The influence of intelligence and cognitive abilities on the reading ability of Japanese students with developmental disorders.

OBJECTIVE: We examined the differences in reading skills between Japanese students with developmental dyslexia (DD) having developmental disorders who had borderline IQ (BIQ) and those who had normal IQ (NIQ), and the influence of cognitive factors through subscale scores of the Wechsler Intelligence Scale for Children - Fourth Edition on the reading skills of all students with DD having developmental disorders. METHODS: One-way analysis of variance revealed differences in reading scores among the four groups (DD with NIQ, DD with BIQ, as well as non-DD with NIQ and non-DD with BIQ as control groups). To examine the influence of cognitive factors, we used multiple regression analysis for all participants, and then for participants with DD. RESULTS: Regarding hiragana nonword fluency reading, no difference was observed between the two DD groups, and cognitive factors did not affect the performance of all participants with DD. Concerning hiragana word fluency reading, DD with NIQ group performed better than DD group with BIQ, and working memory index affected reading skills of participants with DD. Regarding kanji accuracy reading, DD with NIQ group performed better than DD with BIQ group, and processing speed index affected performance of participants with DD. CONCLUSIONS: The results of hiragana reading suggest that the two DD groups shared similar weak sub-lexical route processing, while the acquisition of lexical route processing was hindered by lower IQ and weak phonological working memory in transparent phonographic hiragana reading. For kanji reading, lower IQ and weak visuomotor processing ability hampered the learning of visually complex logographic kanji characters.

Differential association of elevated inflammatory cytokines with postoperative fibrous proliferation and neovascularization after unsuccessful vitrectomy in eyes with proliferative diabetic retinopathy.

BACKGROUND: Pars plana vitrectomy is the only treatment for advanced proliferative diabetic retinopathy (PDR). However, vitrectomy is not always successful despite current progress in vitreoretinal surgical techniques. The aim of our study was to investigate whether the vitreal concentrations of MCP-1, IL-6, IL-8, and VEGF are elevated after unsuccessful vitrectomy in patients with PDR and to investigate whether the altered levels of these cytokines are associated with the cause for the reoperation. PATIENTS AND METHODS: Vitreous samples were collected from 263 eyes of 233 patients: PDR (n=129 eyes), proliferative vitreoretinopathy (PVR; n=24 eyes) and nondiabetic controls (n=110 eyes) prior to vitrectomy. Vitreous samples were also collected from 14 eyes of 14 patients with PDR before vitrectomy and from the same 14 eyes before a second vitrectomy for reoperation. The levels of MCP-1, IL-6, IL-8, and VEGF were measured by flow cytometry using a cytometric bead array (CBA) assay. RESULTS: The mean concentrations of vitreal MCP-1, IL-6, IL-8, and VEGF were significantly higher in patients with PDR and PVR (P<0.01). There were significantly high correlations among the concentrations of MCP-1, IL-6, and IL-8, whereas the correlation of VEGF with the other 3 cytokines was lower. Among the 14 patients who required reoperation, the mean vitreal concentrations of MCP-1, IL-6, and IL-8 were higher than that at the time of the initial vitrectomy (P<0.01). At the time of the reoperation vitrectomy, the mean vitreous level of MCP-1, IL-6, and IL-8 in eyes with fibrous proliferation was higher than in those without fibrous proliferation (P<0.05). In contrast, VEGF in eyes with neovascular glaucoma (NVG) or anterior hyaloidal fibrovascular proliferation (AHFVP) was higher than in the eyes without NVG and AHFVP (P<0.05). CONCLUSION: The elevated levels of MCP-1, IL-6, and IL-8 may be the cause of the postoperative fibrous proliferation. In contrast, VEGF may be the cause of the neovascularization after unsuccessful vitrectomy in the eyes of PDR patients.

Increased vitreous concentrations of MCP-1 and IL-6 after vitrectomy in patients with proliferative diabetic retinopathy: possible association with postoperative macular oedema.

