng/ml; P < 0.001) and PDR (26. 2 +/- 93.5 ng/ml; P < 0.01) when compared to control vitreous (17.7 +/- 7.8 ng/ml). The vitreous levels of sICAM-1 were higher in cases of PDR which developed recurrent proliferative disease (P < 0.01) and recurrent RD (P = 0.01), whereas the levels of sICAM-1 in PVR and sVCAM-1 in PDR and PVR did not significantly correlate with these clinical parameters. CONCLUSIONS. Soluble forms of ICAM-1 and VCAM-1 are increased in the vitreous cavity of patients with RD due to PDR or PVR, reflecting the inflammatory nature of these conditions and suggesting a possible role for these mediators in the pathogenesis of proliferative retinal disease. The vitreous levels of these sCAMs at the time of surgery may serve as a marker of inflammation, but their specific levels do not predict the likelihood of recurrent proliferation or surgical anatomic success in most cases of PVR and PDR.     

Tenascin-C levels in the vitreous of patients with proliferative vitreoretinopathy

PURPOSE: To determine whether tenascin-C levels are elevated in the vitreous of patients with proliferative vitreoretinopathy (PVR). METHODS: We assayed tenascin-C levels in vitreous samples of 110 consecutive patients with PVR (30 eyes), rhegmatogenous retinal detachment (RRD; 32 eyes), and macular hole or idiopathic epiretinal membrane (controls, 48 eyes) using an enzyme-linked immunosorbent assay. RESULTS: Vitreous levels of tenascin-C (median [range]) were significantly greater in PVR (845.0 ng/ml [411.0-1,050.0]) than in RRD (21.9 ng/ml [13.2-127.0]) and in the controls (18.0 ng/ml [9.9-199.0]) (p < 0.0001). CONCLUSION: The results indicate the possibility that tenascin-C is involved in the pathogenesis of PVR.     

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.     

Syndecan-1在视网膜脱离患者玻璃体液中的表达

目的检测孔源性视网膜脱离（RRD）及增生型糖尿病视网膜病变（PDR）并发牵拉性视网膜脱离（TRD）患者玻璃体液中syndecan-1的浓度。方法酶联免疫吸附法检测对照组正常人、RRD组、PDR合并TRD组患者玻璃体液中syndecan-1的浓度。采用Kruskal—Wallis秩和检验进行组间比较。结果9例正常人玻璃体液中syndecan-1的浓度[中位数（四分位数间距）]为0．31（0．22）ng／mL,10例RRD患者玻璃体液中syndecan-1的浓度为1．89（1．89）ng／mL,29例PDR并发TRD患者玻璃体液中syndecan-1的浓度为3．64（4．00）ng／mL。3组间syndecan-1浓度的差异有统计学意义（χ2=23．65,P〈0．0001）。与对照组syndecan．1的浓度相比,RRD玻璃体液（χ2=8．18,P=0．0167）及PDR并发TRD玻璃体液（χ2=23．57,P〈0．0001）中的浓度差异均有统计学意义。结论在RRD及PDR并发TRD的玻璃体液中,syndecan-1的水平较正常均显著升高。     

Monocyte chemotactic protein-1 levels in the vitreous of patients with proliferative vitreoretinopathy

PURPOSE: To assess the potential role of monocyte chemotactic protein-1 (MCP-1) in the pathogenesis of proliferative vitreoretinopathy (PVR) and to investigate its possible interaction with the macrophage migration inhibitory factor (MIF). METHODS: We assayed MCP-1 and MIF levels in the vitreous samples of 85 consecutive patients with PVR (29 eyes), rhegmatogenous retinal detachment (RRD; 22 eyes), and macular hole or idiopathic epimacular membrane (controls; 34 eyes), by enzyme-linked immunosorbent assay. RESULTS: Vitreous levels of MCP-1 were 1760.7 +/- 471.3 pg/mL (mean +/- SD) in PVR patients, 1200.4 +/- 579.8 pg/mL in RRD patients, and 436.3 +/- 286.1 pg/mL in the controls. Vitreous MCP-1 levels in PVR patients were significantly higher than those in RRD patients and in the controls (P <.0001, respectively). MCP-1 levels in grade C of PVR (1883.7 +/- 479.5 pg/mL) were significantly greater than those in grade D (1437.8 +/- 258.8 pg/mL) (P =.0112). Vitreous concentrations of MCP-1 had no correlation with those of MIF. CONCLUSIONS: The results indicate the possibility that MCP-1 may have a role mainly in the early stage of PVR and that the role of MCP-1 in PVR may differ from that of MIF.     

