Central serous choroidopathy in pregnancy.
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Central serous choroidopathy is a spontaneous serous detachment of the sensory retina, usually affecting adults between 20 to 50 years of age but is also found in patients older than 60 years of age. This disease usually affects males with a male to female ratio of 8-10 to 1. Many aetiological or associated factors have been described. Here we report a 39-year-old pregnant lady presented with left central serous chorioretinopathy preceded by an unusual emotional disturbance. She was not given any photocoagulative treatment to avoid possible photocoagulative complications. Post delivery, she presented with resolution of the CSC. (+info)
Hypoxic induction of vascular endothelial growth factor is markedly decreased in diabetic individuals who do not develop retinopathy.
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OBJECTIVE: A small percentage of patients do not develop any evidence of diabetic retinopathy (DR) even after many years of diabetes. Vascular endothelial growth factor (VEGF) has been implicated in the development of DR. Therefore, we sought to determine if the regulation of VEGF differs in those patients who develop DR after many years of diabetes compared with those who do not develop DR. RESEARCH DESIGN AND METHODS: We performed standard 7-field stereoscopic fundus photography on 95 consecutive patients with type 1 and type 2 diabetes. Patients were categorized into 3 groups according to the presence or absence of DR and the duration of diabetes: group 1 was defined by presence of DR, group 2 was defined by absence of DR after >10 years duration of diabetes, and group 3 was defined by absence of DR with long-standing diabetes (> or =20 years for type 1 diabetes and > or =15 years for type 2 diabetes). Monocytes from 40 ml peripheral blood were isolated from all patients, and the hypoxic induction of VEGF was determined in vitro. RESULTS: We found no significant difference in the basal level of VEGF in patients with and without DR. However, we did find a markedly significant difference in the hypoxic induction of VEGF between patients from group 1 and group 3 (4.35+/-0.55 vs. 1.87+/-0.3, P<0.00013). CONCLUSIONS: This study suggests that 1 mechanism for the absence of DR in patients with long-standing diabetes is a decreased hypoxic induction of VEGF. (+info)
Vasoproliferative tumours of the retina.
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BACKGROUND: Vasoproliferative tumours of the retina (VPTR) are benign tumours of unknown origin, occurring mostly in otherwise healthy patients. VPTR may be associated with other chorioretinal diseases, such as uveitis. The tumours, which histologically represent reactive gliovascular proliferations, are characterised by a pink to yellow appearance on funduscopy and are accompanied by exudative and haemorrhagic changes of the retina. METHODS: 22 cases of VPTR in 21 patients were examined with a follow up period between 1 month and 6 years. Ophthalmological changes associated with VPTR were intraretinal and subretinal exudations (n=18), exudative detachments of the surrounding sensory retina (n=13), intraretinal and subretinal haemorrhages (n=10), exudative changes within the macula (n=10), hyperpigmentation of the retinal pigment epithelium at the border of the exudative retinal changes (n=9), and vitreous haemorrhages (n=4). Tumour biopsy was performed in two cases. Treatment consisted of plaque radiotherapy (n=14), plaque radiotherapy and cryotherapy (two), cryotherapy only (two), observation (three), and enucleation in one case of a blind and painful eye. RESULTS: Regression of the tumour and the associated exudative changes could be observed in all treated cases. Visual acuity at last follow up improved two lines or more in two cases, remained within two lines of the initial visual acuity in 15 cases, and worsened in the remaining five. Histopathological examination of the biopsy specimens and the tumour of the enucleated eye showed massive capillary proliferation with perivascular spindle-shaped glial cells of retinal origin. CONCLUSION: The correct diagnosis of VPTR is of importance as these lesions may lead to visual loss. Further, VPTR must be differentiated from angiomas associated with von Hippel-Lindau disease as well as from ocular and systemic malignancies. Regression of tumour thickness and associated retinal changes can be achieved with brachytherapy or cryotherapy. (+info)
A high association with cone dystrophy in Fundus albipunctatus caused by mutations of the RDH5 gene.
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PURPOSE: To analyze the RDH5 gene in patients with fundus albipunctatus with and without cone dystrophy and to determine whether the disease is stationary or progressive and whether the cone dystrophy is a part of fundus albipunctatus or a separate disease. METHODS: Fourteen patients from 12 separate Japanese families with fundus albipunctatus were examined. Six of the patients from 6 families also had a cone dystrophy. Genomic DNA was extracted from leukocytes of the peripheral blood, and exons 2, 3, 4, and 5 of the RDH5 gene were amplified by polymerase chain reaction and were directly sequenced. A complete ophthalmic examination was performed including best-corrected visual acuity, slit-lamp examination, indirect ophthalmoscopy, fundus photography, and electroretinography. RESULTS: In all the patients, either a homozygous mutation or compound heterozygous mutations in the RDH5 gene were identified. The identified mutations were nucleotide position (nt) 103 G to A (Gly35Ser), nt 319 G to C (Gly107Arg), nt 394 G to A (Val132Met), nt 719 G insertion (frame shift), nt 839 G to A (Arg280His), nt 841 T to C (Tyr281His), and nt 928 C to GAAG (Leu310 to GluVal). All these mutations except the Arg280His were new. The nt 928 C to GAAG mutation was detected in patients with and without cone dystrophy. Cone dystrophy was most frequently seen in patients over 40 years old. CONCLUSIONS: Fundus albipunctatus either with or without cone dystrophy is caused by mutations of the RDH5 gene. Cone dystrophy is frequently observed in elderly patients with fundus albipunctatus. The conclusion was reached that the mutations of the RDH5 gene caused a progressive cone dystrophy as well as night blindness. (+info)
Mutations in the 11-cis retinol dehydrogenase gene in Japanese patients with Fundus albipunctatus.
