Eyes with a refractive error of more than − 6 diopters or an axial length of more than 26.5 mm and with typical pathologic changes at fundus are defined as having pathologic myopia (PM).1 A recent systematic review has indicated that the prevalence of PM is 1–3% in adults, and that 5–11% of patients with PM develop CNV.2 Several of the phenotypic features of PM are associated with increased risk of myopic choroidal neovascularisation (mCNV)—these include patchy atrophy, lacquer cracks,3 thinning of the choroid and choriocapillaris,4 and CNV in the other eye.5 Choroidal neovascularisation (CNV) is the sight-threatening complication occurring in approximately 5.2–10.2% of highly myopic eyes.6,7 CNV is one of the most common causes of irreversible central vision loss, deteriorates quality of life, and generates huge socioeconomic burdens. CNV secondary to PM has a very high incidence in Asian populations, and it mainly affects the population aged 40 and above.8 The traditional therapeutic modalities for CNV secondary to PM include thermal laser photocoagulation, surgical management, transpupillary thermotherapy, and photodynamic therapy with verteporfin. Verteporfin photodynamic therapy has been an established treatment for sub-foveal mCNV for many years; however, this treatment is not satisfactory in restoring visual acuity and is associated with long-term chorioretinal atrophy. In recent years, anti-vascular endothelial growth factor (anti-VEGF) agents in patients with mCNV have demonstrated substantial visual acuity gains, and the quality of life of patients undergoing anti-VEGF therapy has increased compared with photodynamic therapy.
The anti-VEGF agents have been proposed as the first-line therapy for sub-foveal and juxtafoveal CNV secondary to PM.9 Administration of anti-VEGF biological agents, including ranibizumab, aflibercept, and conbercept has demonstrated promising outcomes in recent years.
Idiopathic choroidal neovascularisation (iCNV) is defined as CNV occurring in patients younger than 50 years without detectable primary ocular or systemic diseases, including PM, angioid streak, trauma, or other inflammatory or hereditary disorders.10,11 iCNV is a distinct clinical entity that accounts for 17% of cases12 of CNV in patients less than 50 years old. Treatments including intravitreal and subtenon steroids, transpupillary thermotherapy, surgical removal, and photodynamic therapy with verteporfin13,14 have varying success in preventing visual loss in patients with iCNV. The visual prognosis and natural progression of iCNV are more favourable than those of CNV in age-related macular degeneration (AMD), and patients suffering from iCNV respond well to anti-VEGF therapy. Anti-VEGF regimens are effective in improving visual acuity, reducing metamorphosis, and reducing central retinal thickness compared to traditional modalities. These anti-VEGF agents have become the first-line treatment for mCNV and iCNV. Conbercept (or KH902, Lumitin; Chengdu Kang Hong Biotech Co, Ltd., Sichuan, People’s Republic of China) is an anti-VEGF multitarget drug developed in China for intraocular injection. It can bind to all isoforms of VEGF-A, VEGF-B, and placental growth factors. Conbercept is larger than aflibercept and contains a fourth binding domain of VEGFR-2. It has several advantages, including a lower VEGF dissociation rate, higher binding affinity, lower isoelectric point, and longer clearance time. Since conbercept was approved by the China State Food and Drug Administration (FDA) in 2013 for the treatment of neovascular AMD, diabetic macular oedema, and CNV in pathological myopia, it has become one of the most commonly used anti-VEGF drugs in China.15–17 Zhang et al.18 found that conbercept inhibited the VEGF-induced proliferation of human umbilical vein endothelial cells in a dose-dependent manner. Intravitreal injection of high-dose conbercept (300 µg and 500 µg) significantly reduced neovascular leakage, as examined by fluorescence fundus angiography and optical coherence tomography (OCT), and prevented the formation of fibrovascular membranes, as revealed by tissue staining. More importantly, multifocal ERG showed improvement in visual function after the administration of high-dose conbercept. In a cohort study, the same research group demonstrated a significant improvement in the leakage of laser-induced CNV after monkeys in the control group were switched to the conbercept treatment group, suggesting the therapeutic effects of conbercept on pre-existing laser-induced CNV in animals.19
As with any general intraocular operation, intravitreal injection of anti-VEGF agents is associated with risks of infection, bleeding, glaucoma, and cataracts.20 The risk of retinal damage after intravitreal injections is increased in myopic eyes, where degenerative changes at the posterior segment may have already existed.21 Comprehensive ophthalmic tests should therefore be performed in myopic patients prior to intravitreal injections.
It is now recognised that mCNV can occur at any degree of myopia and in eyes without typical myopic degenerative fundus changes.22,23 The mechanical theory is based on the assumption that the progressive and excessive elongation of the anteroposterior axis causes mechanical stress on the retina, leading to an imbalance between pro-angiogenic and anti-angiogenic factors, resulting in mCNV.24 The heredodegenerative theory states that myopic refractive errors are genetically predetermined.25, 26, 27 In support, studies have shown that single nucleotide polymorphisms in several genes (e.g. pigment epithelium-derived factor) are associated with the development and progression of mCNV.28 29 30
This study, we retrospectively reviewed the records of 20 consecutive eyes with mCNV and 18 consecutive eyes with iCNV which were treated with intravitreal conbercept and were followed up for 24 months. All eyes underwent two monthly injections, followed by an additional injection based on monthly visits.