Nonproliferative Diabetic RetinopathyPhase 4NCT02834663
Effects of Intravitreal Ranibizumab for Macular Edema With Nonproliferative Diabetic Retinopathy
A Phase 4 study testing Lucentis in people with Nonproliferative Diabetic Retinopathy, run by Wonkwang University Hospital.
Trial summary
Title of study: Effects of Ranibizumab to delay or regression non-proliferative diabetic retinopathy(NPDR) with DME assessed by microaneurysm changes: A pilot study Objectives Diabetic retinopathy (DR) is a major cause of visual impairment. Read more about this study
- Who is it for?
- Ages 40 years and older
- Conditions the study is for
- Nonproliferative Diabetic Retinopathy
- What is being tested?
- Lucentis
- Type of treatment
- Injection or infusion
- Could I receive a placebo?
- No, everyone receives an active treatment
- How many people
- 25 participants
- Where
- No sites listed yet
- Study dates
- Aug 2016to Dec 2019
- Phase
- Phase 4
- Are there results?
- Yes, posted in the registrySummary in the doctors' view
Key requirements
Who can take part, as listed by the sponsor. Only the study team can confirm whether you are eligible, so take this list to your doctor.
- Ages 40 years and older
- All sexes
- No healthy volunteers
- Adult, Older adult
Who may be able to join
- Patients (Male \& female) ≥40 years of age
- Type 2 DM
- Best corrected visual acuity ≥ 20/200 (Snellen equivalent using Early Treatment Diabetic Retinopathy Study chart)
- central retinal thickness of ≥300 µm on optical coherence tomography
- nonproliferative diabetic retinopathy (NPDR) with diabetic macular edema
Who cannot join
- proliferative diabetic retinopathy
- Vitreous hemorrhage
- previous history of vitreoretinal surgery, post-cataract operation status (≤4 months before participation in this study)
- prior treatment with anti-VEGF drugs, intraocular corticosteroids, and/or retinal laser application
- Uncontrolled hypertension.
- Uncontrolled glaucoma.
- If both eyes met the study inclusion criteria, the more severely affected eye was selected
About this study
Official title: Prospective, Single-center, Six-month Study of Intravitreal Ranibizumab for Macular Edema With Nonproliferative Diabetic Retinopathy: Effects on Microaneurysm Turnover and Non-perfused Retinal Area
Title of study:
Effects of Ranibizumab to delay or regression non-proliferative diabetic retinopathy(NPDR) with DME assessed by microaneurysm changes: A pilot study Objectives Diabetic retinopathy (DR) is a major cause of visual impairment. Anti-vascular endothelial growth factors have demonstrated therapeutic benefits in diabetic macular edema (DME). We aimed to prospectively analyze the effects of early intensive treatment using intravitreal ranibizumab (IVR) injections in nonproliferative diabetic retinopathy patients with macular edema.
Read more
Primary objective:
To investigate other efficacy endpoints including other visual acuity, anatomical change in mild-to-moderate NPDR with DME after intravitreal Ranibizumab injection from baseline through 6 months after treatment.
Secondary objectives:
To compare microvascular changes assessed by microaneurysm counts and perifoveal non-perfusion area changes and safty in eyes of mild-to-moderate NPDR with DME after intravitreal Ranibizumab injection from baseline through 6 months after treatment.
Read the detailed description
Title of study:
Effects of Ranibizumab to delay or regression non-proliferative diabetic retinopathy(NPDR) with DME assessed by microaneurysm changes: A pilot study
Study Rationale:
Diabetic retinopathy is the leading disease that causes acquired vision loss after 20 by making diabetic macular edema and neovascularization. In recent young generation, as prevalence of type 2 diabetes is growing, the burden of sight-threatening retinopathy is increasing on trend.1 Pathologically, angiogenesis is a main cause that destroys the structure of the eye and induces the visual function disorder as VEGF playing an important role in increasing the migration and proliferation of endothelial cells and increasing the permeability of the blood vessels.2,3 VEGF is made from the endothelial cells of retinal tissue, perivascular cells, pigment endothelial cells by hypoxia. And hypoxic condition of intraocular tissues is a key regulator of intra ocular angiogenesis by VEGF, the balance between VEGF and angiogenesis inhibitors determines the neovascular proliferation in diabetic retinopathy.4 VEGF is also inducing the expression of cell-to-cell contact molecule (intracellular adhesion molecule-1, ICM-1) and the adhesion of leukocytes to help the inflammatory response5, as mediator which destroys the blood retinal barrier, affecting the protein of tight junctions, making a microaneurysm and increasing permeability of capillary, that makes the liquid leakage and macular edema.5,6 Microanuerysm is the earliest clinical manifestations, the saccular local lesion that perivascular cells protruding in damaged areas on the capillary wall. According to Stitt AW et al9, diabetic microaneurysm is non-functioning extrusion of the vascular system from the deep part of inner retinal capillary plexus.
It is sometimes disappeared by being blocked with blood clots, on the other hand, new microanerysm is occurred in the other vascular bed structure.