A proposed new classification for diabetic retinopathy: the concept of primary and secondary vitreopathy

BACKGROUND: Many eyes with proliferative diabetic retinopathy (PDR) require vitreous surgery despite complete regression of new vessels with pan retinal laser photocoagulation (PRP). Changes in the vitreous caused by diabetes mellitus and diabetic retinopathy may continue to progress independent of laser regressed status of retinopathy. Diabetic vitreopathy can be an independent manifestation of the disease process. AIM: To examine this concept by studying the long-term behavior of the vitreous in cases of PDR regressed with PRP. MATERIALS AND METHODS: Seventy-four eyes with pure PDR (without clinically evident vitreous traction) showing fundus fluorescein angiography (FFA) proven regression of new vessels following PRP were retrospectively studied out of a total of 1380 eyes photocoagulated between March 2001 and September 2006 for PDR of varying severity. Follow-up was available from one to four years. RESULTS: Twenty-three percent of eyes showing FFA-proven regression of new vessels with laser required to undergo surgery for indications produced by vitreous traction such as recurrent vitreous hemorrhage, tractional retinal detachment, secondary rhegmatogenous retinal detachment and tractional macular edema within one to four years. CONCLUSION: Vitreous changes continued to progress despite regression of PDR in many diabetics. We identifies this as "clinical diabetic vitreopathy" and propose an expanded classification for diabetic retinopathy to signify these changes and to redefine the indications for surgery.     

Interleukin (IL)-6, interleukin (IL)-8 levels and cellular composition of the vitreous humor in proliferative diabetic retinopathy, proliferative vitreoretinopathy, and traumatic proliferative vitreoretinopathy

PURPOSE: To investigate the interleukin (IL)-6 levels, IL-8 levels, and cellular composition of the vitreous humor in patients with proliferative diabetic retinopathy (PDR), proliferative vitreoretinopathy (PVR), and traumatic PVR. METHODS: Vitreous samples from 14 patients with PDR, 10 patients with PVR, and 10 patients with traumatic PVR were analyzed. Fifteen cadaver eyes were used as controls. Cytokine levels were measured by ELISA. RESULTS: Elevated IL-6 levels were detected in the vitreous of 12 (85.7%) of the PDR patients, eight (80%) of the PVR patients, and all (100%) of the traumatic PVR patients. None of the control IL-6 results were elevated. Vitreous IL-8 levels were elevated in 12 (85.7%) of the PDR patients, six (60%) of the PVR patients, all (100%) of the traumatic PVR patients, and one (6.7%) of the control eyes. Cytological examination of the vitreous specimens revealed a predominance of macrophages (50%) in the PDR samples and a predominance of retinal pigment epithelial (RPE) cells (60%) in the PVR samples. In contrast, neutrophils predominated (88%) in the traumatic PVR samples. CONCLUSION: The findings suggest that IL-6 and IL-8 may be involved in the pathogenesis of PDR, PVR, and traumatic PVR. High proportions of RPE cells and macrophages are associated with elevated IL-6 and IL-8 levels in the vitreous of PDR and PVR patients; however, the fact that these cells are not predominant in traumatic PVR suggests that different immune response mechanisms may be active in the pathogenesis of these disorders.     

Vitreous leptin levels in retinal disease

BACKGROUND/AIMS: The purpose of this study was to investigate the relationship between vitreous leptin levels and retinal diseases. METHODS: Levels of vitreous leptin were evaluated in proliferative diabetic retinopathy (PDR) and a variety of other retinopathies including: macular disease, neovascular maculopathies, primary retinal detachments, and vascular occlusive disease. RESULTS: In patients with PDR (N=7), the average vitreous level of leptin (37.4 ng/ml) was significantly higher than that in patients with PVR (<1.0 ng/ml, P<0.05). Vitreous leptin level in patients with PVR or macular disease (N=18), with or without diabetes, was not significantly different from the control subjects who had retinal detachment only (N=7). CONCLUSION: The results show that the leptin level in vitreous taps is elevated in PDR. We suggest that leptin plays an active role in PDR.     