PURPOSE: To determine whether vitreal concentrations of MCP-1, IL-6 and IL-8 are altered after vitrectomy in patients with proliferative diabetic retinopathy (PDR) and to investigate whether the altered levels of these cytokines are associated with postoperative macular oedema. METHODS: Vitreous samples were collected from 36 eyes of 33 patients with PDR before pars plana vitrectomy without intraocular lens (IOL) implantation, and also from the same 36 eyes during IOL implantation surgery approximately 7 months after the initial vitrectomy. Levels of MCP-1, IL-6, IL-8 and vascular endothelial growth factor were measured by flow cytometry using cytometric bead array (CBA) technology. RESULTS: The mean vitreous levels of MCP-1, IL-6 and IL-8 in the samples collected before vitrectomy were significantly higher in patients with PDR than in control patients (p<0.0001). The levels of MCP-1 and IL-6 in the samples collected at the time of IOL implantation were significantly higher than those collected before vitrectomy (p<0.05). In contrast, the level of IL-8 was significantly lower after vitrectomy (p<0.05). The levels of IL-6 and IL-8, but not MCP-1, in the vitreous from eyes with PDR were inversely correlated with the interval between the initial vitrectomy and the time of implantation surgery. Among the vitrectomised patients, the mean vitreous level of MCP-1 in eyes with diabetic macular oedema (DME) was significantly higher than in those without DME (p=0.028). CONCLUSIONS: The elevated levels of MCP-1 and IL-6 may indicate prolonged inflammation even after successful vitrectomy, which can cause postoperative DME.

Microarray analysis of gene expression in fibrovascular membranes excised from patients with proliferative diabetic retinopathy.

PURPOSE: We determined the profile of genes expressed in fibrovascular membranes (FVMs). METHODS: Six FVMs were surgically removed from patients with proliferative diabetic retinopathy (PDR) during pars plana vitrectomy with membrane peeling. The FVMs were classified into three active FVMs or three inactive FVMs according to the presence or absence of neovascularization (NV) in the membranes. Total RNA was isolated from the six FVMs and also from three normal human retinas. The DNA microarray analysis was performed to compare the genes expressed in the FVMs to those in normal human retinas, and also between active and inactive FVMs. Ingenuity pathway analysis (IPA) was used to determine the key biological networks related to the genes that were significantly altered. Quantitative RT-PCR and immunohistochemistry were performed to validate the microarray analyses. RESULTS: There were 87 genes expressed at significantly higher levels in FVMs than in normal human retinas. Functional classification of these genes showed that the most clustered genes were those related to extracellular matrix formation. The top biological network generated by the IPA was cellular assembly and organization involving nodes of genes related to extracellular matrix formation. These networks included the collagen family and matricellular proteins, THBS2, POSTN, and TNC. There were 91 genes significantly upregulated in active FVMs, and the most clustered functional category was angiogenesis. In contrast, 89 genes were significantly upregulated in inactive FVMs, and the most clustered functional category was metabolism. The IPA revealed that the top biological network related to the genes that were significantly altered in this comparison was cell-to-cell signaling, and interactions involving the PDGF and TGFß families. The results of quantitative RT-PCR analyses and immunohistochemistry for several selected molecules were in good agreement with the microarray data. CONCLUSIONS: Our data indicate that extracellular matrix-related molecules such as POSTN, TNC, TGFß, and angiogenic factors have important roles in promoting the development of FVMs associated with PDR.

Overexpression of CD163 in vitreous and fibrovascular membranes of patients with proliferative diabetic retinopathy: possible involvement of periostin.