Through these changes, the investigators know the course of a diabetic retinopathy and it is known that the generation rate of microaneurysm is associated with the clinically significant progression of macular edema (CSME) in mild-to-moderate nonproliferative diabetic retinopathy .10,11 In addition, the number of microanerysm is an important prognostic indicator which can estimate the progression or regression of diabetic retinopathy, as predicting whether becoming better or worse in diabetic retinopathy.12 Kohner and Sleightholm13 describe this concept at first time in 1986, its association with the number of microvascular flow and the severity of diabetic retinopathy. In recent years it is reported that measuring the number of microaneurysm and the turnover rate associated with the appearance or disappearance of microaneurysm, are predictors in progression of diabetic retinopathy and macular edema.14 To delay the progression of diabetic retinopathy and to improve macular edema, the laser photocoagulation have been the important role.15 Although the laser photocoagulation have had treatment effect in the diabetic retinopathy by reducing the amount of VEGF in micraneurysm and by degenerating the neovascularization after laser therapy, there was a problem that has many limitations - peripheral visual field defects, night blindness, progression of macular edema etc., and that the disease does not cured in a good time because of limits of laser therapy due to cataract, vitreous hemorrhage and turbidity. As an alternative method to solve these limitations, there is an anti-VEGF therapy.6 According to a previous study result, intraocular injection of Bevacizumab inhibits occurring of neovascularization by blocking the VEGF receptor .17 Recently, several studies have been reported that when injected intravitreal anti-VEGF, macular edema is improved and neovascularization is inhibited, by reducing the leakage of neovascularization.3 Especially, Leicht SF et al18 reported the number of microaneurysms and turnover rate in NPDR(non-proliferative diabetic retinopathy) patients injected with Ranibizumab. And the result showed entire number of the microaneurysms and turnover rate are decreased, which could be mean the regression of diabetic retinopathy and it could decide the therapeutic effect.
On this study, through the fluorescein fundus angiography, the average number of microaneurysms was significantly decreased after intravitreal injection of anti-VEGF therapy (p<0.05). The decrease of 35.70±24.79% in the treatment group was statistically higher than 13.95±38.21% in the control group of the fellow eye (p<0.05).
The result is found because decreased concentration of intravitreal VEGF inhibits the progression of diabetic retinopathy, such as endothelial cell proliferation and endothelial cell damage on retinal capillary and perivascular cells.
Sjølie AK et al12 reported up-regulation of VEGF occuring microaneurysms causes endothelial cell proliferation and inflammation and effusion reaction, so anti-VEGF is effective in early diabetic retinopathy. But there is less effectiveness in late diabetic retinopathy as it reaches the non-changing point. Also Kohner EM et al19 reported diabetic retinopathy lesions are reversible and could be delayed in early diabetic retinopathy.
So far, changes of microaneurysms in late diabetic retinopathy is uncertain, and if there would be a finding according to anti-VEGF therapy, the investigators could get a clue of surrogate marker which represents treatment results in diabetic retinopathy.
This study was designed to find the clinical evaluation and reduction rate through fluorescein angiography as microaneurysm examination tools to research NPDR with DME treatment results assessed by microaneurysm counts, timely monitored with anti-VEGF therapy.
Objectives To evaluate the effects of intravitreal Ranibizumab injection on microvascular changes in eyes of mild-to-moderate NPDR with DME.
Primary objective:
To investigate other efficacy endpoints including other visual acuity, anatomical change in mild-to-moderate NPDR with DME after intravitreal Ranibizumab injection from baseline through 6 months after treatment.
Secondary objectives:
To compare microvascular changes assessed by microaneurysm counts and perifoveal non-perfusion area changes and safty in eyes of mild-to-moderate NPDR with DME after intravitreal Ranibizumab injection from baseline through 6 months after treatment.
Primary and secondary endpoints:
Primary endpoint:
To compare other visual acuity, anatomical changes after intravitreal Ranibizumab injection from baseline through 6 months after treatment.
- The changes in best corrected visual acuity (BCVA) using ETDRS chart. ii) The central macular thickness - Circle Diameters : 1 mm ETDRS by spectralis OCT ; Heidelberg Engineering.
Secondary endpoints:
To compare microaneurysmal changes and perifoveal non-perfusion area and safty after intravitreal Ranibizumab injection from baseline through 6 months after treatment.
- The total number of microaneurysm by fundus photo using Retmarker DR(version 1.0.2) software. ii) The microaneurysm formation rate : Number of new MAs detected/month. iii) The microaneurysm disappearance rate : Number of MAs that resolved/month. iv)The microaneurysm turnover. v) Perifoveal non-perfusion area in FAG (mm²) using ImageJ software (version 1.52a) by FAG image. vi) Safety parameters : Systemic adverse events (MI, CVA, etc), Ocular adverse events (retinal detachment, RPE tear, endophthalmitis, uveitis, vitreous hemorrhage, subretinal hemorrhage, cataract , IOP elevation, etc).
Methodology:
single center, prospective, interventional, one arm, pilot study
Evaluation Participants will be evaluated with a full ocular examination at each visit (VA measurement, tonometry, slit lamp exam). Fluorescein angiography (FA) will be performed at baseline, at 3 months after baseline and at the last visit(6 months after baseline), and OCT will be performed monthly (baseline and 1, 2, 3, 4, 5, 6 months from baseline).
The MAs and perifoveal non-perfused areas in individual retinas were evaluated at 6 months using fundus photography and FA imaging. The Retmarker (version 1.0.2 by Retmarker Ltd, Coimbra, Portugal) software was used for automatic measurement and analysis of changes in number and extent of MAs on fundus photographs and to calculate the total number and turnover of MAs.
