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  1. Article ; Online: Drusen maculopathy: a risk factor for visual deterioration.

    Algvere, Peep V / Kvanta, Anders / Seregard, Stefan

    Acta ophthalmologica

    2016  Volume 94, Issue 5, Page(s) 427–433

    Abstract: Age-related macular degeneration (AMD), the most common cause of visual loss after the age of 65, displays a degeneration of the retinal pigment epithelial (RPE) cells and photoreceptors in the retinal centre (macula). The central macula (fovea) that ... ...

    Abstract Age-related macular degeneration (AMD), the most common cause of visual loss after the age of 65, displays a degeneration of the retinal pigment epithelial (RPE) cells and photoreceptors in the retinal centre (macula). The central macula (fovea) that contains mostly cone photoreceptors mediates the high visual acuity. Drusen maculopathy may lead to visual deterioration. Drusen are extracellular deposits of debris that accumulate on Bruch's membrane. Drusen attract inflammatory, immunological and vasoactive stimuli. RPE and photoreceptor cells overlying drusen exhibit biochemical and morphological signs of degeneration. Strong and intermittent light exposure (photons) induces the formation of free radicals in the very high oxygen tension milieu of the retina. The negative effects of irradiation stimulate accumulation of lipofuscin in RPE and photoreceptor cells leading to mitochondrial dysfunction and apoptotic cell death. A hydrophobic barrier is built up in Bruch's membrane reducing diffusion to the choroid. Hereditary and inflammatory factors modify the risk for AMD. There is a genetic dysregulation of the complement system leading to inappropriate complement activation. The genetic polymorphism of complement factor H (CFH) and age-related maculopathy susceptibilty 2 (ARMS2) increase the risk of progression to advanced AMD. The photoelectric effect creates free radicals, resulting in a continuous increase of lipofuscin formation and impairing mitochondrial activity. In addition, inflammation and complement dysregulation contribute to the formation of drusen and vasoproliferative reactions with neovascularization. Antioxidants neutralize reactive oxygen species and reduce lipofuscin accumulation in RPE and photoreceptor cells. For prophylactic treatment of drusen maculopathy, high doses of antioxidants such as vitamins C and E, lutein, zeaxanthine and zinc are used according to the Age-Related Eye Disease Study 2 (AREDS 2). The risk of developing advanced AMD was reduced by 27% at 10 years follow-up. No adverse events were noted.
    MeSH term(s) Antioxidants/therapeutic use ; Humans ; Macular Degeneration/etiology ; Macular Degeneration/prevention & control ; Photoreceptor Cells, Vertebrate/pathology ; Retinal Drusen/complications ; Retinal Drusen/drug therapy ; Retinal Pigment Epithelium/pathology ; Risk Factors ; Vision Disorders/etiology ; Vision Disorders/prevention & control
    Chemical Substances Antioxidants
    Language English
    Publishing date 2016-08
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 2408333-1
    ISSN 1755-3768 ; 1755-375X
    ISSN (online) 1755-3768
    ISSN 1755-375X
    DOI 10.1111/aos.13011
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article: Drusen maculopathy: a risk factor for AMD. Can we prevent visual loss?

    Algvere, Peep V / Seregard, Stefan

    Acta ophthalmologica Scandinavica

    2003  Volume 81, Issue 5, Page(s) 427–429

    MeSH term(s) Humans ; Macular Degeneration/complications ; Macular Degeneration/etiology ; Retinal Drusen/complications ; Risk Factors ; Vision Disorders/etiology ; Vision Disorders/prevention & control
    Language English
    Publishing date 2003-10
    Publishing country Denmark
    Document type Comment ; Editorial ; Review
    ZDB-ID 1230907-2
    ISSN 1600-0420 ; 1395-3907
    ISSN (online) 1600-0420
    ISSN 1395-3907
    DOI 10.1034/j.1600-0420.2003.00157.x
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Shall we use Avastin or Lucentis for ocular neovascularization?