Increased glutamate levels in the vitreous of patients with retinal detachment

Experimental models have implicated glutamate in the irreversible damage to retinal cells following retinal detachment. In this retrospective study we investigated a possible role for glutamate and other amino acid neurotransmitters during clinical rhegmatogenous retinal detachment (RRD). Undiluted vitreous samples were obtained from 176 patients undergoing pars plana vitrectomy. The study group consisted of 114 patients (114 eyes) with a rhegmatogenous retinal detachment. Controls included 52 eyes with an idiopathic macular hole or idiopathic epiretinal membrane and 10 eyes with a traction retinal detachment due to proliferative diabetic retinopathy. Vitreous concentrations of glutamate, gamma-aminobutyric acid (GABA), taurine, glycine, and aspartate were determined by high-pressure liquid chromatography (HPLC). Multivariate analysis was used to examine a possible association between amino acid neurotransmitter levels and several clinical variables including visual acuity. The mean vitreous concentration of glutamate in eyes with a rhegmatogenous retinal detachment (16.6 +/- 5.6 microM) was significantly higher as compared to the controls (13.1 +/- 5.2 microM) (P = 0.001). Taurine levels were also increased in RRD, whereas no significant difference could be observed in glycine, aspartate and GABA levels when comparing RRD with controls. A correlation was found between increased vitreous glutamate and a lower pre-operative visual acuity. No association was, however, observed between post-operative visual acuity and the level of any of the five amino acid neurotransmitters. RRD was associated with a significantly increased vitreous glutamate concentration. Using visual acuity as a functional parameter in this study, we could not demonstrate a correlation between vitreous glutamate, or any of the other tested amino acid neurotransmitters and visual outcome.     

Surgical outcomes of epiretinal membrane removal after successful pars plana vitrectomy for retinal diseases

PURPOSE: To evaluate visual outcomes after a removal of an epiretinal membrane (ERM) secondary to rhegmatogenous retinal detachment (RRD), proliferative vitreoretinopathy (PVR), or proliferative diabetic retinopathy (PDR). METHODS: The medical charts of 51 consecutive patients who underwent PPV to remove an ERM were reviewed in an institutional setting. The preoperative best-corrected visual acuity (BCVA) was evaluated to determine if it was a possible predictor of the postoperative BCVA. The visual outcomes in the RRD, PVR, and PDR groups were compared. Follow-up periods ranged from 13 to 90 months (mean, 40.9 months). RESULTS: After the ERM was removed, the postoperative BCVA improved significantly by 0.471 logarithm of the minimum angle of resolution units for all groups (t = 8.99; P < 0.001). The postoperative BCVA improved by two or more lines in 43 eyes (84.3%). Patient age and the preoperative BCVA significantly correlated with the visual improvement (P = 0.0082 and P = 0.035, respectively). CONCLUSION: The BCVA improves after removal of an ERM following PPV for eyes with RRD, PVR, or PDR. Patient age and preoperative BCVA correlated with the visual improvement after the ERM removal.     

Interleukin (IL)-6, Interleukin (IL)-8 Levels and Cellular Composition of the Vitreous Humor in Proliferative Diabetic Retinopathy,Proliferative Vitreoretinopathy,and Traumatic Proliferative Vitreoretinopathy

Purpose: To investigate the interleukin (IL)-6 levels, IL-8 levels, and cellular composition of the vitreous humor in patients with proliferative diabetic retinopathy (PDR), proliferative vitreoretinopathy (PVR), and traumatic PVR. Methods: Vitreous samples from 14 patients with PDR, 10 patients with PVR, and 10 patients with traumatic PVR were analyzed. Fifteen cadaver eyes were used as controls. Cytokine levels were measured by ELISA. Results: Elevated IL-6 levels were detected in the vitreous of 12 (85.7%) of the PDR patients, eight (80%) of the PVR patients, and all (100%) of the traumatic PVR patients. None of the control IL-6 results were elevated. Vitreous IL-8 levels were elevated in 12 (85.7%) of the PDR patients, six (60%) of the PVR patients, all (100%) of the traumatic PVR patients, and one (6.7%) of the control eyes. Cytological examination of the vitreous specimens revealed a predominance of macrophages (50%) in the PDR samples and a predominance of retinal pigment epithelial (RPE) cells (60%) in the PVR samples. In contrast, neutrophils predominated (88%) in the traumatic PVR samples. Conclusion: The findings suggest that IL-6 and IL-8 may be involved in the pathogenesis of PDR, PVR, and traumatic PVR. High proportions of RPE cells and macrophages are associated with elevated IL-6 and IL-8 levels in the vitreous of PDR and PVR patients; however, the fact that these cells are not predominant in traumatic PVR suggests that different immune response mechanisms may be active in the pathogenesis of these disorders.     