AIM: To determine whether CD163, a specific marker for M2 macrophages, is involved in the formation of preretinal fibrovascular membranes (FVMs) present in eyes with proliferative diabetic retinopathy (PDR). METHODS: We measured the levels of soluble (s)CD163, periostin and vascular endothelial growth factor by sandwich ELISA in vitreous samples from 74 eyes of 62 patients with PDR, 20 eyes of 18 patients with proliferative vitreoretinopathy, and 56 eyes of 54 patients with non-diabetic ocular diseases (control group). Immunohistochemical analyses were performed to determine the expressions of CD68, CD163 and periostin in the surgically resected FVMs and idiopathic epiretinal membranes (ERMs). RESULTS: The concentrations of sCD163 and periostin in the vitreous were significantly higher in patients with PDR than in non-diabetic controls (p<0.0001). There was a strong correlation between the vitreous concentrations of sCD163 and periostin. The mean vitreous level of sCD163 was significantly higher in eyes with FVMs than in those without FVMs (epicentre only). The number and percentage of CD163+ macrophages were significantly higher in the FVMs than in the idiopathic ERMs. Immunohistochemical analysis showed co-localisation of CD163 and periostin in FVM cells. CONCLUSIONS: These findings indicate that the overexpression of CD163 by macrophages may be involved in the development of FVMs partly through periostin production.

Increased expression of M-CSF and IL-13 in vitreous of patients with proliferative diabetic retinopathy: implications for M2 macrophage-involving fibrovascular membrane formation.

PURPOSE: We recently demonstrated that M2 macrophages were involved in the development of fibrovascular membranes (FVM) associated with proliferative diabetic retinopathy (PDR) possibly through the induction of periostin. The purpose of this study was to determine whether macrophage colony-stimulating factor (M-CSF) and interleukin (IL)-13, inducers of the M2 polarisation of macrophages from monocytes, are elevated in the vitreous of patients with PDR, and whether M2-polarised macrophages induce periostin production. METHODS: We measured the levels of M-CSF, granulocyte-macrophage colony-stimulating factor (GM-CSF), IL-4, IL-13, soluble (s)CD163, periostin and vascular endothelial growth factor by sandwich ELISA in vitreous samples collected from 61 eyes of 47 patients with PDR, and 39 eyes of 36 patients with non-diabetic ocular diseases (control group). Human monocytes were polarised in vitro with GM-CSF, interferon-γ, and lipopolysaccharide for M1 macrophages, and M-CSF, IL-4, and IL-13 for M2 macrophages. Quantitative real-time PCR was used to determine the mRNA level of periostin. RESULTS: The concentrations of M-CSF and IL-13 in the vitreous were significantly higher in patients with PDR than in non-diabetic controls (p<0.0001). There was a strong positive correlation between the vitreous concentrations of M-CSF and sCD163 and periostin. The mean vitreous level of IL-13 was significantly higher in eyes with FVMs than in those without FVMs (epicentre only). In vitro studies showed that M2-polarlised macrophages significantly increased the expression of the mRNA of periostin. CONCLUSIONS: These findings indicate that the M2 polarisation of macrophages is induced by M-CSF and IL-13 in diabetic retinas. The presence of M-CSF and IL-13 would then promote FVM formation by periostin production.

Periostin promotes the generation of fibrous membranes in proliferative vitreoretinopathy.

Proliferative vitreoretinopathy (PVR) is a severe, vision-threatening disorder characterized by the fibrous membrane formation that leads to tractional retinal detachment. There has been no effective therapeutic approach other than vitreoretinal surgery. In this study, DNA microarray analysis of the fibrous membranes revealed significant up-regulation of periostin. We also found increased periostin expression in the vitreous and retinal pigment epithelial (RPE) cells from fibrous membranes of PVR patients. In vitro, periostin increased proliferation, adhesion, migration, and collagen production in RPE cells through integrin αV-mediated FAK and AKT phosphorylation. Periostin blockade suppressed migration and adhesion induced by TGFß2 and PVR vitreous. In vivo, periostin inhibition had the inhibitory effect on progression of experimental PVR in rabbit eyes without affecting the viability of retinal cells. These results identified periostin as a pivotal molecule for fibrous membrane formation as well as a promising therapeutic target for PVR.