    Algvere, Peep V / Kvanta, Anders / Seregard, Stefan

    Acta ophthalmologica

    2008  Volume 86, Issue 4, Page(s) 352–355

    MeSH term(s) Angiogenesis Inhibitors/therapeutic use ; Antibodies, Monoclonal/therapeutic use ; Antibodies, Monoclonal, Humanized ; Bevacizumab ; Choroidal Neovascularization/drug therapy ; Humans ; Randomized Controlled Trials as Topic ; Ranibizumab
    Chemical Substances Angiogenesis Inhibitors ; Antibodies, Monoclonal ; Antibodies, Monoclonal, Humanized ; Bevacizumab (2S9ZZM9Q9V) ; Ranibizumab (ZL1R02VT79)
    Language English
    Publishing date 2008-06
    Publishing country England
    Document type Editorial
    ZDB-ID 2408333-1
    ISSN 1755-3768 ; 1755-375X
    ISSN (online) 1755-3768
    ISSN 1755-375X
    DOI 10.1111/j.1755-3768.2008.01317.x
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article: Age-related maculopathy: pathogenetic features and new treatment modalities.

    Algvere, Peep V / Seregard, Stefan

    Acta ophthalmologica Scandinavica

    2002  Volume 80, Issue 2, Page(s) 136–143

    Abstract: A considerable amount of new information on putative pathogenetic mechanisms in age-related maculopathy and degeneration has emerged in recent years. This comprises experimental studies on retinal pigment epithelium (RPE) and rod photoreceptor ageing, ... ...

    Abstract A considerable amount of new information on putative pathogenetic mechanisms in age-related maculopathy and degeneration has emerged in recent years. This comprises experimental studies on retinal pigment epithelium (RPE) and rod photoreceptor ageing, lipofuscin accumulation, the roles of oxidative stress and free radical formation, as well as antioxidants and other defensive mechanisms operating against environmental factors and ageing. The current application of photodynamic therapy (PDT) using verteporfin marks a new era in the treatment of subfoveal classical choroidal neovascularization. Several new treatment modalities, such as transpupillary thermotherapy (TTT) and anti-vascular endothelial growth factor (VEGF) agents for inhibition of neovascularization, have emerged and are undergoing multicentre clinical trials. A period of dynamic development in this field has commenced.
    MeSH term(s) Aging ; Cellular Senescence ; Clinical Trials as Topic ; Endothelial Growth Factors/antagonists & inhibitors ; Humans ; Hyperthermia, Induced ; Lymphokines/antagonists & inhibitors ; Macular Degeneration/pathology ; Macular Degeneration/therapy ; Oxidative Stress ; Photochemotherapy/methods ; Pigment Epithelium of Eye/physiology ; Retinal Rod Photoreceptor Cells/physiology ; Vascular Endothelial Growth Factor A ; Vascular Endothelial Growth Factors
    Chemical Substances Endothelial Growth Factors ; Lymphokines ; Vascular Endothelial Growth Factor A ; Vascular Endothelial Growth Factors
    Language English
    Publishing date 2002-04
    Publishing country Denmark
    Document type Journal Article ; Review
    ZDB-ID 1230907-2
    ISSN 1600-0420 ; 1395-3907
    ISSN (online) 1600-0420
    ISSN 1395-3907
    DOI 10.1034/j.1600-0420.2002.800204.x
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Bevacizumab for macular edema in central retinal vein occlusion: a prospective, randomized, double-masked clinical study.

    Epstein, David L J / Algvere, Peep V / von Wendt, Gunvor / Seregard, Stefan / Kvanta, Anders

    Ophthalmology

    2012  Volume 119, Issue 6, Page(s) 1184–1189

    Abstract: Purpose: To evaluate the efficacy of intraocular injections with bevacizumab in patients with macular edema (ME) secondary to central retinal vein occlusion (CRVO).: Design: Prospective, randomized, sham injection-controlled, double-masked clinical ... ...