Elevated vitreous nitric oxide levels in patients with proliferative diabetic retinopathy

PURPOSE: The aim of this study was to determine nitric oxide levels in the vitreous of patients with proliferative diabetic retinopathy. METHODS: Using the spectrophotometric method based on Griess reaction, we measured levels of nitrite, the stable product of nitric oxide, in the vitreous of 21 eyes of 21 patients who underwent vitrectomy for the treatment of proliferative diabetic retinopathy with tractional retinal detachment, prospectively. Three samples were excluded from the study because of blood contamination. The control group was made up of vitreous samples from 15 eyes of 15 normal cadavers and five eyes of five patients who were undergoing vitrectomy for macular hole surgery.RESULTS: Nitrite levels were 0. 524 +/- 0.27 microM and 0.383 +/- 0.17 microM in the vitreous of patients with proliferative diabetic retinopathy of diabetes type I and type II, respectively. In 15 cadaver eyes and five vitreous samples from patients who underwent macular hole surgery, nitrite levels were below the detection limit (less than 0.08 microM). There was no significant difference between nitrite levels in patients with type I and type II diabetes (P =.56), whereas there was a significant difference between diabetes groups and controls (P <. 00001).CONCLUSION: Vitreous nitric oxide levels are elevated in patients with proliferative diabetic retinopathy with tractional retinal detachment. Nitric oxide may play a role in the pathogenesis of proliferative diabetic retinopathy.     

Vascular adhesion molecules in vitreous from eyes with proliferative diabetic retinopathy.

PURPOSE: To investigate whether proliferative vitreoretinopathy (PDR) is associated with a selective increase in vitreous levels of soluble vascular cell adhesion molecules that mediate leukocyte extravasation and interaction with endothelium during processes of inflammation and neovascularization. METHODS: Vitreous from 55 patients undergoing vitrectomy for treatment of PDR complicated by vitreous hemorrhage and/or traction retinal detachment was assayed for the presence of the soluble vascular cell adhesion molecules sICAM-1, sVCAM-1, and sE-selectin using a standard enzyme-linked immunosorbent assays (ELISA). Vitreous from 12 cadaveric eyes matching age and sex of the patients were used as control samples. RESULTS: Vitreous levels of sICAM-1, sVCAM-1, and sE-selectin were significantly higher in eyes with PDR than in control cadaveric vitreous, and levels of all three molecules did not relate to the type or duration of diabetes mellitus. However, eyes with either traction retinal detachment alone or both traction retinal detachment and vitreous hemorrhage exhibited significantly higher levels of sICAM-1 and sE-selectin than eyes with vitreous hemorrhage alone. Vitreous levels of sVCAM-1 were similar in eyes with either vitreous hemorrhage or traction retinal detachment alone. CONCLUSIONS: The present observations suggest that molecular inflammatory mechanisms may contribute to processes of neovascularization and fibrosis observed in PDR, possibly not as the causative event, but as a result of endothelial, Müller, and retinal pigment epithelial cell activation. The results also indicate that retinal detachment amplifies the existing inflammation within the diabetic retina. Identification of any abnormalities in the production and control of specific adhesion molecules could have important implications in the design of new therapeutic regimens to treat and prevent this sight-threatening complication of diabetes mellitus.     