Perifoveal non-perfused area was estimated using the early FA image (from each of the three examinations) in which both the vascular arch and the non-perfused area were clearly visualized. Subsequently, the ImageJ software (version 1.25a 23/04/2018 by ImageJ, USA) was used for scaling each image to 200 µm and for equalizing the contrast and sensitivity of each picture to the maximum possible extent, by auto-adjustment of brightness and contrast. The raw red-green-blue (RGB) images were then converted to 8-bit images, with the threshold set for optimal visualization of the non-perfused area. The same threshold was applied to all images of the same patient.
Result analysis The investigators compare the differences between at baseline, at 3 month, and at 6 month. Statistical analyses will be performed using SPSS ver.18.0 (SPSS Inc., Chicago, Il, USA). Kolmogorov-Smirnov test was applied to test for normality of sample group data. the paired T-test was used for comparative statistical analysis of these parameters. (BCVA, CRT, total number of MAs, MA formation rate, MA disappearance rate, MA turnover, and perifoveal non-perfused area)
- Conditions
- Nonproliferative Diabetic Retinopathy
- Being tested
- Lucentis
- Keywords
- Nonproliferative diabetic retinopathy, Microaneurysms
- Medical subject headings
- Microaneurysm
What participants receive
What participants receive. In a randomised study each person is assigned to one group by chance.
LucentisDrug
Also called Intravitreal Lucentis injection
Local anesthesia with T-caine with Saline irrigation. Routine eye drap was done by potadine-cotton ball. Lucentis injected to vitreous cavity, finally dressing.
| Study group | Role | What they receive |
|---|---|---|
| Lucentis | Experimental | Patients were administered 0.5-mg IVR injections monthly for 6 months. Receives: Drug: Lucentis |
What is being measured
The primary outcome is the main question the study is designed to answer.
The Best Corrected Visual Acuity (BCVA)
BCVA was performed using the Early Treatment Diabetic Retinopathy Study (ETDRS) chart at baseline and 6 months. The BCVA compare the degree of improvement or worsening of vision at baseline and 6 months. (value at 6 months minus value at baseline)
Measured: 6 months
Central Macular Thickness(CMT)
CRT was performed using OCT at each visit. The OCT measured at each visit was analyzed statistically. the CMT compare the degree of improvement or worsening of vision at baseline and 6 months. (value at 6 months minus value at baseline)
Measured: 6 months
Secondary outcomes (6)
The Total Number of Microaneurysm
The number of MAs in individual retinas were evaluated during 6 months using fundus photography and FA imaging. The Retmarker software was used for automatic measurement and analysis of changes in number and extent of MAs on fundus photographs and to calculate the total number and turnover of MAs. Changes in MAs were analyzed statistically. the total number of MAs compare the degree of improvement or worsening of vision at baseline and 6 months. (value at 6 months minus value at baseline)
Measured: 6 months
The Microaneurysm Formation Rate
number of new MAs detected/month The MAs in individual retinas were evaluated at 6 months using fundus photography. The Retmarker (version 1.0.2 by Retmarker Ltd, Coimbra, Portugal) software was used for automatic measurement and analysis of changes in number and extent of MAs on fundus photographs and to calculate the total number and turnover of MAs. MA turnover was calculated by adding the MA formation rate (number of new MAs detected/month) to the MA disappearance rate (number of MAs that resolved/month). The microaneurysm formation rate compare the degree of improvement or worsening of vision at baseline and 6 months. (value at 6 months minus value at baseline)
Measured: 6 months
The Microaneurysm Disappearance Rate
Number of MAs that resolved/month The MAs in individual retinas were evaluated at 6 months using fundus photography. The Retmarker (version 1.0.2 by Retmarker Ltd, Coimbra, Portugal) software was used for automatic measurement and analysis of changes in number and extent of MAs on fundus photographs and to calculate the total number and turnover of MAs. MA turnover was calculated by adding the MA formation rate (number of new MAs detected/month) to the MA disappearance rate (number of MAs that resolved/month). The microaneurysm disappearance rate compare the degree of improvement or worsening of vision at baseline and 6 months. (value at 6 months minus value at baseline)
Measured: 6 months
The Microaneurysm Turnover
The microaneurysm formation rate + The microaneurysm disappearance rate The MAs in individual retinas were evaluated at 6 months using fundus photography. The Retmarker (version 1.0.2 by Retmarker Ltd, Coimbra, Portugal) software was used for automatic measurement and analysis of changes in number and extent of MAs on fundus photographs and to calculate the total number and turnover of MAs. MA turnover was calculated by adding the MA formation rate (number of new MAs detected/month) to the MA disappearance rate (number of MAs that resolved/month). The microaneurysm turnover compare the degree of improvement or worsening of vision at baseline and 6 months. (value at 6 months minus value at baseline)
Measured: 6 months
Perifoveal Non-perfusion Area in FAG (mm²)
Using ImageJ software (version 1.52a) by FAG image. The Perifoveal non-perfusion area in FAG compare the degree of improvement or worsening of vision at baseline and 6 months. (value at 6 months minus value at baseline)
Measured: 6 months
Safety Parameters
Systemic adverse events (MI, CVA, etc), Ocular adverse events (retinal detachment, RPE tear, endophthalmitis, uveitis, vitreous hemorrhage, subretinal hemorrhage, cataract , IOP elevation, etc) at baseline and each visit.