    Abstract Purpose: To evaluate the efficacy of intraocular injections with bevacizumab in patients with macular edema (ME) secondary to central retinal vein occlusion (CRVO).
    Design: Prospective, randomized, sham injection-controlled, double-masked clinical trial.
    Participants: Sixty patients with ME secondary to CRVO.
    Methods: At baseline, patients were randomized 1:1 to receive intraocular injections of bevacizumab or sham injections every 6 weeks for 6 months.
    Main outcome measures: The primary outcome measure was the proportion of patients gaining at least 15 letters at 6 months. Secondary outcome measures included mean change from baseline best-corrected visual acuity (BCVA), foveal thickness, and neovascular glaucoma.
    Results: At the end of follow-up, 18 of 30 patients (60.0%) in the study group had gained ≥15 letters compared with 6 of 30 patients (20.0%) in the control group (P=0.003). The BCVA improved by 14.1 letters at 24 weeks compared with a decrease of 2.0 letters in the control group (P < 0.003). The mean decrease in central retinal thickness (CRT) was significantly greater in the study group (426 μm) than in the control group (102 μm) at all time points up to week 24 (P < 0.001). No residual edema, defined as CRT <300 μm at 24 weeks, was found in 26 of 30 patients (86.7%) in the treatment group compared with 6 of 30 patients (20%) in the control group (P < 0.001). In the sham group, 5 of 30 patients (16.7%) had developed iris rubeosis at week 24. No patients in the study group had rubeosis at week 24 (P=0.052). There were no events of endophthalmitis, retinal tear, or retinal detachment during the 24-week treatment period. No serious non-ocular adverse events were reported.
    Conclusions: Intraocular injections of bevacizumab given every 6 weeks for 6 months improve visual acuity (VA) and reduce ME significantly compared with sham.
    Financial disclosure(s): Proprietary or commercial disclosure may be found after the references.
    MeSH term(s) Aged ; Aged, 80 and over ; Angiogenesis Inhibitors/administration & dosage ; Angiogenesis Inhibitors/therapeutic use ; Antibodies, Monoclonal, Humanized/administration & dosage ; Antibodies, Monoclonal, Humanized/therapeutic use ; Bevacizumab ; Double-Blind Method ; Female ; Follow-Up Studies ; Humans ; Intravitreal Injections ; Macular Edema/drug therapy ; Macular Edema/etiology ; Macular Edema/physiopathology ; Male ; Middle Aged ; Prospective Studies ; Retinal Vein Occlusion/complications ; Retinal Vein Occlusion/drug therapy ; Retinal Vein Occlusion/physiopathology ; Tomography, Optical Coherence ; Treatment Outcome ; Vascular Endothelial Growth Factor A/antagonists & inhibitors ; Visual Acuity/physiology
    Chemical Substances Angiogenesis Inhibitors ; Antibodies, Monoclonal, Humanized ; VEGFA protein, human ; Vascular Endothelial Growth Factor A ; Bevacizumab (2S9ZZM9Q9V)
    Language English
    Publishing date 2012-06
    Publishing country United States
    Document type Journal Article ; Randomized Controlled Trial
    ZDB-ID 392083-5
    ISSN 1549-4713 ; 0161-6420
    ISSN (online) 1549-4713
    ISSN 0161-6420
    DOI 10.1016/j.ophtha.2012.01.022
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: Benefit from bevacizumab for macular edema in central retinal vein occlusion: twelve-month results of a prospective, randomized study.

    Epstein, David L / Algvere, Peep V / von Wendt, Gunvor / Seregard, Stefan / Kvanta, Anders

    Ophthalmology

    2012  Volume 119, Issue 12, Page(s) 2587–2591

    Abstract: Purpose: To evaluate the efficacy of intraocular injections with bevacizumab over 12 months in patients with macular edema (ME) secondary to central retinal vein occlusion (CRVO).: Design: A prospective study including a randomized 6-month, sham ... ...

