[Show abstract][Hide abstract] ABSTRACT: Aims:
Nitric oxide (NO) is associated with neuroinflammation in the central nervous system. We determined whether NO increases the expression of aquaporin-4 (AQP4) in optic nerve astrocytes of rats.
Isolated astrocytes were incubated under normoxic or hypoxic conditions with or without glucose (5.5 mM). The astrocytes were also exposed to different concentrations of S-nitroso-N-acetyl-DL-penicillamine (SNAP, 1.0-100 μM), an NO donor. The expression of AQP4 was determined by Western blot analyses, and NO formation was measured by the Griess reaction. The changes in astrocytic cellular volumes were determined by flow cytometry.
Hypoxia and glucose deprivation increased AQP4 expression and NO formation. Inhibition of NO synthetase (NOS) significantly suppressed these changes. SNAP caused a significant increase in AQP4 expression, and the increase was significantly suppressed by carboxy-PTIO, a scavenger of NO. Incubation with 8-Br-cyclic guanosine monophosphate (cGMP) mimicked the effects of SNAP, while the addition of either 1H-[1,2,4]oxadiazolo[4,3,-a]quinoxalin-1-one (ODQ; inhibitor of soluble guanylate cyclase) or KT5823 (protein kinase G inhibitor) suppressed the SNAP-induced increase in AQP4 significantly. SNAP also caused a significant increase in astrocytic cellular volume through the AQP4 channels.
NO increased the AQP4 expression of optic nerve astrocytes through the cGMP/protein kinase G pathway and enlarged their volume.
Ophthalmic Research 11/2015; 54(4):212-221. DOI:10.1159/000440846 · 1.42 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: Purpose:
To evaluate the effect of the postoperative administration of rebamipide ophthalmic suspension on the success rate of lacrimal stent intubation (LSI) for the treatment of primary acquired nasolacrimal duct obstruction (PANDO).
This comparative interventional cohort study investigated 110 consecutive patients with PANDO who were treated with LSI and followed up for 12 months postoperatively at one institution. LSI was performed by one surgeon, and all patients received identical postoperative care. Among the total 110 patients, 71 underwent LSI with postoperative administration of rebamipide ophthalmic suspension, and 39 underwent LSI without administration of the suspension. Data related to patient age, gender, laterality, and postoperative administration of rebamipide ophthalmic suspension were collected and used as independent variables, and logistic regression analyses were performed to compare the anatomical success rate at 12 months postoperatively between patients with and without postoperative administration of the suspension.
The anatomical success rate of LSI in patients with and without postoperative administration of rebamipide ophthalmic suspension was 90.1 and 69.2 %, respectively. A comparison of these success rates showed statistical significance, in that the rate of treatment success was higher in PANDO patients who underwent LSI with postoperative administration of the suspension [odds ratio (OR), 3.37; P < 0.05].
The findings of this study show that postoperative administration of rebamipide ophthalmic suspension increases the rate of anatomical success in patients who undergo LSI for the treatment of PANDO.
Albrecht von Graæes Archiv für Ophthalmologie 10/2015; DOI:10.1007/s00417-015-3190-0 · 1.91 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: Purpose:
To determine whether insulin induces nitric oxide (NO) formation in retinal microvessels and to examine the effects of high glucose on the formation of NO.
Freshly isolated rat retinal microvessels were incubated in normal (5.5 mM) or high (20 mM) glucose with or without insulin (100 nM). The levels of insulin-induced NO and reactive oxygen species (ROS) in the retinal microvessels were determined semiquantitatively using fluorescent probes, 4,5-diaminofluorescein diacetate, and hydroethidine, respectively, and a laser scanning confocal microscope. The insulin-induced changes of NO in rat retinal endothelial cells and pericytes cultured at different glucose concentrations (5.5 and 25 mM) were determined using flow cytometry. Nitric oxide synthase (NOS) protein levels were determined by Western blot analysis; intracellular levels of ROS were determined using fluorescence-activated cell sorting (FACS) analysis of ethidium fluorescence; and nicotinamide adenine dinucleotide phosphate (NADPH) oxidase RNA expression was quantified using real-time PCR.
Exposure of microvessels to insulin under normal glucose conditions led to a significant increase in NO levels; however, this increase was significantly suppressed when the microvessels were incubated under high glucose conditions. Intracellular levels of ROS were significantly increased in both retinal microvessels and cultured microvascular cells under high glucose conditions. The expression of NOS and NADPH oxidase were significantly increased in endothelial cells and pericytes under high glucose conditions.