Measured: 6 months
Timeline
From the start of the study to its completion; the mark is today. Estimated dates are the sponsor’s plan.
- First posted15 Jul 2016 (estimated)
- Study startAug 2016
- Primary completionFeb 2019
- Study completionDec 2019
Resources
- Official record on ClinicalTrials.govThe registry entry this page is built from, with its full change history.
- Posted resultsParticipant flow, outcome measures and adverse events reported by the sponsor.
- Publications (19)Papers the sponsor has linked to this study.
- Other trials for Nonproliferative Diabetic RetinopathyStudies of the same condition, open and under way.
- What the trial phases meanHow a treatment moves from first tests in people to approval.
More details
For doctors and researchers: how the study is designed, who runs it, and its registry IDs.
Study design
- Study type
- Interventional
- Phase
- Phase 4
- Primary purpose
- Other
- Allocation
- Not applicable
- Intervention model
- Single group
- Masking
- None (open label)
- Enrolment
- 25 participants (actual)
Sponsor and investigators
- Lead sponsor
- Wonkwang University Hospital
- Sponsor type
- University, hospital or other
- Collaborators
- Novartis Korea Ltd.
- Responsible party
- Principal investigator, Yun-Sik Yang, Wonkwang University Hospital
- Investigators
- Yunsik Yang, MD, Ph D, Study chair, Department of Ophthalmology, Wonkwang University School of MedicineSeungjoon Lee, MD, Ph D, Principal investigator, Study Official Affiliation should have no more than 80 characters.
IDs, dates and publications
- ClinicalTrials.gov ID
- NCT02834663
- Sponsor's protocol ID
- CRFB002DKR03T
- Status last verified
- May 2020
- First submitted
- 26 Jun 2016
- Last updated
- 22 May 2020
- Results posted
- Yes, on ClinicalTrials.gov
- Data monitoring committee
- No
- Individual data sharing
- No
Publications
Liinamaa MJ, Savolainen MJ. High vitreous concentration of vascular endothelial growth factor in diabetic patients with proliferative retinopathy using statins. Ann Med. 2008;40(3):209-14. doi: 10.1080/07853890701749209.
PubMed 18382886Noma H, Funatsu H, Yamasaki M, Tsukamoto H, Mimura T, Sone T, Hirayama T, Tamura H, Yamashita H, Minamoto A, Mishima HK. Aqueous humour levels of cytokines are correlated to vitreous levels and severity of macular oedema in branch retinal vein occlusion. Eye (Lond). 2008 Jan;22(1):42-8. doi: 10.1038/sj.eye.6702498. Epub 2006 Jul 7.
PubMed 16826241Crawford TN, Alfaro DV 3rd, Kerrison JB, Jablon EP. Diabetic retinopathy and angiogenesis. Curr Diabetes Rev. 2009 Feb;5(1):8-13. doi: 10.2174/157339909787314149.
PubMed 19199892Usui T, Ishida S, Yamashiro K, Kaji Y, Poulaki V, Moore J, Moore T, Amano S, Horikawa Y, Dartt D, Golding M, Shima DT, Adamis AP. VEGF164(165) as the pathological isoform: differential leukocyte and endothelial responses through VEGFR1 and VEGFR2. Invest Ophthalmol Vis Sci. 2004 Feb;45(2):368-74. doi: 10.1167/iovs.03-0106.
PubMed 14744874Hoeben A, Landuyt B, Highley MS, Wildiers H, Van Oosterom AT, De Bruijn EA. Vascular endothelial growth factor and angiogenesis. Pharmacol Rev. 2004 Dec;56(4):549-80. doi: 10.1124/pr.56.4.3.
PubMed 15602010Roy S, Ha J, Trudeau K, Beglova E. Vascular basement membrane thickening in diabetic retinopathy. Curr Eye Res. 2010 Dec;35(12):1045-56. doi: 10.3109/02713683.2010.514659. Epub 2010 Oct 7.
PubMed 20929292Hammes HP. Pericytes and the pathogenesis of diabetic retinopathy. Horm Metab Res. 2005 Apr;37 Suppl 1:39-43. doi: 10.1055/s-2005-861361.
PubMed 15918109Stitt AW, Gardiner TA, Archer DB. Histological and ultrastructural investigation of retinal microaneurysm development in diabetic patients. Br J Ophthalmol. 1995 Apr;79(4):362-7. doi: 10.1136/bjo.79.4.362.
PubMed 7742285Ribeiro ML, Nunes SG, Cunha-Vaz JG. Microaneurysm turnover at the macula predicts risk of development of clinically significant macular edema in persons with mild nonproliferative diabetic retinopathy. Diabetes Care. 2013 May;36(5):1254-9. doi: 10.2337/dc12-1491. Epub 2012 Nov 30.
PubMed 23204247Haritoglou C, Kernt M, Neubauer A, Gerss J, Oliveira CM, Kampik A, Ulbig M. Microaneurysm formation rate as a predictive marker for progression to clinically significant macular edema in nonproliferative diabetic retinopathy. Retina. 2014 Jan;34(1):157-64. doi: 10.1097/IAE.0b013e318295f6de.