    Abstract Purpose: To evaluate the efficacy of intraocular injections with bevacizumab over 12 months in patients with macular edema (ME) secondary to central retinal vein occlusion (CRVO).
    Design: A prospective study including a randomized 6-month, sham injection-controlled, double-masked clinical trial followed by a 6-month open-label extension.
    Participants: Sixty patients with ME secondary to CRVO.
    Methods: At baseline, patients were randomized 1:1 to receive intraocular injections of bevacizumab or sham injections every 6 weeks for 6 months. From month 6, all patients received intraocular injections of bevacizumab every 6 weeks for 6 months.
    Main outcome measures: The primary outcome measure was the proportion of patients gaining at least 15 letters at 12 months. Secondary outcome measures included mean change from baseline best-corrected visual acuity (BCVA), change in foveal thickness, and development of neovascular glaucoma.
    Results: At the end of follow-up, 18 of 30 patients (60.0%) in the bevacizumab/bevacizumab (bz/bz) group had gained ≥ 15 letters compared with 10 of 30 patients (33.3%) in the sham/bevacizumab (sh/bz) group (P < 0.05). The BCVA improved by 16.0 letters at 12 months in the bz/bz group compared with 4.6 letters in the sh/bz group (P < 0.05). In an unplanned retrospective analysis, patients aged >70 years had a significantly worse outcome when receiving delayed treatment, losing 1.4 letters (95% confidence interval [CI], -9.7 to 8.4) in the sh/bz group compared with a gain of 20.1 letters (95% CI, 13.9-26.3) in the bz/bz group in patients aged <70 years (P < 0.003). The mean decrease in central retinal thickness (CRT) was 435 μm in the bz/bz group compared with 404 μm in the sh/bz group (P = not significant). No patients developed iris rubeosis during the 6-month open-label extension period. There were no events of endophthalmitis, retinal tear, or retinal detachment during the 12-month treatment period. No serious nonocular adverse events were reported.
    Conclusions: Intraocular injections of bevacizumab given every 6 weeks for 12 months improve visual acuity (VA) and reduce ME significantly. Patients receiving delayed treatment have a limited visual improvement.
    Financial disclosure(s): Proprietary or commercial disclosure may be found after the references.
    MeSH term(s) Aged ; Angiogenesis Inhibitors/therapeutic use ; Antibodies, Monoclonal, Humanized/therapeutic use ; Bevacizumab ; Double-Blind Method ; Female ; Gonioscopy ; Humans ; Intravitreal Injections ; Macular Edema/drug therapy ; Macular Edema/etiology ; Macular Edema/physiopathology ; Male ; Prospective Studies ; Retinal Vein Occlusion/complications ; Retinal Vein Occlusion/physiopathology ; Tomography, Optical Coherence ; Treatment Outcome ; Vascular Endothelial Growth Factor A/antagonists & inhibitors ; Visual Acuity/physiology
    Chemical Substances Angiogenesis Inhibitors ; Antibodies, Monoclonal, Humanized ; VEGFA protein, human ; Vascular Endothelial Growth Factor A ; Bevacizumab (2S9ZZM9Q9V)
    Language English
    Publishing date 2012-12
    Publishing country United States
    Document type Journal Article ; Randomized Controlled Trial
    ZDB-ID 392083-5
    ISSN 1549-4713 ; 0161-6420
    ISSN (online) 1549-4713
    ISSN 0161-6420
    DOI 10.1016/j.ophtha.2012.06.037
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article ; Online: Combination therapy with low-dose transpupillary thermotherapy and intravitreal ranibizumab for neovascular age-related macular degeneration: a 24-month prospective randomised clinical study.

    Söderberg, Anne-Catherine / Algvere, Peep V / Hengstler, Jürg C / Söderberg, Pär / Seregard, Stefan / Kvanta, Anders

    The British journal of ophthalmology

    2012  Volume 96, Issue 5, Page(s) 714–718

    Abstract: Aim: To compare the effect of combined low-dose transpupillary thermotherapy (TTT) and intravitreal ranibizumab with sham TTT and intravitreal ranibizumab in patients with neovascular age-related macular degeneration (AMD).: Methods: A 24-month, ... ...