The increased formation of NO by insulin and its suppression by high glucose conditions suggests that ROS production mediated by NADPH oxidase is important by insulin's effect on the retinal microvasculature.
[Show abstract][Hide abstract] ABSTRACT: The purpose of this study was to report the surgical outcomes after creating a 120° intentional giant retinal tear for use in removing hemorrhage and subretinal proliferative tissue in patients with polypoidal choroidal vasculopathy (PCV) or age-related macular degeneration (ARMD). This study involved 12 eyes of 12 patients (10 eyes: PCV, 2 eyes: ARMD). After removal of the lens in phakic eyes, we performed a vitrectomy with artificial posterior vitreous detachment. Subsequently, a 120° intentional giant retinal tear was created in the temporal periphery, the retina was then turned, and the subretinal hemorrhage and proliferative tissue were removed. In order to preserve as much of the retinal pigment epithelium (RPE) as possible, we used a bimanual technique under direct visualization. After stretching the retina by use of perfluorocarbon liquid (PFCL), we performed endophotocoagulation around the tear followed by PFCL/silicone oil exchange. Except for 1 eye in which extensive loss of the RPE occurred, the fundus findings and the visual acuity (VA) improved in all patients. In addition, postoperative VA improved to ≥20/50 in 3 eyes in which the macular RPE was preserved. This surgical procedure is an effective treatment for PCV or ARMD patients with extensive subretinal hemorrhage and proliferative tissue.
International Ophthalmology 07/2015; DOI:10.1007/s10792-015-0102-6 · 0.55 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: Müller cells are dedifferentiated after retinal injuries and are transformed into nestin-positive progenitor cells that play crucial roles in remodeling. The purpose of this study was to determine the changes in the expression of nestin, CD44 (a receptor of hyaluronan), vascular endothelial growth factor (VEGF), and glutamine sythetase in cultured Müller cells after dedifferentiation by basic fibroblast growth factor (bFGF) and insulin.
Cells from a rat retinal Müller cell line (TR-MUL5) and from primary rat retinal Müller cells were grown in culture. The cells were incubated in various concentrations of bFGF (1.0, 10, 100 ng/mL) with or without insulin (5 μM) for 48 h. Changes in the expression of nestin, CD44, VEGF, and glutamine synthetase were determined by immunoblot and immunohistochemistry.
Exposure of TR-MUL5 cells to 10 ng/mL of bFGF led to the maximum increase in nestin by 1.5-fold, whereas the exposure had no effects on the expression of CD44. Addition of insulin (5 μM) to the bFGF significantly increased the CD44 level in TR-MUL5 cells by 1.4-fold. Immunohistochemistry showed that the combined treatments also upregulated the expression of nestin and CD44 in primary retinal Müller cells. Immunoblot analyses showed that exposure to bFGF and insulin caused significant increases of nestin (4.9-fold), CD44 (3.4-fold), and VEGF (1.44-fold) and decreases in glutamine synthetase (0.7-fold).
The inflammation and angiogenesis that develop after retinal injuries may be due to an upregulation of CD44 and VEGF by the dedifferentiated Müller cells.
Journal of ocular pharmacology and therapeutics: the official journal of the Association for Ocular Pharmacology and Therapeutics 06/2015; 31(8). DOI:10.1089/jop.2014.0117 · 1.47 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: To investigate the pathogenesis of idiopathic epiretinal membrane (ERM) from a biochemical perspective, the relationships between ERM and tryptase activity, a serine protease, and the levels of anti-type II collagen (anti-IIC) antibodies in the serum.
Vitreous samples for measurement of tryptase activity were obtained from 54 eyes of 54 patients who underwent a vitrectomy for vitreoretinal disease, ie, 14 eyes of 14 patients with idiopathic macular hole, 14 eyes of 14 patients with proliferative diabetic retinopathy (PDR), 13 eyes of 13 patients with ERM, and 13 eyes of 13 patients with rhegmatogenous retinal detachment (RRD). Tryptase activity was measured by spectrophotometry. Anti-IIC antibodies were measured in the serum obtained from 17 patients with ERM, eight patients who underwent cataract surgery, 12 patients with PDR, and nine patients with RRD. In these 46 patients, the anti-IIC antibodies were measured using a Human/Monkey Anti-Type I and Type II Collagen IgG Assay Kit.
