Sadao Hori

Influence of phacoemulsification and intraocular lens implantation on the course of diabetic retinopathy

PURPOSEnTo study the effect of phacoemulsification and posterior chamber intraocular lens implantation on the course of diabetic retinopathy using the nonoperated fellow eye as a control.nnnSETTINGnDepartments of Ophthalmology, Diabetes Center, Tokyo Womens Medical University, and University of Tokyo School of Medicine, Tokyo, Japan.nnnMETHODSnOne eye of 66 diabetic patients who preoperatively had a similar stage of retinopathy in both eyes or no retinopathy bilaterally had cataract surgery. The course of diabetic retinopathy was followed for 1 year postoperatively. Patients were placed into 1 of 2 groups: Group A, progression of retinopathy in the operated eye was attributable to the surgical invasion (i.e., there was progression of retinopathy only in the operated eye or more progression in the operated eye than in the nonoperated fellow eye); Group B, no deterioration of retinopathy bilaterally, comparable level of deterioration in both eyes, or greater progression in the nonoperated eye than in the operated eye.nnnRESULTSnSurgery resulted in retinopathy progression in 16 patients (24.2%, Group A): 13 with unilateral deterioration and 3 with greater progression in the operated than in the nonoperated fellow eye. Of the remaining 50 patients (75.8%, Group B), 39 presented no significant progression in either eye, 8 had bilaterally comparable progression, and 3 showed progression in the nonoperated fellow eye only. Retinopathy worsened in the operated eye in 24 cases (36.3%); of these, changes in 16 patients were attributed to surgical influence. There was no significant difference between Groups A and B in age, diabetes mellitus duration, diabetes treatment method, and preoperative and postoperative hemoglobin A1c levels. The distribution of preoperative retinopathy stage significantly differed between groups, with more patients without retinopathy in Group A and more patients with advanced retinopathy in Group B.nnnCONCLUSIONnFactors such as age, diabetes mellitus duration, diabetes treatment method, and hemoglobin A1c level did not affect the progression of retinopathy; however, preoperative status of retinopathy may influence the susceptibility of the retinopathy to surgical invasion. A considerable proportion of eyes with aggravation of retinopathy would reflect the natural course of the disease, systemic factors, or both rather than the influence of cataract surgery.

Vascular endothelial growth factor in diabetic retinopathy.

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Intravitreal injection of erythropoietin protects against retinal vascular regression at the early stage of diabetic retinopathy in streptozotocin-induced diabetic rats.

A single intravitreal injection of erythropoietin (EPO) (50xa0ng/eye) or phosphate-buffered saline was administered to 5-week-old Sprague-Dawley rats at the onset of diabetes mellitus (DM) to determine and evaluate the protective effect of EPO on retinal microvessels. DM was induced by an intraperitoneal injection of streptozotocin (STZ; 60xa0mg/kg body weight). Morphological changes in microvessels in flat retinal preparations were evaluated during the subsequent 4 weeks by three-dimensional imaging of all blood vessels stained with fluorescein isothiocyanate-conjugated tomato lectin, following immunofluorescence techniques. No marked differences were observed in the shape or density of retinal vessels and the number of retinal capillary branches of the four groups [control, EPO, DM, and DM/EPO] up to 4 weeks after STZ administration. We also observed unique type IV collagen-positive filamentous structures that lacked both cellular elements and blood circulation (lectin-/type IV+ acellular strands), suggesting regressed vessel remnants. The lectin-/type IV+ acellular strands were detected soon after the onset of DM in the diabetic rats, and the number of these structures increased in the DM group (Pxa0<xa00.01). A single intravitreal injection of EPO caused a significant reduction in the number of lectin-/type IV+ acellular strands to levels observed in the control group. However, the lectin-/type IV+ acellular strands were observed in the central area of the retina near the optic disc in all four groups. Intravitreal injection of EPO resulted in downregulation of the EPO receptor, vascular endothelial growth factor (VEGF), and VEGF receptor at 4 weeks. We conclude that EPO may play a primary role against the progression of diabetic retinopathy by reducing blood vessel degeneration at a very early disease stage.