    Abstract Aim: To compare the effect of combined low-dose transpupillary thermotherapy (TTT) and intravitreal ranibizumab with sham TTT and intravitreal ranibizumab in patients with neovascular age-related macular degeneration (AMD).
    Methods: A 24-month, double-masked, randomised, active-controlled clinical trial. 100 patients with primary neovascular AMD were randomly assigned (1:1) to receive intravitreal ranibizumab and sham TTT or intravitreal ranibizumab and low-dose TTT. After an initial loading phase of ranibizumab patients were assigned to receive quarterly low-dose TTT (136 mW/mm) or sham TTT for 24 months. Retreatment with ranibizumab was allowed in both treatment groups using a variable dosing regimen. The primary endpoint was the number of intravitreal injections with ranibizumab. Secondary endpoints included change in best corrected visual acuity (BCVA), central retinal thickness (CRT) and lesion area.
    Results: In the per protocol (PP) population (78 patients) the mean number of ranibizumab injections was 8.0 in the sham TTT group versus 6.3 in the TTT group (p<0.05). The mean number of injections between 0-12 months and 13-24 months was 4.8 versus 4.6 (p>0.05) and 3.2 versus 1.7 (p<0.01) in the sham TTT and TTT groups, respectively. There was no statistically significant difference in BCVA (+4.0 vs +0.9 ETDRS letters), CRT (-49.9% vs -36.4%) or lesion area (-0.3% vs -10.6%) between the treatment groups at the final examination. The results of the intent-to-treat population (92 patients) were similar to the PP population.
    Conclusions: Treatment with low-dose TTT significantly reduced the number or intravitreal injections of ranibizumab over 24 months. The results suggest that low-dose TTT can serve as an adjuvant in combination with intravitreal ranibizumab for neovascular AMD.
    Clinical trial registration number: The trial is registered at http://clinicaltrials.gov (no NCT00599222).
    MeSH term(s) Aged ; Angiogenesis Inhibitors/administration & dosage ; Antibodies, Monoclonal, Humanized/administration & dosage ; Combined Modality Therapy ; Double-Blind Method ; Female ; Fluorescein Angiography ; Humans ; Hyperthermia, Induced ; Intravitreal Injections ; Male ; Prospective Studies ; Pupil ; Ranibizumab ; Retina/pathology ; Retreatment ; Time Factors ; Tomography, Optical Coherence ; Visual Acuity/physiology ; Wet Macular Degeneration/drug therapy ; Wet Macular Degeneration/physiopathology ; Wet Macular Degeneration/therapy
    Chemical Substances Angiogenesis Inhibitors ; Antibodies, Monoclonal, Humanized ; Ranibizumab (ZL1R02VT79)
    Language English
    Publishing date 2012-05
    Publishing country England
    Document type Comparative Study ; Journal Article ; Randomized Controlled Trial
    ZDB-ID 80078-8
    ISSN 1468-2079 ; 0007-1161
    ISSN (online) 1468-2079
    ISSN 0007-1161
    DOI 10.1136/bjophthalmol-2011-300721
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  8. Article: Photochemical damage of the retina.

    Wu, Jiangmei / Seregard, Stefan / Algvere, Peep V

    Survey of ophthalmology

    2006  Volume 51, Issue 5, Page(s) 461–481

    Abstract: Visual perception occurs when radiation with a wavelength between 400 and 760 nm reaches the retina. The retina has evolved to capture photons efficiently and initiate visual transduction. The retina, however, is vulnerable to damage by light, a ... ...

    Abstract Visual perception occurs when radiation with a wavelength between 400 and 760 nm reaches the retina. The retina has evolved to capture photons efficiently and initiate visual transduction. The retina, however, is vulnerable to damage by light, a vulnerability that has long been recognized. Photochemical damage has been widely studied, because it can cause retinal damage within the intensity range of natural light. Photochemical lesions are primarily located in the outer layers at the central region of the retina. Two classes of photochemical damage have been recognized: Class I damage, which is characterized by the rhodopsin action spectrum, is believed to be mediated by visual pigments, with the primary lesions located in the photoreceptors; whereas Class II damage is generally confined to the retinal pigment epithelium. The action spectrum peaks in the short wavelength region, providing the basis for the concept of blue light hazard. Several factors can modify the susceptibility of the retina to photochemical damage. Photochemical mechanisms, in particular mechanisms that arise from illumination with blue light, are responsible for solar retinitis and for iatrogenic retinal insult from ophthalmological instruments. Further, blue light may play a role in the pathogenesis of age-related macular degeneration. Laboratory studies have suggested that photochemical damage includes oxidative events. Retinal cells die by apoptosis in response to photic injury, and the process of cell death is operated by diverse damaging mechanisms. Modern molecular biology techniques help to study in-depth the basic mechanism of photochemical damage of the retina and to develop strategies of neuroprotection.
    MeSH term(s) Animals ; Humans ; Oxidants, Photochemical/radiation effects ; Oxidative Stress/radiation effects ; Photobleaching/radiation effects ; Pigment Epithelium of Eye/radiation effects ; Radiation Injuries/etiology ; Retina/radiation effects ; Retinal Degeneration/etiology ; Vision, Ocular/radiation effects
    Chemical Substances Oxidants, Photochemical
    Language English
    Publishing date 2006-09
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 391346-6
    ISSN 1879-3304 ; 0039-6257
    ISSN (online) 1879-3304
    ISSN 0039-6257
    DOI 10.1016/j.survophthal.2006.06.009
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  9. Article: Age-related maculopathy and the impact of blue light hazard.

