CNV相关知识
CNV(Choroidal neovascularization,脈絡膜新生血管)類型：
【1】中CNV被分為4種：
| CNV類型 | CNV癥狀 | 人群比例【3】 | 人群比例【4】 | 經VEGF治療， BCVA惡化比例 |
| 隱匿型【1】 | 新生血管膜在RPE下方 | 40% | 47% | 27.9% |
| 經典型【1】 | 刺破RPE，損害神經感覺視網膜 | 9% | 12% | 30.0% |
| 視網膜血管瘤增生【1】 | 34% | 24.1% | 【1】中沒有研究 | |
| 前面兩種的組合【1】 | 分別位于RPE下方和刺破RPE | 17% | 16.9% | 4.2% |
BCVA：
best-corrected visual acuity（最佳矯正視力）
The minimally classic type(指的是上述表格中的類型4)?of CNV demonstrated a poorer functional and anatomical response to treatment. So, the CNV type can be a predictor to the change of BCVA after anti-VEGF treatment.【3】
?It is estimated that 1.4 million people have CNV in the United States every year3,4. In addition, CNV causes blindness in approximately 7 million people worldwide5. To date, there are no eye drops for CNV treatment, and this is an important unmet medical need.
討論了nalfurafine抑制CNV的作用【5】
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?In fact, inflammation represents the third most common cause of choroidal neovascularization (CNV), behind age-related macular degeneration (AMD) and pathologic myopia [1]. Regardless of the aetiology, what these entities have in common is a disruption in Bruch's membrane combined with an inflammatory and angiogenic cascade [3]. Endothelial and inflammatory cell invasion leads to the formation of neovascular membranes with associated leakage and haemorrhage and, consequently, a variable degree of vision loss [1, 3].【6】
（炎癥、近視、黃斑變性）是導致CNV的三大原因
炎癥性CNV分為感染性和非感染性兩種：
| CNV類型 | 致病原因 |
| 感染性 | Multiple evanescent white dot syndrome（多發性消失性白點綜合征） |
| 非感染性 | Tuberculosis（肺結核） |
Nevertheless, the risk of developing CNV in patients with these conditions varies considerably [4]. I-CNV is better documented in noninfectious than in infectious etiologies [1]
（然而，患有這些疾病的患者發生CNV的風險差異很大[4]。I-CNV在非感染性疾病中的記錄比在感染性疾病中的記錄更好[1]）
Even though CNV is a relatively rare complication of inflammatory diseases, it can result in severe vision loss and it has a big impact on patients' work ability and productivity, since it happens commonly during active years [4–6]. This correlates with the incidence of uveitis, which also tends to affect a younger population [4]. Usual presenting symptoms are distortion and metamorphopsia, which can be accompanied by decreased visual acuity or scotoma [1]. Yet, many patients are asymptomatic, so new-onset neovascular membranes are often diagnosed by imaging techniques during follow-up of their inflammatory condition [4].
?In fact, in I-CNV, there are two disease processes we aim to control: neovascularization itself and the underlying inflammatory cause. It is consensual nowadays that a combined approach with both local and systemic therapies results in better disease control and overall visual prognosis. Accordingly, intravitreal anti-VEGF agents, such as bevacizumab, aflibercept, and ranibizumab, in association with systemic immunosuppressive/anti-inflammatory drugs, with or without corticosteroids, are now the standard of care for these patients. As a matter of fact, directly addressing the inflammatory environment, which is itself the root of I-CNV formation, will probably terminate the angiogenic drive, therefore leading to better outcomes [1, 5]. Other therapies, such as photodynamic therapy (PDT) with verteporfin, can also be used to manage the disease [1].（事實上，在I-CNV中，我們旨在控制兩種疾病過程：新生血管本身和潛在的炎癥原因。如今，人們一致認為，結合局部和全身治療的方法可以更好地控制疾病和改善整體視覺預后。因此，玻璃體內抗血管內皮生長因子藥物，如貝伐單抗、阿曲貝西普和雷尼珠單抗，與全身免疫抑制/抗炎藥物聯合使用，加或不加皮質類固醇，現在是這些患者的標準護理。事實上，直接解決炎癥環境本身就是I-CNV形成的根源，這可能會終止血管生成驅動，從而導致更好的結果[1,5]。其他療法，如維特泊芬光動力療法（PDT），也可用于治療該疾病[1]。）
3.5. Systemic Treatment（全身治療）
From all 17 patients, 10 received oral corticosteroids (58.82%).