PubMed 23792485Sjolie AK, Klein R, Porta M, Orchard T, Fuller J, Parving HH, Bilous R, Aldington S, Chaturvedi N. Retinal microaneurysm count predicts progression and regression of diabetic retinopathy. Post-hoc results from the DIRECT Programme. Diabet Med. 2011 Mar;28(3):345-51. doi: 10.1111/j.1464-5491.2010.03210.x.
PubMed 21309844Kohner EM, Sleightholm M. Does microaneurysm count reflect severity of early diabetic retinopathy? Ophthalmology. 1986 May;93(5):586-9. doi: 10.1016/s0161-6420(86)33692-3.
PubMed 3725317Nunes S, Pires I, Rosa A, Duarte L, Bernardes R, Cunha-Vaz J. Microaneurysm turnover is a biomarker for diabetic retinopathy progression to clinically significant macular edema: findings for type 2 diabetics with nonproliferative retinopathy. Ophthalmologica. 2009;223(5):292-7. doi: 10.1159/000213639. Epub 2009 Apr 16.
PubMed 19372723Photocoagulation treatment of proliferative diabetic retinopathy. Clinical application of Diabetic Retinopathy Study (DRS) findings, DRS Report Number 8. The Diabetic Retinopathy Study Research Group. Ophthalmology. 1981 Jul;88(7):583-600.
PubMed 7196564Ferrara N, Hillan KJ, Gerber HP, Novotny W. Discovery and development of bevacizumab, an anti-VEGF antibody for treating cancer. Nat Rev Drug Discov. 2004 May;3(5):391-400. doi: 10.1038/nrd1381. No abstract available.
PubMed 15136787
Study at a glance
From the registry record, last updated by the sponsor on 22 May 2020. Recruitment status is as the sponsor reported it: confirm with the study team.
- Official title
- Prospective, Single-center, Six-month Study of Intravitreal Ranibizumab for Macular Edema With Nonproliferative Diabetic Retinopathy: Effects on Microaneurysm Turnover and Non-perfused Retinal Area
- ClinicalTrials.gov ID
- NCT02834663
- Acronym / sponsor ID
- CRFB002DKR03T
- Conditions
- Nonproliferative Diabetic Retinopathy
- Keywords
- Nonproliferative diabetic retinopathy, Microaneurysms
- Phase
- Phase 4
- Study type
- Interventional
- Recruitment status
- Completed
- Enrolment
- 25 participants (actual)
- Lead sponsor
- Wonkwang University HospitalUniversity, hospital or other
- Collaborators
- Novartis Korea Ltd.
- Study start
- Aug 2016 (actual)
- Primary completion
- Feb 2019 (actual)
- Study completion
- Dec 2019 (actual)
- First posted
- 15 Jul 2016 (estimated)
- Results
- Posted 22 Apr 2020
Clinical summary
The research question as the sponsor registered it. This describes what the study plans to test, not what it found.
Title of study:
Effects of Ranibizumab to delay or regression non-proliferative diabetic retinopathy(NPDR) with DME assessed by microaneurysm changes: A pilot study Objectives Diabetic retinopathy (DR) is a major cause of visual impairment. Anti-vascular endothelial growth factors have demonstrated therapeutic benefits in diabetic macular edema (DME). We aimed to prospectively analyze the effects of early intensive treatment using intravitreal ranibizumab (IVR) injections in nonproliferative diabetic retinopathy patients with macular edema.
Primary objective:
To investigate other efficacy endpoints including other visual acuity, anatomical change in mild-to-moderate NPDR with DME after intravitreal Ranibizumab injection from baseline through 6 months after treatment.
Secondary objectives:
To compare microvascular changes assessed by microaneurysm counts and perifoveal non-perfusion area changes and safty in eyes of mild-to-moderate NPDR with DME after intravitreal Ranibizumab injection from baseline through 6 months after treatment.
Detailed description
Title of study:
Effects of Ranibizumab to delay or regression non-proliferative diabetic retinopathy(NPDR) with DME assessed by microaneurysm changes: A pilot study
Study Rationale:
Diabetic retinopathy is the leading disease that causes acquired vision loss after 20 by making diabetic macular edema and neovascularization. In recent young generation, as prevalence of type 2 diabetes is growing, the burden of sight-threatening retinopathy is increasing on trend.1 Pathologically, angiogenesis is a main cause that destroys the structure of the eye and induces the visual function disorder as VEGF playing an important role in increasing the migration and proliferation of endothelial cells and increasing the permeability of the blood vessels.2,3 VEGF is made from the endothelial cells of retinal tissue, perivascular cells, pigment endothelial cells by hypoxia. And hypoxic condition of intraocular tissues is a key regulator of intra ocular angiogenesis by VEGF, the balance between VEGF and angiogenesis inhibitors determines the neovascular proliferation in diabetic retinopathy.4 VEGF is also inducing the expression of cell-to-cell contact molecule (intracellular adhesion molecule-1, ICM-1) and the adhesion of leukocytes to help the inflammatory response5, as mediator which destroys the blood retinal barrier, affecting the protein of tight junctions, making a microaneurysm and increasing permeability of capillary, that makes the liquid leakage and macular edema.5,6 Microanuerysm is the earliest clinical manifestations, the saccular local lesion that perivascular cells protruding in damaged areas on the capillary wall. According to Stitt AW et al9, diabetic microaneurysm is non-functioning extrusion of the vascular system from the deep part of inner retinal capillary plexus.