    Algvere, Peep V / Marshall, John / Seregard, Stefan

    Acta ophthalmologica Scandinavica

    2006  Volume 84, Issue 1, Page(s) 4–15

    Abstract: The pathogenesis of age-related maculopathy (ARM), the most common cause of visual loss after the age of 60 years, is indeed a complicated scenario that involves a variety of hereditary and environmental factors. The pathological cellular and molecular ... ...

    Abstract The pathogenesis of age-related maculopathy (ARM), the most common cause of visual loss after the age of 60 years, is indeed a complicated scenario that involves a variety of hereditary and environmental factors. The pathological cellular and molecular events underlying retinal photochemical light damage, including photoreceptor apoptosis, have been analysed in experimental animal models. Studies of age-related alterations of the retina and photoreceptors, the accumulation of lipofuscin in retinal pigment epithelium (RPE) cells, and the formation of drusen have greatly contributed to our knowledge. A new concept of an inflammatory response to drusen has emerged, suggesting immunogenic and systemic reactions in Bruch's membrane and the subretinal space. Oxidative stress and free radical damage also impact on the photoreceptors and RPE cells in the ageing eye. Based on the photoelectric effect, a fundamental concept in quantum physics, the consequences of high-energy irradiation have been analysed in animal models and cell culture. Short-wavelength radiation (rhodopsin spectrum), and the blue light hazard (excitation peak 440 nm), have been shown to have a major impact on photoreceptor and RPE function, inducing photochemical damage and apoptotic cell death. Following cataract surgery, there is a dramatic change in ocular transmittance. In aphakic or pseudophakic eyes (with clear intraocular lenses), high-energy (blue) and ultraviolet-A radiation strikes the retina. Epidemiological data indicate a significantly increased 5-year incidence of late ARM in non-phakic eyes compared with phakic eyes. In recent years, putative prophylactic measures against ARM have emerged. The implantation of 'yellow' intraocular lenses (IOLs) that absorb high-energy blue radiation is, from a theoretical point of view, the most rational approach, and, from a practical point of view, is easy to accomplish. With increasing age, RPE cells accumulate lipofuscin (chromophore A2E). It is noteworthy that the yellow IOL not only protects A2E-laden human RPE cells from blue light (peak 430 nm) damage, but also alleviates the detrimental effects of green (peak 550 nm) and white light. A prophylactic treatment using antioxidants is aimed at counteracting oxidative stress and free radical cellular damage. The Age-Related Eye Disease Study (AREDS), a randomized clinical trial, showed a significantly lower incidence of late ARM in a cohort of patients with drusen maculopathy treated with high doses of antioxidants than in a placebo group. In recent years, considerable progress in retinal research has been achieved, creating a platform for the search for new prophylactic and therapeutic measures to alleviate or prevent photoreceptor and RPE degeneration in ARM.
    MeSH term(s) Animals ; Antioxidants/therapeutic use ; Aphakia, Postcataract/complications ; Free Radicals ; Humans ; Incidence ; Lens Implantation, Intraocular ; Lenses, Intraocular/adverse effects ; Light/adverse effects ; Macular Degeneration/epidemiology ; Macular Degeneration/etiology ; Macular Degeneration/prevention & control ; Oxidative Stress ; Photoreceptor Cells, Vertebrate/radiation effects ; Pseudophakia/complications ; Radiation Injuries/epidemiology ; Radiation Injuries/etiology ; Radiation Injuries/prevention & control
    Chemical Substances Antioxidants ; Free Radicals
    Language English
    Publishing date 2006-02
    Publishing country Denmark
    Document type Journal Article ; Review
    ZDB-ID 1230907-2
    ISSN 1600-0420 ; 1395-3907
    ISSN (online) 1600-0420
    ISSN 1395-3907
    DOI 10.1111/j.1600-0420.2005.00627.x
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article ; Online: Intravitreal bevacizumab in central retinal vein occlusion: 18-month results of a prospective clinical trial.