Only one patient had intravenous corticosteroids (P16, 5.88%). He had oral and intravenous prednisolone in Brazil to treat Vogt–Koyanagi–Harada disease. One patient (P8, 5.88%) was treated with intravitreal CCTs (triamcinolone) to help control PIC/MFC activity.
Oral immunosuppressive therapy was used in 6 patients (35.29%): 5 (P4, P8, P11, P12, and P13) had cyclosporin and 1 (P14) had methotrexate. P4 changed immunosuppressive treatment from cyclosporin to azathioprine because of cyclosporine adverse effects. He afterwards initiated treatment with biologic therapy using adalimumab due to severe refractory disease and high risk of central vision loss. He was the only patient in our study receiving biologic therapy.
Absence of systemic treatment can be explained, on the one hand, because the inflammatory condition stayed inactive during follow-up in some patients. On the other hand, in patients belonging to the infectious group, direct treatment of infection would almost certainly control the inflammatory process. In fact, none of the two patients (P15 and P17) belonging to the infectious aetiology subgroup were treated with corticosteroids.
Regarding the infectious etiologies, P15 did not receive specific therapy to treat toxoplasmosis, since this condition was inactive at presentation and during follow-up. In contrast, P17 presented with a recrudescence from a previous Nocardia infection, this time with eye involvement. An anti-Nocardia therapy was used, specifically a combined therapy of trimethoprim-sulfamethoxazole (TMP-SMX) and a beta-lactam antibiotic. The patient was hospitalised for systemic study, so he underwent intravenous treatment with TMP-SMX and a carbapenem firstly and ceftriaxone secondly. Oral treatment was then continued for 12 months with TMP-SMX and cefixime.
Complications included cataract and ocular hypertension. Cataract was seen in 6 patients (P1, P3, P5, P6, P13, and P14). Five had bilateral cataract and one (P13) had unilateral on the left side. Three patients underwent phacoemulsification with intraocular lens implantation (P5, P6, and P14).
Four patients (P4, P6, P11, and P14) developed ocular hypertension. All were treated using topical medication. P16 also underwent trabeculectomy and cyclophotocoagulation.
Details about CNV recurrence, treatment suspension, and complications are described in Supplementary Tables 2 and 3 (see Supplementary Material).
Practically all patients, except for one, presented with posterior uveitis. Other studies have reported CNV occurring more commonly in posterior and panuveitis [4]. Choroidal neovascularization had a predominant subfoveal location (12 eyes), followed by juxtafoveal (7 eyes) and peripapillary locations (1 eye).
I-CNV had a symptomatic presentation in the majority of the affected eyes (85%). Reported symptoms in our patients were compatible with typical CNV symptoms, for instance, metamorphopsia, vision loss, and scotoma [1]. This high incidence of CNV-related symptoms may be associated with the predominant subfoveal location of the neovascular membranes, in addition to the low mean age of the sample and alleged good previous visual acuities. Nevertheless, some eyes with I-CNV were only found through ancillary imaging, while they were being followed either for their primary inflammatory condition or for CNV in the contralateral eye. As a matter of fact, an active inflammatory state and a prior CNV diagnosis in the contralateral eye have been reported as increasing risk factors for CNV development [4]. Therefore, patients with ocular inflammatory conditions or already with I-CNV in the contralateral eye must have a tight follow-up to guarantee prompt diagnosis and treatment.