Upregulation of RAGE and its ligands in proliferative retinal disease

We sought to study the presence of the receptor for advanced glycation endproducts (RAGE) and its ligands, advanced glycation endproducts (AGEs), S100/calgranulins and amphoterin (high mobility group box 1 protein; HMGB1), in the vitreous cavity and epiretinal membranes (ERMs) of eyes of patients with proliferative diabetic retinopathy (PDR) and proliferative vitreoretinopathy (PVR). Undiluted vitreous specimens were collected from 30 eyes of 30 patients undergoing pars plana vitrectomy for repair of retinal detachment (RD) secondary to PDR (n = 15) or PVR (n = 15). The vitreous samples obtained from 10 eyes undergoing macular hole repair were used as controls. Epiretinal membranes were obtained from eight eyes with PDR and from 10 eyes with PVR. The levels of AGEs in the vitreous were measured using ELISA. The vitreous levels of soluble RAGE (sRAGE), S100/calgranulins and amphoterin were measured using Western blot analyses. The localization of RAGE and its ligands in ERMs was determined with immunohistochemistry. The vitreous levels of sRAGE were significantly increased in both PDR and PVR (p < or = 0.05) compared to control vitreous. In both PDR and PVR, the vitreous levels of AGEs (p < or = 0.01), S100/calgranulins (p < or = 0.05), and amphoterin (p < or = 0.01) were also elevated compared to control eyes. Expression of RAGE was detected in six of eight ERMs from eyes with PDR and eight of 10 ERMs from eyes with PVR. Many cells expressing RAGE also expressed vimentin, suggesting a glial cell origin. Ligands for RAGE were also detected in ERMs, with AGEs detected in five eyes with PDR and eight eyes with PVR. Similarly, S100 and amphoterin ERM expression was observed in six eyes with PDR; these ligands were also expressed in ERMs from eyes with PVR (8 and 7 cases, respectively). We conclude that RAGE and its ligands are increased in the vitreous cavity of eyes with PDR and PVR and are present in ERMs of eyes with these proliferative retinal disorders. These findings suggest a role for the proinflammatory RAGE axis in the pathogenesis of proliferative retinal diseases.     

Levels of human tissue kallikrein in the vitreous fluid of patients with severe proliferative diabetic retinopathy

The aim of this study was to determine the levels of human tissue kallikrein in the vitreous fluid of patients with severe proliferative diabetic retinopathy (PDR). Tissue kallikrein levels were measured using a specific ELISA (range: 0.4-25 ng/ml) in 7 vitreous fluids from eyes with severe PDR. Seven vitreous samples from eyes which underwent vitrectomy because of rhegmatogenous retinal detachment served as non-PDR controls. Enzymatic activity was also tested by an amidolytic assay using a chromogenic substrate. In the PDR patients, vitreous tissue kallikrein was <0.4 ng/ml (5 eyes) or very low (0.52 and 0.58 ng/ml). Vitreous tissue kallikrein was <0.4 ng/ml in all non-PDR controls. These results were confirmed by the amidolytic test. Results suggest that vitreous tissue kallikrein probably plays either a secondary or no role in the pathogenesis of PDR.     

增生性糖尿病视网膜病变患者玻璃体内血管内皮生长因子的表达

目的 探讨增生性糖尿病视网膜病变(PDR)患者玻璃体内血管内皮生长因子(VEGF)的表达及相关影响因素.方法 病例对照研究.对50例(50只眼)接受玻璃体切除治疗的PDR患者进行分析.术中获取玻璃体标本,并用双抗体夹心酶联免疫吸附试验ELISA法对术中获取的玻璃体标本进行VEGF含量的定量检测,并分析增生性糖尿病视网膜病变患者玻璃体内VEGF的表达情况.平均随访9个月(6～26个月).用成组t检验比较PDR组和正常对照组玻璃体VEGF含量差异,以及硅油填充组与非硅油填充组VEGF含量差异.用方差分析方法比较PDR进展组、稳定组和好转组玻璃体VEGF含量有无差异.用单因素方差分析方法分析玻璃体VEGF含量对PDR术后疗效的影响.结果 PDR组玻璃体VEGF含量平均(592.4801±587.4267)ng/L,正常对照组玻璃体VEGF含量平均(131.3022±26.9192)ng/L.PDR组玻璃体VEGF含量高于对照组(t=3.2315,P＜0.05).术后PDR进展有10只眼(20%),稳定10只眼(20%),好转30只眼(60%).PDR进展组玻璃体VEGF含量显著高于PDR稳定和好转组(q=-3.3187,-4.0843;P＜0.05).术前未接受视网膜光凝组玻璃体VEGF含量显著高于接受全视网膜光凝或局部视网膜光凝组(q=-4.2187,-3.9672;P＜0.05).结论玻璃体VEGF表达与PDR严重程度有一定关系.术后PDR稳定或好转者玻璃体VEGF水平呈相对低表达.(中华眼科杂志,2009,45:206-209)     

Quantitative analysis of interleukin-6 in vitreous from patients with proliferative vitreoretinal diseases