    Algvere, Peep V / Epstein, David / von Wendt, Gunvor / Seregard, Stefan / Kvanta, Anders

    European journal of ophthalmology

    2011  Volume 21, Issue 6, Page(s) 789–795

    Abstract: Purpose: To evaluate the long-term visual results in central retinal vein occlusion (CRVO) following repeated intravitreal injections of bevacizumab (IVB).: Methods: Thirteen patients (aged 34 to 79 years) with a duration of CRVO of 2 weeks to 6 ... ...

    Abstract Purpose: To evaluate the long-term visual results in central retinal vein occlusion (CRVO) following repeated intravitreal injections of bevacizumab (IVB).
    Methods: Thirteen patients (aged 34 to 79 years) with a duration of CRVO of 2 weeks to 6 months (mean 2.5 months) had a best-corrected visual acuity (BCVA) 0.05 to 0.4 (mean 0.13) as determined by Early Treatment Diabetic Retinopathy Study (ETDRS) chart. Clinical examination was carried out at baseline and every 6 to 8 weeks. Intravitreal bevacizumab (1.25 mg) was given every 6 weeks during the first 6 months, and after that at the discretion of the attending physician.
    Results: In total, 96 IVB (average 7.4/patient) were given: 50 IVB during the first 6 months, 28 from 6 to 12 months, and 18 from 12 to 18 months. Average BCVA had improved 15 ETDRS letters at 3 months, 24 letters at 6 months, 24 letters at 12 months, and 18 letters at 18 months (p<0.05). Eight patients (62%) had gained >15 ETDRS letters at 12 months, and 7 subjects (54%) >15 ETDRS letters at 18 months. Foveal thickness decreased from 596 µm at baseline to 294 µm at 18 months (p<0.05) and mean IOP from 15.2 mmHg to 15.8 mmHg. No serious adverse events occurred.
    Conclusions: Following repeated IVB, there was a significant gain of BCVA during the follow-up of 18 months. To maintain visual gain, regular ophthalmologic examinations and repeated injections seem to be necessary as long as the disease is active.
    MeSH term(s) Adult ; Aged ; Angiogenesis Inhibitors/administration & dosage ; Angiogenesis Inhibitors/therapeutic use ; Antibodies, Monoclonal, Humanized/administration & dosage ; Antibodies, Monoclonal, Humanized/therapeutic use ; Bevacizumab ; Female ; Fluorescein Angiography ; Follow-Up Studies ; Gonioscopy ; Humans ; Intraocular Pressure/physiology ; Intravitreal Injections ; Male ; Middle Aged ; Prospective Studies ; Retinal Vein Occlusion/diagnosis ; Retinal Vein Occlusion/drug therapy ; Retinal Vein Occlusion/physiopathology ; Retreatment ; Vascular Endothelial Growth Factor A/antagonists & inhibitors ; Visual Acuity/physiology
    Chemical Substances Angiogenesis Inhibitors ; Antibodies, Monoclonal, Humanized ; VEGFA protein, human ; Vascular Endothelial Growth Factor A ; Bevacizumab (2S9ZZM9Q9V)
    Language English
    Publishing date 2011-11
    Publishing country Italy
    Document type Clinical Trial ; Journal Article
    ZDB-ID 1089461-5
    ISSN 1724-6016 ; 1120-6721
    ISSN (online) 1724-6016
    ISSN 1120-6721
    DOI 10.5301/EJO.2011.6522
    Database MEDical Literature Analysis and Retrieval System OnLINE

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