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PURPOSE: To detect mutations in the RDH5 gene encoding 11-cis retinol dehydrogenase in patients from Japan with fundus albipunctatus. METHODS: Polymerase chain reaction and direct genomic sequencing techniques were used to detect mutations of the RDH5 coding exons (exons 2-5) in two unrelated patients with fundus albipunctatus. Selected alleles that altered the coding region or intron splice sites were evaluated further through segregation analysis in the families of the index cases. RESULTS: Two novel RDH5 mutations were identified. One of these was a missense mutation Val264Gly in exon 5, and the other was an in-frame insertion of 3 bp in exon 5. CONCLUSIONS: The data indicate that mutations in RDH5 are the primary cause of fundus albipunctatus. (+info)
Superselective ophthalmic artery fibrinolytic therapy for the treatment of central retinal vein occlusion.
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AIM: To study the effect of superselective ophthalmic artery fibrinolysis as a treatment for central retinal vein occlusion (CRVO). METHODS: Retrospective, university based single centre study. The charts of 26 eyes of 26 patients treated were reviewed. Among the 26 patients, there were nine cases of combined artery and vein occlusion, three cases of combined cilioretinal artery and CRVO, and 14 cases of classic CRVO. Complete preoperative and postoperative ophthalmological examination and fluorescein angiography were performed in all cases. The therapeutic procedure comprised the infusion of urokinase through a microcatheter into the ostium of the ophthalmic artery, via a femoral artery approach. The main outcome measure was the improvement in visual acuity 48 hours after the procedure. RESULTS: Six eyes of six patients exhibited significant improvement in visual acuity immediately after the fibrinolysis procedure. Among them, four had a initial funduscopic appearance suggestive of combined occlusion of the central retinal artery (CRAO) and vein. For these patients, the visual benefit was maintained in the long term. Intravitreal haemorrhage occurred in two patients. There were no extraocular complications linked to the procedure. CONCLUSIONS: Selective ophthalmic artery infusion of urokinase was followed by improvement in VA in six out of 26 cases of CRVO. Eyes with combined CRAO and CRVO with recent visual loss appeared to be the most responsive. This treatment did not prevent the occurrence of ischaemia in the failure cases. The efficacy of in situ fibrinolysis for treatment of CRVO needs to be further evaluated in a controlled study. (+info)
Optical and visual impact of tear break-up in human eyes.
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PURPOSE: The purpose of this study was to examine the optical and visual impact of tear break-up. METHODS: Optical quality of the eye was assessed during periods of nonblinking by quantifying vessel contrast in the fundus image and by monitoring the psychophysical contrast sensitivity and the spatial distribution of tear thickness changes by retroillumination. All measures were obtained from three eyes either with or without a soft contact lens. RESULTS: A noticeable decrease in retinal vessel contrast and contrast sensitivity were observed soon after a blink. Both of these measures of optical quality of the eye showed a similar pattern of image degradation both with and without a soft contact lens. Although trial-to-trial variability was considerable, sample means show that image contrast in the low spatial frequency range can drop to between 20% and 40% of initial values after 60 seconds of nonblinking. Retroillumination of the tear film showed local intensity fluctuations that progressively spread across the pupil with increasing time after the blink. CONCLUSIONS: Optical aberrations created by tear break-up contribute to the decline in image quality observed objectively and psychophysically. The decline in image quality that accompanies tear break-up may be a direct cause of the blurry vision complaints commonly encountered in dry-eye patients. (+info)
Ocular fundus abnormalities detected by fluorescein and indocyanine green angiography in the Royal College of Surgeons dystrophic rat.
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The ocular fundi of the Royal College of Surgeons (RCS) dystrophic rats were examined by conventional fundus photography, fluorescein angiography (FA) and indocyanine green angiography (IA). In the fundus, a reddish colored background was observed in the RCS dystrophic rats at 3 weeks of age. At 9 weeks of age, the background had changed to pale in color. In FA, the RCS dystrophic rats at 3 week of age demonstrated background fluorescence with homogeneous brightness. Fluorescent dye leakage was observed in the late phase of the postinjection period at 9 weeks of age. In IA, the RCS dystrophic rats at 3 weeks of age had background fluorescence with homogeneous brightness, and at 5 weeks of age, spots of hyperfluorescence were scattered over the dark background. At 7 weeks of age, numerous delimited, irregular round spots of hyperfluorescence appeared over the dark background. Such hyperfluorescent lesions had further increased in number and size in the RCS dystrophic rats at 9 weeks of age. In this way, ocular findings related to abnormalities in the retinal pigment epithelium and choroid in the RCS dystrophic rat were demonstrated by fundus photography, fluorescein angiography and indocyanine green angiography. (+info)