Management of type 2 diabetics requiring panretinal photocoagulation and cataract surgery

PURPOSE: To evaluate the outcomes in patients with diabetic retinopathy and cataract who had panretinal photocoagulation (PRP) first and cataract surgery second in 1 eye and cataract surgery followed by PRP in the fellow eye. SETTING: Department of Ophthalmology, Saiseikai Kurihashi Hospital, Saitama, Japan. METHODS: Fifty‐eight eyes of 29 patients with similar bilateral cataracts and severe nonproliferative or early proliferative diabetic retinopathy were randomly assigned for treatment with cataract surgery performed after PRP (PRP‐first group) or before PRP (surgery‐first group). Treatment was performed in the opposite order in the contralateral eye. The main outcome measure was best corrected visual acuity (BCVA) 12 months after surgery. The secondary outcome measures were the laser parameters, progression of retinopathy and macular edema, and aqueous flare intensity. RESULTS: The percentage of eyes with a BCVA of 20/40 or better was statistically significantly higher in the surgery‐first group (96.6%) than in the PRP‐first group (69.0%) (P = .012). The rate of the progression of macular edema was significantly decreased in the surgery‐first group (P = .033). There was no significant difference between the 2 groups in the other outcome measures. CONCLUSION: Although the order in which PRP and cataract surgery were performed had no effect on postoperative retinopathy, the BCVA was better and the rate of the progression of macular edema was decreased in the surgery‐first group.

Changes of vascular endothelial growth factor after vitrectomy for macular edema secondary to retinal vein occlusion

Purpose To examine whether vitrectomy combined with retinal photocoagulation reduces the vitreous level of vascular endothelial growth factor (VEGF) in patients with macular edema associated with retinal vein occlusion (RVO). Methods The authors measured VEGF levels in vitreous samples from four eyes of four patients with RVO during vitrectomy and fluid samples obtained during revitrectomy 3 to 9 months postoperatively for complications: an epiretinal membrane in two patients, macular holes in one patient, and vitreous hemorrhage in one patient. During vitrectomy, retinal photocoagulation was performed on the ischemic region of the retina in all cases (mean of 510 shots). Results In four eyes with RVO, there was a difference in the vitreous VEGF levels between the vitreous samples obtained during vitrectomy (mean of 2692 pg/mL, range of 15.6–9040 pg/mL) and the fluid samples obtained at the time of revitrectomy (mean of 947 pg/mL, range of 15.6–3430 pg/mL). Conclusions The results suggest that the vitreous levels of VEGF may be reduced by vitrectomy combined with retinal photocoagulation for macular edema with RVO. It may be important to reduce the vitreous levels of VEGF by vitrectomy and retinal photocoagulation for ischemic retina in macular edema with RVO.

Transport of fluorescein in the rabbit eye after treatment with sodium iodate

The outward active transport and the inward permeability of the blood-retinal barrier were studied in the rabbit eye after i.v. administration of sodium iodate. The active transport was evaluated from the half-time of disappearance of the vitreous fluorescein following intravitreal administration, and the inward permeability was evaluated from the vitreous concentration of fluorescein monoglucuronide after i.v. administration. The half-time of the vitreous fluorescein was 3.5 +/- 0.3 (mean +/- S.D.) hr, and 3.9 +/- 0.2 hr before and within 6 hr after iodate administration, respectively. After 24 hr, the half-time was 11.7 +/- 1.7 hr, similar to that of fluorescein monoglucuronide, 12.0 +/- 2.7 hr. The vitreous and the anterior chamber concentration of fluorescein monoglucuronide was measured at 1 hr after the i.v. dye injection. The vitreous concentration in the rabbits given iodate 3 hr before the dye injection was significantly greater than in the normal eyes, while the anterior chamber concentration was not different. Since fluorescein is rapidly metabolized to fluorescein monoglucuronide, differences in parameters determined using systemic fluorescein under two treatments or in disease states may be the result of alteration of the dynamics of fluorescein, fluorescein monoglucuronide, or both.

Glial Cells in Culture of Preretinal Membrane of Proliferative Vitreoretinopathy

Nine preretinal membranes surgically obtained from seven patients with proliferative vitreoretinopathy were cultured in Eagles minimal essential medium or RPMI 1640 medium, both with addition of 10% fetal bovine serum, in order to assess the proliferative capacity of the cells in the membrane. In addition, glial fibrillary acidic protein (GFAP, protein specific for glial cells) was stained in the cultured cells, by the immunoperoxidase method (peroxidase-antiperoxidase technique). Cellular outgrowth consisted of five types of cells; 1) spindle-shaped cells, 2) flat round or polyhedral cells, 3) semilunar cells, 4) stellate cells and 5) polygonal cells in close contact with each other and extending in monolayer. The spindle-shaped cells, the flat round or polyhedral cells, and the semilunar cells were dominant in all cases, and they showed vigorous proliferation and migration. Many of these cells were GFAP-positive, indicating their glial origin. The stellate cells were GFAP-positive, but they were few in number. The polygonal cells were near the explants and were GFAP-negative; they were thought to be derived from the retinal pigment epithelial cells. It was confirmed that the glial cells are the major cellular component of the proliferative preretinal membrane, and that they show vigorous proliferative capacity. It may be concluded that the glial cells play the major role in the formation of the preretinal membrane in proliferative vitreoretinopathy.