Vitreal tryptase activity (mean ± standard deviation [SD]) in macular hole, PDR, ERM, and RRD was 0.0146±0.0053, 0.0018±0.0018, 0.0166±0.0046, and 0.0117±0.0029 mU/mg protein, respectively. Vitreal tryptase activity was significantly higher in macular hole and ERM than in PDR and RRD (P<0.05, Fisher's protected least significant difference). The serum levels of anti-IIC immunoglobulin G (IgG) antibody (mean ± SD) in ERM, cataract surgery, PDR, and RRD were 58.222±30.986, 34.890±18.165, 55.760±26.008, and 35.453±12.769 units/mL, respectively. The serum levels of anti-IIC IgG antibody were significantly higher in ERM and PDR than in cataract surgery and RRD (P<0.05, Fisher's protected least significant difference, two-sided).
In the pathogenesis of ERM, increased vitreal tryptase activity may be involved in tissue fibrosis, and elevated serum anti-IIC antibodies may lead to an immune response at the vitreoretinal interface, thus resulting in membrane formation.
[Show abstract][Hide abstract] ABSTRACT: To report a case of Coats' disease in which spontaneous reattachment occurred after total retinal detachment.
A young boy (patient age: 4 years and 11 months) presented with leukocoria in the left eye. Slit-lamp examination revealed total retinal detachment with abnormal retinal blood vessels and subretinal exudation just behind the lens. Computed tomography imaging showed no solid mass lesion in the intraocular space. Secondary total retinal detachment as a complication of Coats' disease was diagnosed. No light perception was detected, so we determined that surgical treatment was not indicated.
Four months after the initial diagnosis, the retina showed complete reattachment with a large amount of subretinal hard exudate. Visual acuity remained unchanged, with no light perception.
We speculate that the spontaneous retinal reattachment in the present case was caused by the decreased permeability of the abnormal retinal vessels and the good functional effect of the retinal pigment epithelium.
Case Reports in Ophthalmology 05/2015; 6(2):200-3. DOI:10.1159/000434676
[Show abstract][Hide abstract] ABSTRACT: Walker-Warburg syndrome (WWS) is a type of congenital muscular dystrophy (CMD) characterised by severe brain malformation, lissencephaly, and congenital eye abnormalities. Despite the coexistence of various eye abnormalities, results from optical coherence tomography (OCT) in WWS have not previously been reported. We herein report specific OCT findings in an infant with WWS.
The patient was a 14-day-old boy delivered by caesarean section at 38 weeks and 4 days of gestation and with a birth weight of 2,543 g. A cranial MRI showed lissencephaly, hydrocephalus, an encephalocele, and cerebellar hypoplasia, consistent with the diagnosis of WWS.
A bilateral ocular examination showed no abnormalities of the anterior eye segment. A fundus examination showed a persistent hyaloid artery in the vitreous cavity, a widespread loss of fundus pigmentation, transparent choroidal vessels (some choroidal vessel sections were visible), and the absence of a distinct macular reflex. OCT showed no foveal pit and an indistinct laminar structure of the retina. The infant subsequently developed congenital glaucoma and he then died of respiratory failure at the age of 8 months.
WWS is associated with a high incidence of congenital eye abnormalities, and this infant showed findings consistent with WWS. OCT revealed a marked retinal dysplasia.
Case Reports in Ophthalmology 05/2015; 6(2):210-5. DOI:10.1159/000435771
[Show abstract][Hide abstract] ABSTRACT: To study the indications for and effectiveness of Nunchaku-style silicone tube intubation (NSTI) in treating primary acquired lacrimal drainage obstruction (PALDO).
In this interventional cohort study, 235 consecutive patients in 1 institution who had complete lacrimal obstruction were investigated. Of those, 212 PALDO patients were enrolled, and 156 of the PALDO patients ultimately satisfied our treatment protocol and were then followed up for 12 months postsurgery. Patients without dacryocystitis underwent NSTI, while those with dacryocystitis underwent NSTI or endonasal dacryocystorhinostomy (EN-DCR) using the NST as a stent. The tubes were left in place for 8 weeks, and all patients received identical postoperative care. Resolution was deemed as patency assessed by irrigation. Logistic regression analyses were performed to compare the success of NSTI for upper (puncta and canaliculus) and lower (lacrimal sac and nasolacrimal duct) obstruction, NSTI for lower obstruction with and without dacryocystitis, and NSTI and EN-DCR for lower obstruction with dacryocystitis.