Altered vascular microenvironment by bevacizumab in diabetic fibrovascular membrane.

PURPOSE: The purpose of this study was to evaluate the impact of intravitreal bevacizumab (IVB) on three cellular components (vascular endothelial cells, pericytes, and myofibroblasts) of the vascular microenvironment in fibrovascular membranes (FVMs) of patients with proliferative diabetic retinopathy. METHODS: Immunohistological studies with antibodies of CD34, αSMA, and transforming growth factor-ß were performed on 20 surgical specimens obtained during a pars plana vitrectomy from 8 IVB-treated eyes, whereas 12 remained untreated. Four different indexes of vascular phenotype (vascular area, vascular major axis, CD34 endothelial area, and blood vessel density) and αSMA expression in vascular and stromal components were quantitatively analyzed. RESULTS: The intraluminal area of blood vessels, CD34 endothelial area, and the blood vessel density in IVB-treated FVMs were significantly less than in untreated FVMs. The number of CD34 blood vessels in IVB-treated FVMs was similar to that in untreated FVMs. Intravitreal bevacizumab could not affect vascular and stromal αSMA area significantly. However, the ratio of vascular αSMA area/CD34 area was significantly higher in IVB-treated FVMs than in untreated FVMs. Transforming growth factor-ß expression could be observed in the IVB-treated FVM. CONCLUSION: Intravitreal bevacizumab might primarily affect blood vessels, and the effects on pericytes and myofibroblasts might be secondary. Intravitreal bevacizumab treatment regulates vascular microenvironment by the contraction of blood vessels, the increasing pericyte ratio, and transforming growth factor-ß expression in FVMs of patients with proliferative diabetic retinopathy.

Comparison of gene expression profile of epiretinal membranes obtained from eyes with proliferative vitreoretinopathy to that of secondary epiretinal membranes.

BACKGROUND: Proliferative vitreoretinopathy (PVR) is a destructive complication of retinal detachment and vitreoretinal surgery which can lead to severe vision reduction by tractional retinal detachments. The purpose of this study was to determine the gene expression profile of epiretinal membranes (ERMs) associated with a PVR (PVR-ERM) and to compare it to the expression profile of less-aggressive secondary ERMs. METHODOLOGY/PRINCIPAL FINDINGS: A PCR-amplified complementary DNA (cDNA) library was constructed using the RNAs isolated from ERMs obtained during vitrectomy. The sequence from the 5' end was obtained for randomly selected clones and used to generate expressed sequence tags (ESTs). We obtained 1116 nonredundant clusters representing individual genes expressed in PVR-ERMs, and 799 clusters representing the genes expressed in secondary ERMs. The transcriptome of the PVR-ERMs was subdivided by functional subsets of genes related to metabolism, cell adhesion, cytoskeleton, signaling, and other functions, by FatiGo analysis. The genes highly expressed in PVR-ERMs were compared to those expressed in the secondary ERMs, and these were subdivided by cell adhesion, proliferation, and other functions. Querying 10 cell adhesion-related genes against the STRING database yielded 70 possible physical relationships to other genes/proteins, which included an additional 60 genes that were not detected in the PVR-ERM library. Of these, soluble CD44 and soluble vascular cellular adhesion molecule-1 were significantly increased in the vitreous of patients with PVR. CONCLUSIONS/SIGNIFICANCE: Our results support an earlier hypothesis that a PVR-ERM, even from genomic points of view, is an aberrant form of wound healing response. Genes preferentially expressed in PVR-ERMs may play an important role in the progression of PVR and could be served as therapeutic targets.

Antiangiogenic shift in vitreous after vitrectomy in patients with proliferative diabetic retinopathy.