Adequate individualised treatment prevents disease progression and additional visual loss [5]. In fact, if choroidal neovascularization is adequately and opportunistically addressed and inflammatory pathology is concomitantly managed, it is possible to stabilise or even improve patient's visual acuity from their nadir at the time of CNV presentation/decompensation [5, 8]. In our study, CNV was approached with intravitreal anti-VEGF injections and uveitis was treated with anti-inflammatory/immunosuppressive agents (i.e., corticosteroids and cyclosporin). Several studies have shown the benefit of intravitreal anti-VEGF therapy in patients with CNV secondary to various inflammatory aetiologies. For instance, a retrospective multicentre case series of patients with I-CNV was one of the early and largest studies demonstrating the benefit of bevacizumab in CNV regression and significant visual improvement. In this study, from 76 eyes with I-CNV, 58 improved, 15 registered no change, and 3 worsened their visual acuities after intravitreal bevacizumab. Additionally, visual improvement was significant in punctate inner choroidopathy, multifocal choroiditis, and Vogt–Koyanagi–Harada disease [15].
We found a wide variation in the number of performed intravitreal anti-VEGF injections (range: 2 to 111, median: 7 injections). Some patients were able to stabilise the disease with a smaller number of injections, whereas others needed a substantially greater number. I-CNV recurrence was seen in 15% of eyes. This percentage seems to be lower than in myopic CNV or neovascular AMD [17–20]. In fact, since CNV was secondary to an inflammatory aetiology, managing the primary disease with an anti-inflammatory/immunosuppressive approach allows better disease control, reducing recurrence and need for anti-VEGF injections. In comparison, in a previous retrospective study of CNV secondary to PIC, the authors compared 14 eyes treated with ranibizumab monotherapy with 10 eyes treated with a combination of corticosteroids and ranibizumab. Patients treated with a combined approach received fewer ranibizumab injections, had a greater mean visual acuity improvement, and never recurred, compared with the ranibizumab monotherapy group [21].
Additionally, 25% of eyes maintained treatment during all follow-up period, never suspending anti-VEGF therapy. In one of these cases, I-CNV had been diagnosed only 10 months before, so we can speculate that more time would be needed to achieve CNV remission. All the other 4 cases had more than 3 years of follow-up. This significant variability between patient's responses to treatment emphasises the importance of an individual on demand approach, which had also been proven effective in other studies [8, 9, 22].
Follow-up in our care centre required frequent consultation with continuous patient evaluation. This allowed detection and immediate management of active CNV through patients de novo symptoms and suggestive imaging findings. Median follow-up time was 46 months, ranging from 10 to 188 months.
Complications seen in our sample were cataract and ocular hypertension. Cataract development correlated with a higher mean number of anti-VEGF intravitreal injections (35 versus 7, p=0.031).
上面內容來自【6】
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下面內容來自【7】
The appearance of CNV in posterior uveitis on FA has not been as well characterized. CNV lesions on FA present with early iso- or hyperfluorescence with late leakage (Fig. 1) [32]. The presence of surrounding mild hemorrhage causing masking effect on FA may also lead to the diagnosis of CNV. However, the inflammatory retinochoroidal lesions of posterior uveitis may present with markedly similar findings making the differentiation very challenging. Active uveitic chorioretinal lesions show early isofluorescence (but mostly hypofluorescent) with late leakage. On the other hand, inactive atrophic lesions show early hypo-/isofluorescence with late staining (indicating RPE window defect) without any leakage [1–3]. Thus, there are very subtle differences in the appearance of FA between CNV lesions and active/inactive retinochoroidal inflammatory lesions. In the presence of extensive retinal involvement resulting in scars and pigmentary changes, which may happen in conditions like multifocal choroiditis, serpiginous choroiditis, and VKH disease, the detection of hyperfluorescence due to CNV may be very challenging.