Comparison of the success rates at 12 months postsurgery showed significance as follows: treatment with NSTI was more successful for upper obstruction (94.6 %) than for lower obstruction (71.4 %) [odds ratio (OR) 8.23; P < 0.01]; treatment with NSTI was more successful for lower obstruction without dacryocystitis (82.9 %) than for dacryocystitis (52.4 %) (OR 4.96; P < 0.05); and treatment with EN-DCR (95.5 %) was more successful than NSTI (52.4 %) for treating lower obstruction with dacryocystitis (OR 16.99; P < 0.001).
NSTI is effective for treating PALDO; however, EN-DCR is more effective for treating PALDO cases complicated by dacryocystitis.
Japanese Journal of Ophthalmology 04/2015; 59(4). DOI:10.1007/s10384-015-0381-5 · 1.68 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: Estrogen, a female hormone, activates collagenase and might be associated with the pathogenesis of vitreoretinal collagen fiber disease. The purpose of the present study was to investigate the vitreous levels of estrone (E1) and estradiol (E2) in subjects with an idiopathic macular hole (IMH).
Vitreous samples were obtained from ten female patients with an IMH and from nine female patients with other retinal diseases (six with rhegmatogenous retinal detachment and three with age-related macular degeneration) as a control at the time of vitreous surgery. E1 and E2 levels in the vitreous samples were then determined using the Coat-A-Count(®) Estradiol Radioimmunoassay (RIA) Kit and the DSL-70 Estrone RIA Kit, respectively.
The mean vitreous levels of E1 and E2 in the subjects with IMH were 1.83±2.00 pg/mL and 7.03±2.97 pg/mL, respectively, whereas in the control subjects they were 2.42±1.25 pg/mL and 4.90±2.90 pg/mL, respectively. Thus, the vitreous E2 levels in the subjects with IMH were significantly higher than in the controls (P<0.05).
The findings of this study suggest that E2 might be associated with the pathogenesis of IMH, but further investigation is needed to elucidate that association.
[Show abstract][Hide abstract] ABSTRACT: Autoimmune mechanisms have been postulated as a cause of diabetic retinopathy (DR), as several autoantibodies have reportedly been detected in the serum of DR patients. In this present study, we measured serum and vitreous levels of anti-type II collagen (anti-II-C) antibodies in DR patients and investigated their association with the mechanism of development of DR.
Blood samples were obtained from patients with proliferative DR and from patients with diabetic macular edema who underwent vitrectomy at Osaka Medical College, Takatsuki City, Osaka, Japan. Diabetic patients without DR were also included. The control group consisted of age- and sex-matched patients with noninflammatory eye diseases who underwent eye surgery for retinal detachment or for cataracts. The levels of anti-II-C immunoglobulin (Ig)G antibody in the vitreous and serum were measured using a human/monkey anti-II-C IgG assay kit.
The serum levels of anti-II-C IgG antibody were significantly higher in the DR patients than in the patients with noninflammatory eye disease (56.8±33.8 units/mL versus 30.5±13.7 units/mL, respectively; P<0.05, Fisher's exact test). These levels were also significantly higher in the diabetic patients without DR than in the patients with noninflammatory eye disease (76.3±49.7 units/mL versus 30.5±13.7 units/mL, respectively; P<0.01, Fisher's exact test). However, anti-II-C IgG antibody levels were unable to be detected in all of the obtained vitreous fluid samples.
The development and progression of DR may be related to a mechanism involving intraocular type II collagen, which normally has immunological tolerance as a sequestered antigen. In DR, the disruption of the blood-retinal barrier leads to contact between the intraocular type II collagen and immunocompetent cells, and to subsequent activation of the autoimmune mechanism.
[Show abstract][Hide abstract] ABSTRACT: Diabetic macular edema(DME) is a major cause of vision loss and has a remarkable impact on the quality of life of diabetic patients. New pharmacological approaches based on the use of intravitreal drugs, such as corticosteroids and anti-vascular endothelial growth factor, have recently been developed for the treatment of DME. Even though laser therapy has been the standard treatment for DME, the results of several clinical trials have shown the superiority of some of these new agents to laser therapy. The purpose of this review is to briefly summarize the currently available new pharmacological treatments for DME in Japan.
Nippon rinsho. Japanese journal of clinical medicine 03/2015; 73(3):484-8.