PURPOSE: To explore immunological mechanisms in the pathogenesis of proliferative vitreoretinal diseases, we measured the concentration of interleukin-6 in the vitreous body and serum from patients with proliferative diabetic retinopathy (PDR), proliferative vitreoretinopathy (PVR), and premacular fibrosis. To evaluate immunological etiology, interleukin-6 levels in each disease were compared with disease severity. METHODS: Clinical samples were obtained at the beginning of pars plana vitrectomy from 30 eyes of 26 patients with PDR, 12 eyes of 12 patients with PVR, and 10 eyes of 10 patients with premacular fibrosis. Interleukin-6 was quantitated with an enzyme-linked immunosorbent assay. RESULTS: The levels of detectable interleukin-6 in the vitreous specimens ranged from 22.8 to 666.4 pg/mL in the PDR patients and from 28.2 to 416.3 pg/mL in the PVR patients. No interleukin-6 was detected in the vitreous specimens from patients with premacular fibrosis or in any serum samples from patients. Interleukin-6 levels of vitreous specimens from PDR patients were higher than those from PVR patients (P <.02, Mann-Whitney U-test). There was no correlation between clinical severity and interleukin-6 levels in vitreous specimens from either PDR or PVR patients. CONCLUSION: Our results indicated that cell-mediated immunity is involved in the pathogenesis of proliferative vitreoretinal diseases.     

增殖性糖尿病视网膜病变玻璃体SDF-1和VEGF的含量分析

研究增殖性糖尿病视网膜病变患者玻璃体基质细胞衍生因子（Stromalcell—derivedfactor-1。SDF-1）和血管内皮生长因子（Vascularendothelialgrowthfactor，VEGF）的浓度，及其相互作用关系。方法：酶联免疫吸附法（Enzyme-linkedimmunosorbentassay，ELISA）检测玻璃体内SDF-1和VEGF的含量，每个标本重复3次。实验组为增殖性糖尿病视网膜病变（Proliferativediabeticretinopathy，PDR）的住院患者30例，对照组为同期行玻璃体切除术的特发性黄斑裂孔患者12例。结果：PDR患者玻璃体VEGF的平均浓度为（2865．87±387．85）pg／ml，明显高于特发性黄斑裂孔组[（142．42±21．03）pg／ml，P〈0．0001]。增殖性糖尿病视网膜病变患者玻璃体SDF-1的含量平均为（298．40±24．57）pg／ml，对照组为（86．9l±15．89）pg／ml，两组的差异具有统计学意义（P〈0．0001）。在30例PDR患者玻璃体内VEGF和SDF-1的含量表现为正相关（Pearson相关系数r=0．62，P〈0．001）。结论：增殖性糖尿病患者玻璃体SDF-1和VEGF的含量均高于非糖尿病患者，提示SDF-1和VEGF共同参与了增殖性糖尿病视网膜病变患者病理性新生血管的形成过程。     

Comparative study of clinical factors that predispose patients to proliferative vitreoretinopathy in aphakia

To clarify the risk factors of proliferative vitreoretinopathy (PVR) in aphakia, the clinical features of 25 aphakic eyes with PVR were statistically analyzed and compared with a control group of 157 aphakic eyes with non-PVR rhegmatogenous retinal detachment. The statistically significant (P less than 0.05) factors that predisposed patients to PVR in aphakia were as follows: a history of vitreous loss on cataract surgery, retinal detachment developing within 3 months after cataract extraction, duration of retinal detachment longer than 3 months, break larger than three disc diameters, and choroidal detachment. Vitreous loss is believed to play the most important role in the development of PVR in aphakia.     

Incidence of rhegmatogenous retinal detachment after vitrectomy in eyes of diabetic patients

PURPOSE: To assess the incidence of rhegmatogenous retinal detachment (RRD) after pars plana vitrectomy (PPV) among diabetic patients with complications of proliferative diabetic retinopathy. METHODS: Ninety-three eyes of diabetic patients-who underwent PPV with or without intraocular gas tamponade for complications of proliferative diabetic retinopathy-were reviewed retrospectively. Indication for vitrectomy was vitreous hemorrhage in 80 patients (86.1%), tractional retinal detachment in 3 (3.2%), and vitreous hemorrhage associated with tractional retinal detachment in 10 (10.7%). RESULTS: Four (4.3%) of 93 eyes developed an RRD after vitrectomy. The primary reason for vitrectomy was recurrent or nonresolving vitreous hemorrhage. The retina was attached with one additional surgical procedure in two of these eyes; the other two had to undergo a third operation before attachment was achieved. CONCLUSION: RRD occurs in a small percentage of patients after PPV with or without gas tamponade for vitreous hemorrhage or tractional retinal detachment caused by proliferative diabetic retinopathy. Thorough postoperative follow-up is important to make early diagnosis and intervention possible.