Expression of vitreous cytokines in proliferative vitreoretinopathy: a prospective study. (1/877)

PURPOSE: Proliferative vitreoretinopathy (PVR) is a major cause of failure of retinal detachment surgery. It is believed to be a wound-healing process in the retina. Many of the cellular functions are influenced by cytokines and growth factors such as interleukins (ILs). The present study was conducted to investigate the presence of transforming growth factor-beta 2 (TGF-beta2), basic fibroblast growth factor (bFGF), IL-1beta, IL-6, and protein in the vitreous of patients with retinal detachment and to determine the value of these mediators in predicting the future development of PVR. METHODS: A prospective study was conducted in 140 consecutive patients with rhegmatogenous retinal detachment in whom vitrectomy was considered necessary. Vitreous samples were analyzed for the presence of TGF-beta2, bFGF, IL-1beta, IL-6, and protein. Patients were then followed up for 3 months for the development of postoperative PVR. RESULTS: The mean levels of TGF-beta2, bFGF, IL-1beta, and protein in the vitreous were significantly higher (P < 0.05) in patients with preoperative PVR compared with those without. The mean levels of TGF-beta2, bFGF, IL-6, and protein in the vitreous were significantly higher (P < 0.05) in patients who had postoperative PVR compared with those who did not. Multivariate logistic regression analysis showed IL-6 and protein to be significant (P < 0.05), independent, predictive risk factors for the development of PVR. CONCLUSIONS: The various cytokines may play a role in the pathobiology of PVR. High vitreous levels of IL-6 and protein were identified as significant risk factors for PVR. A model was developed to predict the probability of development of postoperative PVR in these patients, and it may be used to indicate intravitreal pharmacologic treatment for those at risk.  (+info)

Radioactive phosphorus uptake testing of choroidal lesions. A report of two false-negative tests. (2/877)

Two false-negative results from 32P testing for histologically verified malignant melanomas of the choroid are reported. In the first case, a haemorrhagic choroidal detachment caused an increase in probe; additionally, the tumour was necrotic. Both factors are likely to have contributed to the false-negative result. A satisfactory explanation for the false-negative result in the second case was not determined, although it may have accurately reflected a period of minimal tumour activity, inasmuch as repeat 32P testing was strongly positive eight months later, when unequivocal evidence of tumour growth was present. An alternative explanation is that the orally administered 32P was incompletely absorbed. Since 32P testing is frequently accompanied by significant manipulation both in the manoeuvre associated with tumour localization and in that associated with the actual radioactive counting, it would seem desirable to perform indicated enucleation immediately after completion of the 32P testing. While the properly performed 32P test remains a valuable diagnostic test for helping to establish the presence or absence of malignancies of the posterior globe, it is important to guard against the tendency to underestimate careful clinical evaluation.  (+info)

High incidence of glucose intolerance in Vogt-Koyanagi-Harada disease. (3/877)

AIMS: To evaluate glucose tolerance of patients with Vogt-Koyanagi-Harada (VKH) disease before systemic corticosteroid therapy, and to assess changes brought on by treatment. METHODS: 20 VKH patients with acute bilateral panuveitis were studied. 20 healthy adults and 11 Behcet's disease patients with active uveoretinitis served as controls. A 75 g oral glucose tolerance test (OGTT) was given in the acute stage of ocular inflammation before systemic corticosteroid therapy. The OGTT was repeated in the convalescent stage of VKH disease in the patients with glucose intolerance before treatment. Insulin response was examined at the same time as the OGTT when possible. RESULTS: 55% of VKH patients (11/20) showed glucose intolerance but no apparent insulin secretion deficiency was detected. Four of seven patients in the convalescent stage showed improvement of glucose tolerance. None of the normal controls or disease controls showed glucose intolerance. CONCLUSION: A high incidence of glucose intolerance was found in the acute stage of VKH disease. However, glucose intolerance improved in most cases after systemic corticosteroid therapy. It is possible that glucose intolerance seen in VKH patients may be related to the autoimmune inflammatory process of this disease.  (+info)

Pathogenesis and classification of massive periretinal proliferation. (4/877)

Massive periretinal proliferation (MPP), a serious complication of retinal detachment, is caused by proliferation and fibrous metaplasia of cells mostly deriving from retinal pigment epithelium and retinal glial cells. Contracting fibrous membranes in the vitreous, and on and also under the retina, cause the intraocular changes of MPP. Early signs such as increased 'tobacco dust', pigmented and unpigmented clumps in the vitreous, and subtle preretinal and even retroretinal membranes are usually overlooked. The late signs such as starfolds, irregular retinal folds, circumferential folds, and funnel-shaped detachments are well known. The pathogenesis of the clinically visible signs is described, and a 4-stage classification of the disease is given.  (+info)

Three widespread founder mutations contribute to high incidence of X-linked juvenile retinoschisis in Finland. (5/877)

X-linked juvenile retinoschisis (RS) is a recessively inherited disorder causing progressive vitreoretinal degeneration in males. The gene defective in retinoschisis, XLRS1, has recently been identified and characterised. This gene consists of six exons encoding a protein with a putative role in cell-cell adhesion and phospholipid binding. Juvenile retinoschisis has been actively studied in Finland over the past 30 years, with over 300 diagnosed RS patients. Based on genealogical studies, approximately 70% of the Finnish RS patients originate from Western Finland and 20% from Northern Finland. In this study, one third of the known Finnish RS patients were screened for mutations of the XLRS1 gene. Haplotype analysis, using nine microsatellite markers spanning 1 cM in Xp22.2, suggested the segregation of eight different mutations in these families. To identify mutations, the six exons were amplified by PCR and analysed by single strand conformation analysis, followed by direct sequencing of the PCR products. We identified seven distinct missense mutations, all in exons 4 and 6. The mutations in exon 4, 214G > A and 221G > T, are accountable for RS in Western Finland. A third mutation in exon 4, 325G > C, gives rise to RS in Northern Finland. These three founder mutations are the predominant cause of RS in Finland and their existence explains the high incidence of the disease. The identification of mutations common in genetically isolated populations, such as Finland, allows the diagnosis of patients with an atypical RS phenotype and enables nationwide carrier testing and improved genetic counselling.  (+info)