[Show abstract][Hide abstract] ABSTRACT: We report a rare case of large cell neuroendocrine carcinoma (LCNEC) of the lung with cancer-associated retinopathy (CAR). To our knowledge, only two cases of LCNEC with CAR have been reported, one in 1995 and another in 2013. CAR, typically associated with small cell lung cancer (SCLC), is one of the paraneoplastic syndromes with deterioration of visual acuity, visual field constriction, and photophobia. CAR is caused by an autoimmune system reaction against the same antigen in the tumor and retinal photoreceptor cells. To diagnose CAR, genetic retinal dystrophies or any other medical causes of retinopathy should be excluded, but there are no standard diagnostic criteria. Anti-retinal antibodies are known to be positive in CAR patients, and anti-recoverin antibodies are thought to be sensitive and specific to CAR. In our case, anti-recoverin antibodies were not detected by serum tests, but CAR could be diagnosed on the basis of ophthalmological findings including clinical symptoms, electroretinographic findings, and visual field tests. CAR with clinical features of rapid visual disorder should be considered in LCNEC patients as well as in SCLC patients.
Case Reports in Oncology 03/2015; 8(1):153-158. DOI:10.1159/000380943
[Show abstract][Hide abstract] ABSTRACT: It was the aim of this study to report a case of a vitreomacular traction-associated macular microhole (MMH) in an eye with focal choroidal excavation (FCE) detected by spectral-domain optical coherence tomography (SD-OCT).
A 38-year-old Japanese female presented to our clinic complaining of metamorphopsia in her left eye. The patient then underwent SD-OCT as well as a routine ophthalmological examination. She had a previous history of a macular hole in her right eye that had been successfully treated by pars plana vitrectomy.
Upon initial examination, her best-corrected visual acuity was 20/25 in the left eye with a refractive error of -10.25 diopters. Examination by SD-OCT revealed an MMH with an outer retinal defect adjacent to the FCE. SD-OCT also revealed an intraretinal cystoid space in the macula with vitreous attachment around the foveal center.
The findings of this report show that variable changes are likely to be associated with FCE. However, the etiology of FCE has yet to be fully elucidated and careful observation is necessary in cases of FCE.
Case Reports in Ophthalmology 02/2015; 6(1):71-5. DOI:10.1159/000377667
[Show abstract][Hide abstract] ABSTRACT: The purpose of this study was to determine the temporal and spatial changes in the expression of AQP4 and AQP9 in the optic nerve after it is crushed. The left optic nerves of rats were either crushed (crushed group) or sham operated (sham group), and they were excised before, and at 1, 2, 4, 7, and 14 days later. Four optic nerves were pooled for each time point in both groups. The expression of AQP4 and AQP9 was determined by western blot analyses. Immunohistochemistry was used to determine the spatial expression of AQP4, AQP9, and GFAP in the optic nerve. Optic nerve edema was determined by measuring the water content in the optic nerve. The barrier function of the optic nerve vessels was determined by the extravasated Evans blue dye on days 7 and 14. The results showed that the expression of AQP4 was increased on day 1 but the level was significantly lower than that in the sham group on days 4 and 7 (P<0.05). In contrast, the expression of AQP9 gradually increased, and the level was significantly higher than that in the sham group on days 7 and 14 (P<0.05, Tukey-Kramer). The down-regulation of AQP4 was associated with crush-induced optic nerve edema, and the water content of the nerve was significantly increased by 4.3% in the crushed optic nerve from that of the untouched fellow nerve on day 7. The expression of AQP4 and GFAP was reduced at the crushed site where AQP4-negative and AQP9-positive astrocytes were present. The barrier function was impaired at the crushed site on days 7 and 14, restrictedly where AQP4-negative and AQP9-positive astrocytes were present. The presence of AQP9-positive astrocytes at the crushed site may counteract the metabolic damage but this change did not fully compensate for the barrier function defect.
PLoS ONE 12/2014; 9(12):e114694. DOI:10.1371/journal.pone.0114694 · 3.23 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: Purpose:
The purpose of this study was to evaluate the correlation between laser speckle flowgraphy measurements of mean blur rate (MBR) and hydrogen gas clearance measurements of capillary blood flow (CBF) in the optic nerve head (ONH) of albino and pigmented rabbits, with or without chronic ischemia-induced ONH atrophy.