It is sometimes disappeared by being blocked with blood clots, on the other hand, new microanerysm is occurred in the other vascular bed structure.
Through these changes, the investigators know the course of a diabetic retinopathy and it is known that the generation rate of microaneurysm is associated with the clinically significant progression of macular edema (CSME) in mild-to-moderate nonproliferative diabetic retinopathy .10,11 In addition, the number of microanerysm is an important prognostic indicator which can estimate the progression or regression of diabetic retinopathy, as predicting whether becoming better or worse in diabetic retinopathy.12 Kohner and Sleightholm13 describe this concept at first time in 1986, its association with the number of microvascular flow and the severity of diabetic retinopathy. In recent years it is reported that measuring the number of microaneurysm and the turnover rate associated with the appearance or disappearance of microaneurysm, are predictors in progression of diabetic retinopathy and macular edema.14 To delay the progression of diabetic retinopathy and to improve macular edema, the laser photocoagulation have been the important role.15 Although the laser photocoagulation have had treatment effect in the diabetic retinopathy by reducing the amount of VEGF in micraneurysm and by degenerating the neovascularization after laser therapy, there was a problem that has many limitations - peripheral visual field defects, night blindness, progression of macular edema etc., and that the disease does not cured in a good time because of limits of laser therapy due to cataract, vitreous hemorrhage and turbidity. As an alternative method to solve these limitations, there is an anti-VEGF therapy.6 According to a previous study result, intraocular injection of Bevacizumab inhibits occurring of neovascularization by blocking the VEGF receptor .17 Recently, several studies have been reported that when injected intravitreal anti-VEGF, macular edema is improved and neovascularization is inhibited, by reducing the leakage of neovascularization.3 Especially, Leicht SF et al18 reported the number of microaneurysms and turnover rate in NPDR(non-proliferative diabetic retinopathy) patients injected with Ranibizumab. And the result showed entire number of the microaneurysms and turnover rate are decreased, which could be mean the regression of diabetic retinopathy and it could decide the therapeutic effect.
On this study, through the fluorescein fundus angiography, the average number of microaneurysms was significantly decreased after intravitreal injection of anti-VEGF therapy (p<0.05). The decrease of 35.70±24.79% in the treatment group was statistically higher than 13.95±38.21% in the control group of the fellow eye (p<0.05).
The result is found because decreased concentration of intravitreal VEGF inhibits the progression of diabetic retinopathy, such as endothelial cell proliferation and endothelial cell damage on retinal capillary and perivascular cells.
Sjølie AK et al12 reported up-regulation of VEGF occuring microaneurysms causes endothelial cell proliferation and inflammation and effusion reaction, so anti-VEGF is effective in early diabetic retinopathy. But there is less effectiveness in late diabetic retinopathy as it reaches the non-changing point. Also Kohner EM et al19 reported diabetic retinopathy lesions are reversible and could be delayed in early diabetic retinopathy.
So far, changes of microaneurysms in late diabetic retinopathy is uncertain, and if there would be a finding according to anti-VEGF therapy, the investigators could get a clue of surrogate marker which represents treatment results in diabetic retinopathy.
This study was designed to find the clinical evaluation and reduction rate through fluorescein angiography as microaneurysm examination tools to research NPDR with DME treatment results assessed by microaneurysm counts, timely monitored with anti-VEGF therapy.
Objectives To evaluate the effects of intravitreal Ranibizumab injection on microvascular changes in eyes of mild-to-moderate NPDR with DME.
Primary objective:
To investigate other efficacy endpoints including other visual acuity, anatomical change in mild-to-moderate NPDR with DME after intravitreal Ranibizumab injection from baseline through 6 months after treatment.
Secondary objectives:
To compare microvascular changes assessed by microaneurysm counts and perifoveal non-perfusion area changes and safty in eyes of mild-to-moderate NPDR with DME after intravitreal Ranibizumab injection from baseline through 6 months after treatment.
Primary and secondary endpoints:
Primary endpoint:
To compare other visual acuity, anatomical changes after intravitreal Ranibizumab injection from baseline through 6 months after treatment.
- The changes in best corrected visual acuity (BCVA) using ETDRS chart. ii) The central macular thickness - Circle Diameters : 1 mm ETDRS by spectralis OCT ; Heidelberg Engineering.
Secondary endpoints:
To compare microaneurysmal changes and perifoveal non-perfusion area and safty after intravitreal Ranibizumab injection from baseline through 6 months after treatment.
- The total number of microaneurysm by fundus photo using Retmarker DR(version 1.0.2) software. ii) The microaneurysm formation rate : Number of new MAs detected/month. iii) The microaneurysm disappearance rate : Number of MAs that resolved/month. iv)The microaneurysm turnover. v) Perifoveal non-perfusion area in FAG (mm²) using ImageJ software (version 1.52a) by FAG image. vi) Safety parameters : Systemic adverse events (MI, CVA, etc), Ocular adverse events (retinal detachment, RPE tear, endophthalmitis, uveitis, vitreous hemorrhage, subretinal hemorrhage, cataract , IOP elevation, etc).
Methodology:
single center, prospective, interventional, one arm, pilot study
Evaluation Participants will be evaluated with a full ocular examination at each visit (VA measurement, tonometry, slit lamp exam). Fluorescein angiography (FA) will be performed at baseline, at 3 months after baseline and at the last visit(6 months after baseline), and OCT will be performed monthly (baseline and 1, 2, 3, 4, 5, 6 months from baseline).