PURPOSE: We determined whether the concentrations of VEGF, erythropoietin, and endostatin in the vitreous are altered after vitrectomy in patient with proliferative diabetic retinopathy (PDR). METHODS: We measured the levels of VEGF, erythropoietin, and endostatin by sandwich ELISA in vitreous samples collected from 38 eyes of 33 patients with PDR before pars plana vitrectomy (without IOL implantation) and the same 38 eyes during IOL implantation 3.1 to 25.7 (mean 6.7) months after the initial vitrectomy. RESULTS: The mean vitreous levels of VEGF (964.5 pg/mL) and erythropoietin (1359.5 pg/mL) in the samples collected before vitrectomy were significantly higher in patients with PDR than in the control patients (0.68 and 70.7 pg/mL, respectively; P < 0.01). The levels of VEGF (292.5 pg/mL) and erythropoietin (557.9 pg/mL) in the samples from eyes with PDR collected at the time of IOL implantation were significantly lower than those collected before vitrectomy (P < 0.01). In contrast, the changes in the level of endostatin were not significant after vitrectomy. The VEGF and erythropoietin levels in the vitreous fluid from patients with PDR were correlated inversely with the interval between the initial vitrectomy and the time of the IOL implantation. CONCLUSIONS: The significant decrease in the intravitreal concentration of VEGF and erythropoietin, and an absence of a significant change in the endostatin indicated a shift in the antiangiogenic balance in the vitreous of patients with PDR after successful vitrectomy.

Intravitreal anti-VEGF therapy blocks inflammatory cell infiltration and re-entry into the circulation in retinal angiogenesis.

PURPOSE: Anti-VEGF-A antibody (Ab) (e.g., bevacizumab, ranibizumab) is widely used as a treatment against retinal angiogenesis and edema. The purpose of this study was to evaluate whether intravitreal anti-VEGF Ab injection modulates inflammatory cells in retinal angiogenesis. METHODS: To investigate whether intravitreal bevacizumab injections affect the number of inflammatory cells in proliferative diabetic retinopathy (PDR) membranes in patients, immunohistochemical staining with CD45 Ab (pan-leukocyte marker) was performed using the surgically obtained membranes in pars plana vitrectomy with or without pretreatment with bevacizumab. To check whether anti-VEGF-A Ab affects leukocytes going in and out of blood vessels during retinal angiogenesis, the authors performed their novel leukocyte transmigration assay and CD45 immunostaining in a mouse model of oxygen-induced retinopathy (OIR). RESULTS: The authors' new imaging approach revealed that intravitreal injection of anti-VEGF-A Ab blocks leukocyte infiltration as well as angiogenesis. The Ab injection inhibited leukocyte transmigration before affecting the angiogenenic area. CD45 staining showed no significant difference in the leukocyte number in the angiogenic retina or the human PDR membranes between the anti-VEGF-A Ab injected group and the control group. Furthermore, VEGF-A inhibition also affected leukocytes going out from the retina. CONCLUSIONS: Intravitreal injection of anti-VEGF-A Ab could inhibit leukocyte trafficking in the retina, suggesting that anti-VEGF-A therapy could serve as a treatment in retinal inflammation.

Increased expression of periostin in vitreous and fibrovascular membranes obtained from patients with proliferative diabetic retinopathy.