The ONH MBR and ONH CBF were measured at baseline, 30 and 60 minutes after the intravenous administration of endothelin-1 (ET-1) (10(-10) mol/kg) in six albino and six pigmented rabbit eyes. The ONH MBR and ONH CBF were also measured in nine pigmented rabbit eyes that underwent the intravitreal administration of ET-1 (20 pmol) twice per week for 4 weeks to provoke chronic ischemia-induced ONH atrophy.
In the group that received intravenous ET-1, average measurements of ONH MBR and ONH CBF at all time points were correlated in both the albino (r = 0.88, P < 0.001, n = 18) and pigmented rabbits (r = 0.85, P < 0.001, n = 18), with no intrarabbit correlations (P = 0.524). The ONH MBR and ONH CBF were also correlated in the model of chronic ischemia-induced ONH atrophy (r = 0.78, P = 0.013, n = 9). Pooled ONH MBR and ONH CBF measurements in both the intravenous and intravitreal groups were also highly correlated (r = 0.87, P < 0.001, n = 45), with no significant intergroup differences in the relationship between ONH MBR and ONH CBF (P = 0.138).
Regardless of the presence of fundus pigmentation or ONH atrophy, ONH MBR and ONH CBF were highly correlated, suggesting that MBR in the ONH tissue is usable for interindividual and intergroup comparisons.
[Show abstract][Hide abstract] ABSTRACT: Purpose:
The incidence of blindness is increasing, in part, because of abnormal ocular neovascularization. Anti-VEGF therapies have yielded impressive results; however, they are not a cure for blindness. Recently, metallothioneins (MTs) 1 and 2 have been implicated in the process of angiogenesis. Therefore, we investigated whether MT-1 and MT-2 were also involved in ocular neovascularization.
The concentrations of MT-1 and MT-2 (hereafter MT-1/2) were observed by ELISA. We examined the role of MT-1/2 in ocular neovascularization by using both an oxygen-induced retinopathy (OIR) model and a laser-induced choroidal neovascularization (CNV) model. We investigated the localization of MT-1/2 in retina. Furthermore, we investigated the expression of hypoxia-inducible factor (HIF)-1α and VEGF in OIR. In vitro, we investigated the degradation of HIF-1α.
The MT-1/2 were significantly elevated in proliferative diabetic retinopathy patients. Ocular neovascularization, which was induced in both the OIR model and the CNV model, was decreased in MT-1/2 knockout (KO) mice. We confirmed that although MT-1/2 was expressed throughout the murine retina, its expression levels were highest in the endothelial cells. Further, OIR enhanced MT-1/2 expression in the retina. Interestingly, in the OIR model, both HIF-1α and VEGF levels were significantly decreased in the retina of MT-1/2 KO mice. In addition, we found that knockdown of MT-1/2 accelerated ubiquitination of HIF-1α.
These results indicate that MT-1/2 are involved in retinal and choroidal neovascularization, and that MT-1/2 might be a new therapeutic target in diseases in which ocular angiogenesis is implicated.
[Show abstract][Hide abstract] ABSTRACT: Background
We report our findings in three cases of unilateral macular edema associated with retinal vein occlusion (RVO) that improved after successful treatment of systemic hypertension alone.
All three cases had systemic hypertension but no diabetes mellitus or other ocular diseases associated with macular edema. All patients were treated only with medication for systemic hypertension. Optical coherence tomography was performed to determine the foveal thickness before and after treatment.
Case one was a 72-year-old woman with a central RVO who had macular edema in her left eye and a visual acuity (VA) of 20/50. Her blood pressure (BP) was 169/96 mmHg. One month after the initiation of a calcium blocker to treat her systemic hypertension, her BP was decreased, macular edema was reduced, and her VA improved to 20/20. Case two was a 62-year-old woman with branch RVO. Her VA was 20/40 and her BP was 165/97 mmHg. Six weeks after initiation of medication to treat her systemic hypertension, her RVO-related macular edema had decreased and her VA improved to 20/20. Case three was a 71-year-old man with branch RVO. His VA was 20/50 and his BP was 165/87 mmHg. One month after initiation of treatment for systemic hypertension, his RVO-related macular edema had disappeared and his VA improved to 20/20. All three cases had nonischemic RVO by fluorescein angiography, and they did not develop ischemic changes for at least 1 year.
The reduction of macular edema following a decrease in the systemic hypertension suggests that the edema was most likely caused by leakage of fluids from the blood vessels. We recommend that the blood pressure should be measured in all patients with macular edema before initiating intravitreal anti-VEGF therapy.