Effect of diode laser trans-scleral cyclophotocoagulation in the management of glaucoma after intravitreal silicone oil injection for complicated retinal detachments. (6/877)

AIMS: To evaluate the effect of trans scleral cyclophotocoagulation (TSCPC) on intraocular pressure (IOP) in the eyes retaining intravitreal silicone oil with medically uncontrolled secondary glaucoma following intravitreal silicone oil injection. METHODS: Medical records of 11 eyes of 11 patients who underwent TSCPC for medically uncontrolled glaucoma without pupillary block following intravitreal silicone oil injection for complicated retinal detachment were reviewed retrospectively. In all cases, intravitreal silicone oil was not removed for fear of retinal redetachment. Diode laser contact TSCPC was performed at a power of 1.5-2.5 W, for a duration of 2 seconds, and with 20-27 applications. IOP, number of glaucoma medications, and success rate were evaluated. RESULTS: After a mean follow up period of 52.5 (SD 8.2) (range 42-68) weeks, the mean pretreatment level of IOP, 43.0 (14.4) (26-67) mmHg, had fallen to 14.5 (4.3) (7-20) mm Hg (p=0.003). The number of glaucoma medications was reduced from 2.6 (0.8) to 0.6 (1.0) (p= 0.005). Qualified success was achieved in nine eyes (81.8%) and complete success in six (54.5%). After TSCPC, patients' retinal status had not changed. CONCLUSION: Patients with medically uncontrolled glaucoma secondary to intravitreal silicone oil injection can be treated with TSCPC in spite of the retained intravitreal silicone oil.  (+info)

Effects of the neurotrophin brain-derived neurotrophic factor in an experimental model of retinal detachment. (7/877)

PURPOSE: To examine the effects of brain-derived neurotrophic factor (BDNF) in an animal model of retinal detachment. METHODS: Cat retinas were detached from the retinal pigment epithelium for either 7 or 28 days. Animals received either an intravitreal injection of BDNF (100 ILg) or phosphate-buffered saline (PBS), the vehicle for BDNF. Retinas were evaluated using morphology and immunocytochemistry. The width of the outer segment zone was measured, and the retinas were evaluated for changes in protein expression by labeling with antibodies to rod opsin, phosducin, synaptophysin, calbindin D, and glial fibrillary acidic protein (GFAP). The effect of BDNF on both proliferation and apoptotic cell death was examined. RESULTS: Although there was variability in the treated retinas, most of the animals receiving BDNF had well-organized outer segments that were longer than those in vehicle-treated controls. Immunocytochemistry revealed that treated retinas had consistently less opsin redistribution to the plasma membrane, less phosducin upregulation, and fewer calbindin D-labeled horizontal cell processes. BDNF did not reduce overall cell death in the detachments or death of photoreceptors by apoptosis. However, it significantly reduced the proliferative response of Miller cells and the extent of upregulation of GFAP. CONCLUSIONS. The results suggest that BDNF may aid in the recovery of the retina after reattachment by maintaining the surviving photoreceptor cells, by reducing the gliotic effects in Muller cells, and perhaps by promoting outer segment regeneration.  (+info)

The etiology and treatment of macular detachment associated with optic nerve pits and related anomalies. (8/877)

PURPOSE: Up to two thirds of patients with optic disc pits develop a sight-limiting maculopathy. There is confusion regarding the etiology and nature of the maculopathy in these cases. We present 7 cases of serous macular detachment occurring in association with optic pits or related cavitary anomalies and identify a rhegmatogenous etiology. METHODS: We reviewed the records of 7 patients with optic nerve anomalies and macular detachment. Patients were treated with observation, barricade laser, vitrectomy, and/or gas tamponade. RESULTS: Seven patients were noted to have serous macular detachment associated with an optic nerve pit or other cavitary anomaly. A hole or tear in the diaphanous tissue overlying the optic pit was identified in all cases. None of the patients had a posterior vitreous detachment. Two were treated with photocoagulation only, and 5 underwent pars plana vitrectomy with fluid-gas exchange with or without photocoagulation. Pretreatment visual acuity ranged from 20/30 to 6/200. Posttreatment acuity ranged from 20/25 to 20/100. Five of 7 eyes had final acuities of 20/30 or better, and all treated eyes improved. CONCLUSIONS: A tear in the diaphanous tissue overlying the optic nerve pit is responsible for the development of serous macular detachment and is consistent with findings in similar conditions, such as retinal detachment in association with chorioretinal coloboma. These tears may be quite subtle, and careful biomicroscopic examination is required to appreciate them. The treatment of this condition remains controversial. However, because of the relatively poor prognosis, we believe treatment should include the formation of a barricade to fluid movement as well as sealing and relief of traction from the hole. The value of laser treatment may be increased by the early identification of a defect in the diaphanous membrane prior to the development of macular detachment. Consideration of prophylactic laser might then reduce the need for later, more invasive measures, and improve the prognosis.  (+info)