The MAs and perifoveal non-perfused areas in individual retinas were evaluated at 6 months using fundus photography and FA imaging. The Retmarker (version 1.0.2 by Retmarker Ltd, Coimbra, Portugal) software was used for automatic measurement and analysis of changes in number and extent of MAs on fundus photographs and to calculate the total number and turnover of MAs.
Perifoveal non-perfused area was estimated using the early FA image (from each of the three examinations) in which both the vascular arch and the non-perfused area were clearly visualized. Subsequently, the ImageJ software (version 1.25a 23/04/2018 by ImageJ, USA) was used for scaling each image to 200 µm and for equalizing the contrast and sensitivity of each picture to the maximum possible extent, by auto-adjustment of brightness and contrast. The raw red-green-blue (RGB) images were then converted to 8-bit images, with the threshold set for optimal visualization of the non-perfused area. The same threshold was applied to all images of the same patient.
Result analysis The investigators compare the differences between at baseline, at 3 month, and at 6 month. Statistical analyses will be performed using SPSS ver.18.0 (SPSS Inc., Chicago, Il, USA). Kolmogorov-Smirnov test was applied to test for normality of sample group data. the paired T-test was used for comparative statistical analysis of these parameters. (BCVA, CRT, total number of MAs, MA formation rate, MA disappearance rate, MA turnover, and perifoveal non-perfused area)
Study design
- Primary purpose
- Other
- Allocation
- Not applicable
- Intervention model
- Single group
- Masking
- None (open label)
- Number of arms
- 1
| Arm | Type | Receives |
|---|---|---|
| Lucentis | Experimental | Drug: LucentisPatients were administered 0.5-mg IVR injections monthly for 6 months. |
Who may qualify
- Ages
- 40 years and older
- Sex
- All
- Healthy volunteers
- Not accepted
- Age groups
- Adult, Older adult
Key inclusion criteria (5 listed)
- Patients (Male \& female) ≥40 years of age
- Type 2 DM
- Best corrected visual acuity ≥ 20/200 (Snellen equivalent using Early Treatment Diabetic Retinopathy Study chart)
- central retinal thickness of ≥300 µm on optical coherence tomography
- nonproliferative diabetic retinopathy (NPDR) with diabetic macular edema
Key exclusion criteria (7 listed)
- proliferative diabetic retinopathy
- Vitreous hemorrhage
- previous history of vitreoretinal surgery, post-cataract operation status (≤4 months before participation in this study)
- prior treatment with anti-VEGF drugs, intraocular corticosteroids, and/or retinal laser application
- Uncontrolled hypertension.
Eligibility is decided by the study team after screening; this overview does not establish that a patient qualifies. Full inclusion and exclusion criteria.
Interventions
| Intervention | Type | Arms |
|---|---|---|
| LucentisAlso: Intravitreal Lucentis injectionLocal anesthesia with T-caine with Saline irrigation. Routine eye drap was done by potadine-cotton ball. Lucentis injected to vitreous cavity, finally dressing. | Drug | Lucentis |
Primary outcome
The Best Corrected Visual Acuity (BCVA)
Time frame: 6 months
BCVA was performed using the Early Treatment Diabetic Retinopathy Study (ETDRS) chart at baseline and 6 months. The BCVA compare the degree of improvement or worsening of vision at baseline and 6 months. (value at 6 months minus value at baseline)
Central Macular Thickness(CMT)
Time frame: 6 months
CRT was performed using OCT at each visit. The OCT measured at each visit was analyzed statistically. the CMT compare the degree of improvement or worsening of vision at baseline and 6 months. (value at 6 months minus value at baseline)
6 secondary outcomes
The Total Number of Microaneurysm
Time frame: 6 months
The Microaneurysm Formation Rate
Time frame: 6 months
The Microaneurysm Disappearance Rate
Time frame: 6 months
The Microaneurysm Turnover
Time frame: 6 months
Perifoveal Non-perfusion Area in FAG (mm²)
Time frame: 6 months
Safety Parameters
Time frame: 6 months
Results and safety
Loading the posted results from ClinicalTrials.gov…
Research links
- Official record on ClinicalTrials.govLast updated by the sponsor 22 May 2020.
- Posted resultsParticipant flow, baseline, all outcome measures and adverse events.
- Background: PubMed 18382886Liinamaa MJ, Savolainen MJ. High vitreous concentration of vascular endothelial growth factor in diabetic patients with proliferative retinopathy using statins. Ann Med. 2008;40(3):209-14. doi: 10.1080/07853890701749209.
- Background: PubMed 16826241Noma H, Funatsu H, Yamasaki M, Tsukamoto H, Mimura T, Sone T, Hirayama T, Tamura H, Yamashita H, Minamoto A, Mishima HK. Aqueous humour levels of cytokines are correlated to vitreous levels and severity of macular oedema in branch retinal vein occlusion. Eye (Lond). 2008 Jan;22(1):42-8. doi: 10.1038/sj.eye.6702498. Epub 2006 Jul 7.
- Background: PubMed 19199892Crawford TN, Alfaro DV 3rd, Kerrison JB, Jablon EP. Diabetic retinopathy and angiogenesis. Curr Diabetes Rev. 2009 Feb;5(1):8-13. doi: 10.2174/157339909787314149.