PURPOSE: Preretinal fibrovascular membranes (FVMs) form as a sequela to proliferative diabetic retinopathy (PDR), and their presence can lead to a severe decrease of vision. The purpose of this study was to determine whether periostin, a matricellular protein that plays a role in cell adhesion and migration, is associated with the formation of FVMs. METHODS: One hundred six vitreous samples and 15 FVMs were obtained during vitrectomy on patients with PDR. Semiquantitative RT-PCR was performed to determine the periostin level of the mRNA. Immunohistochemical analyses were performed to determine the sites of periostin expression in the FVMs. ELISA was used to measure the concentrations of periostin, bFGF, and VEGF in the vitreous. RESULTS: The periostin level of the mRNA was high in 10 of 10 FVMs tested but was barely detectable in the control retinas. Sequencing of the periostin PCR products revealed three splice variants of the FVMs. Immunohistochemical analysis showed colocalization of periostin and α-SMA in FVM cells. The concentration of periostin in the vitreous was significantly higher in patients with PDR than in the 31 eyes of patients with a macular hole or an epiretinal membrane (P < 0.001). Among the PDR patients, the mean vitreous level of periostin in eyes with FVMs was significantly higher than in those without FVMs (epicenter only; P < 0.001). The correlation between the vitreous concentrations of periostin and of bFGF and VEGF was not significant. CONCLUSIONS: These findings indicate that periostin may be involved in the development of FVMs.

Reduced concentrations of angiogenesis-related factors in vitreous after vitrectomy in patients with proliferative diabetic retinopathy.

BACKGROUND: The purpose of this study was to determine whether vitrectomy alters the angiogenic profile in the vitreous of eyes with proliferative diabetic retinopathy (PDR). METHODS: We measured the levels of angiopoietin-2, HGF, bFGF, PDGF, TIMP-1, and TIMP-2 by sandwich enzyme linked immunosorbent assay (ELISA) in vitreous samples from 27 eyes of 26 patients with PDR before pars plana vitrectomy (without IOL implantation) and in 12 fluid samples from 12 patients with PDR obtained during an IOL implantation 3.5 to 9 (mean 4.9) months after an earlier vitrectomy. The levels of these factors were also measured in 12 vitreous samples obtained from 12 eyes that had undergone epiretinal membrane (ERM) or macular hole (MH) surgeries. RESULTS: The mean vitreous levels of both angiopietin-2 (103 pg/ml) and HGF (1091 pg/ml) in the sample from eyes with PDR collected at the time of the IOL implantation were significantly lower than in those collected before the vitrectomy (P < 0.01). On the other hand, the changes in the levels of TIMP-1 and TIMP-2 were both not significant after vitrectomy. CONCLUSION: The significant decrease of angiopietin-2 and HGF in the vitreous fluid after vitrectomy suggests that vitrectomy shifts the eye towards an anti-angiogenic environment.

Gene expression profile of fibrovascular membranes from patients with proliferative diabetic retinopathy.

BACKGROUND/AIMS: The purpose of this study was to generate a profile of genes expressed in preretinal fibrovascular membranes (FVMs) from patients with proliferative diabetic retinopathy. METHODS: A PCR-amplified complementary DNA (cDNA) library was constructed using the RNAs isolated from FVMs obtained during vitrectomy. The sequence from the 5' end was obtained for randomly selected clones and used to generate expressed sequence tags (ESTs). Functional annotation was retrieved from Ensemble database and analysed by FatiGO. The web-based VisANT software was used to identify the molecular networks within the FVMs. RESULTS: A total of 2816 ESTs were assembled in 625 non-redundant clusters. Among these, 515 matched the human cDNA database. The 515 clusters were subdivided by functional subsets of genes related to ribosomal activity, oxidative phosphorylation, focal adhesion, cell adhesion and other functions. Querying against the VisANT database yielded 3175 possible physical relationships to other genes/proteins, which included an additional 2480 genes that were not detected in the FVM library. CONCLUSIONS: The cDNA library constructed from human FVMs will be a valuable source of information. It should facilitate a wide range of studies that can establish the molecular mechanisms underlying the development of FVMs.

TEM7 (PLXDC1) in neovascular endothelial cells of fibrovascular membranes from patients with proliferative diabetic retinopathy.