- Background: PubMed 14744874Usui T, Ishida S, Yamashiro K, Kaji Y, Poulaki V, Moore J, Moore T, Amano S, Horikawa Y, Dartt D, Golding M, Shima DT, Adamis AP. VEGF164(165) as the pathological isoform: differential leukocyte and endothelial responses through VEGFR1 and VEGFR2. Invest Ophthalmol Vis Sci. 2004 Feb;45(2):368-74. doi: 10.1167/iovs.03-0106.
- Background: PubMed 15602010Hoeben A, Landuyt B, Highley MS, Wildiers H, Van Oosterom AT, De Bruijn EA. Vascular endothelial growth factor and angiogenesis. Pharmacol Rev. 2004 Dec;56(4):549-80. doi: 10.1124/pr.56.4.3.
- Background: PubMed 20929292Roy S, Ha J, Trudeau K, Beglova E. Vascular basement membrane thickening in diabetic retinopathy. Curr Eye Res. 2010 Dec;35(12):1045-56. doi: 10.3109/02713683.2010.514659. Epub 2010 Oct 7.
- Background: PubMed 15918109Hammes HP. Pericytes and the pathogenesis of diabetic retinopathy. Horm Metab Res. 2005 Apr;37 Suppl 1:39-43. doi: 10.1055/s-2005-861361.
- Background: PubMed 7742285Stitt AW, Gardiner TA, Archer DB. Histological and ultrastructural investigation of retinal microaneurysm development in diabetic patients. Br J Ophthalmol. 1995 Apr;79(4):362-7. doi: 10.1136/bjo.79.4.362.
- Background: PubMed 23204247Ribeiro ML, Nunes SG, Cunha-Vaz JG. Microaneurysm turnover at the macula predicts risk of development of clinically significant macular edema in persons with mild nonproliferative diabetic retinopathy. Diabetes Care. 2013 May;36(5):1254-9. doi: 10.2337/dc12-1491. Epub 2012 Nov 30.
- Background: PubMed 23792485Haritoglou C, Kernt M, Neubauer A, Gerss J, Oliveira CM, Kampik A, Ulbig M. Microaneurysm formation rate as a predictive marker for progression to clinically significant macular edema in nonproliferative diabetic retinopathy. Retina. 2014 Jan;34(1):157-64. doi: 10.1097/IAE.0b013e318295f6de.
- Background: PubMed 21309844Sjolie AK, Klein R, Porta M, Orchard T, Fuller J, Parving HH, Bilous R, Aldington S, Chaturvedi N. Retinal microaneurysm count predicts progression and regression of diabetic retinopathy. Post-hoc results from the DIRECT Programme. Diabet Med. 2011 Mar;28(3):345-51. doi: 10.1111/j.1464-5491.2010.03210.x.
- Background: PubMed 3725317Kohner EM, Sleightholm M. Does microaneurysm count reflect severity of early diabetic retinopathy? Ophthalmology. 1986 May;93(5):586-9. doi: 10.1016/s0161-6420(86)33692-3.
- Individual participant dataSharing planned: No
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Referral and contact
AzTrials does not enrol participants or take referrals. Contact the study team or a site listed below; they decide who can take part. This study is not recruiting at the moment.
Yunsik Yang, MD, Ph D study chair
Department of Ophthalmology, Wonkwang University School of Medicine
Seungjoon Lee, MD, Ph D principal investigator
Study Official Affiliation should have no more than 80 characters.
Questions about this trial
What is this clinical trial studying?
A Phase 4 study testing Lucentis in people with Nonproliferative Diabetic Retinopathy, run by Wonkwang University Hospital.
The full registered description is in the About this study section and the official record.
Who may be eligible to take part?
The sponsor lists 5 inclusion and 7 exclusion criteria. Eligibility is decided by the study team after screening, so read the full criteria and contact a listed site.
Is this clinical trial currently recruiting?
The record says: finished, as of the sponsor's last update on 22 May 2020. Status can change between updates, so confirm with the study contact before making plans.
What are the possible benefits and risks?
They depend on the study and the treatment, and no study can promise a benefit. The study team explains the known risks during informed consent, before anyone joins; the record itself does not list them.
What does this phase mean?
Phase 4 studies take place after a treatment is approved, to learn more about its long-term benefits and risks in everyday use.
Not every study follows the same path, and some studies (observational studies, device studies) have no phase.
Are results available for this study?
Yes. Results are posted in the registry (first posted 22 Apr 2020). A summary is in the For doctors view, and the full results are on ClinicalTrials.gov.
How can a doctor refer a patient or contact the research team?
The record lists no contact. The official record names the sponsor, who can be asked directly. AzTrials does not enrol participants or take referrals.
What does the primary outcome measure?
The Best Corrected Visual Acuity (BCVA) (time frame: 6 months). The study lists 2 primary outcomes in all. It is what the study was designed to measure, not a finding.
Where can I read the original study information?
On the ClinicalTrials.gov record for NCT02834663, which also lists 19 linked publications.
Does a listing mean the treatment is approved or proven to work?
No. A listing means the study is registered. It does not show that the treatment is safe, works, or is approved by a regulator.
How often is this information updated?
AzTrials copies changed records from ClinicalTrials.gov every night and reloads the whole registry every week. The sponsor last updated this record on 22 May 2020.