PURPOSE: Proliferative diabetic retinopathy (PDR) results from the formation of fibrovascular membranes (FVMs) in the posterior fundus that can lead to a severe decrease of vision. Tumor endothelial marker 7 (TEM7) is a protein that is highly expressed in the endothelial cells of tumors, but whether it plays a role in FVMs is unknown. The purpose of this study was to determine whether TEM7 is associated with the formation of FVMs. METHODS: FVMs were obtained during vitrectomy from patients with PDR. RT-PCR was performed to determine the level of expression of the mRNA of TEM7. The splice variants of TEM7 were identified by direct sequencing. Immunohistochemical analyses and in situ hybridization was performed to determine the sites of TEM7 in the FVMs. RESULTS: The level of the mRNA of TEM7 was high in 10 of 10 FVMs but was barely detectable in the five idiopathic epiretinal membranes. Direct sequencing of subcloned TEM7 PCR products revealed several splice variants (intracellular, secreted, and membrane-bound forms of TEM7) in the FVMs. Immunohistochemical analysis showed a colocalization of TEM7 and CD34, an endothelial cell marker, in most of the neovascular endothelial cells in the FVMs. Immunoelectron microscopy revealed that membrane-bound TEM7 was expressed on the luminal surfaces of the vascular endothelial cells of FVMs. CONCLUSIONS: This study indicates that TEM7 may play a significant role in the proliferation and maintenance of neovascular endothelial cells in the FVMs. If correct, TEM7 may be a molecular target for new diagnostic and therapeutic strategies for PDR.

Scleral resection technique combined with vitrectomy for a macular hole retinal detachment in highly myopic eyes.

PURPOSE: To evaluate scleral resection technique combined with vitrectomy for macular hole retinal detachment of highly myopic eyes. MATERIALS AND METHODS: Seventeencases (17 eyes) of macular hole retinal detachment in highly myopic eyes, in which the patient underwent vitrectomy combined with scleral resection technique formacular hole retinal detachment between January 1996 and December 2003 at Fukuoka University Chikushi Hospital, were studied. Following pars plana vitrectomy, as much as possible of the residual vitreous and/or epiretinal membrane was removed. A scleral resection was performed in 2 quadrants of the equatorial region of the temporal sclera. Finally, a fluid-air exchange with SF(6) gas injection was performed to achieve retinal attachment. Pre- and postoperative axial length of the eyeballs were measured by B-scan ultrasonography. RESULTS: All cases had the retina reattached at the initial surgery, and visual acuities were stabilized or improved after the surgery. The posterior staphyloma became obscure in 13 out of 17 eyes (76.8%). The macular hole closed in 14 of 17 eyes (82.4%) ophthalmoscopically. There were no cases in which retinal redetachment occurred during follow-up periods of more than 6 months. CONCLUSION: In cases of macular hole retinal detachment of a highly myopic eye, scleral resection technique combined with vitrectomy changed the shape of the eyeballs and allowed successful retinal reattachment at the initial surgery.

Long-term results of pars plana vitrectomy combined with filtering surgery for neovascular glaucoma.

BACKGROUND AND OBJECTIVE: To analyze the effectiveness of vitrectomy combined with filtering surgery for neovascular glaucoma. PATIENTS AND METHODS: Twenty-one eyes with neovascular glaucoma underwent pars plana vitrectomy combined with filtering surgery between January 1995 and December 2003. Thirteen eyes (10 cases) had neovascular glaucoma secondary to proliferative diabetic retinopathy and 8 eyes (8 cases) had neovascular glaucoma secondary to central retinal vein occlusion. The initial intraocular pressures ranged from 21 to 70 mm Hg with full medication. All cases were observed for more than 12 months after the last surgery and the ophthalmic records were retrospectively reviewed. RESULTS: During the follow-up period, 19 eyes (90.5%) had intraocular pressures of less than 21 mm Hg with or without antiglaucoma eye drops, whereas 18 eyes (85.7%) had a stable or improved visual acuity. CONCLUSION: Vitrectomy combined with filtering surgery is considered to be an effective treatment for neovascular glaucoma to maintain the visual function for a long period.