Corticosteroid therapy
Mechanism of action Corticosteroids have been used for decades and still represent the commonest choice in the treatment of uveitis due to their strong and rapid anti-inflammatory effects [99]. In addition to the inhibition of pro-inflammatory factors, transcription and the suppression of prostaglandin and interleukin synthesis, corticosteroids interfere with the effects of VEGF [100, 101]. Reducing the VEGF stimulus to the growth of new vessels and decreasing inflammation, the primary cause for VEGF release, these drugs remain a valuable option for the treatment of i-CNVs.
Role of oral corticosteroids Before anti-VEGF agents became available, corticosteroid therapy was the only medical option for the treatment of CNVs [102]. Patients were usually treated with a course of 1 mg/kg/day of oral corticosteroid for approximately 7 days followed by slow tapering. With this approach, several authors reported stabilization of visual acuity in more than 80% of the patients affected by subfoveal i-CNVs [2, 102]. High-dose systemic corticosteroids can control ocular inflammation as well as the stabilization of i-CNV lesions in patients with posterior uveitis.
Local and intravitreal corticosteroids High-dose systemic corticosteroids are limited by their adverse effect profile. Martidis et al. conducted a study comparing high-dose (1 mg/kg) oral prednisolone and a single sub-Tenon injection of triamcinolone acetonide for subfoveal i-CNV due to POHS [102]. In this study, oral prednisone resulted in a short-term improvement in visual acuity, which stabilized over longer follow-up. Sub-Tenon’s triamcinolone group achieved similar final stabilization without the initial improvement. Rechtman et al. also evaluated the use of intravitreal triamcinolone acetonide in ten patients with POHS [103]. Thirty percent patients showed improvement, whereas 50% showed stabilization in visual acuity. Intravitreal dexamethasone implant (Ozurdex?) has not been employed in the management of i-CNV yet.
Combination therapies with corticosteroids
Local [104] or systemic [105, 106] steroid treatment have been combined with photodynamic therapy (PDT), allowing for a decrease in the number of PDT sessions and, for the first time, to achieve an improvement in visual acuity. Intravitreal corticosteroids (triamcinolone acetonide) has been combined with bevacizumab for recurrent i-CNV in VKH disease in a case report by Pai et al. [107] The authors demonstrated complete resolution of i-CNV and ocular inflammation after combined therapy and systemic steroids until 1 year after follow-up.
When VEGF agents demonstrated favorable results in patients affected by i-CNV (both in terms of visual outcomes and their side-effect profile) [45], the use of corticosteroids alone or associated with PDT for the treatment of this condition has gradually decreased. Despite this, with inflammation being the primary trigger for VEGF increase and consequent CNV development in uveitis, corticosteroids are still considered a valuable option in the management of these conditions.
Limitations of the use of corticosteroids There are currently no data available from randomized controlled clinical trials comparing the efficacy of anti-VEGF agents alone versus corticosteroids alone or as a combined therapy. A proper guideline on the use of corticosteroids in i-CNVs is conspicuously absent. In the face of uncertainty, the wisest approach seems to be to control the inflammatory stimulus by the use of systemic steroids [1] while simultaneously treating the neovascular component with intravitreal injections of anti-VEGFs [19].
Immunosuppressive therapy
Pre-clinical evidence and mechanism of action Various corticosteroid-sparing immunosuppressive agents have been used as an off-label therapy in patients with uveitis. As discussed in the preceding sections, most cases with uveitis and i-CNVs are managed using systemic/local corticosteroids and anti-VEGF injections. However, there are situations where corticosteroids may be relatively contraindicated, such as patients with impaired steroid responsiveness or patients with a history of severe systemic/ocular corticosteroid-related adverse events. Immunosuppressive agents, by the virtue of their anti-inflammatory action, can curb angiogenesis and therefore limit the development of CNV.
In an experimental study of laser-induced CNV in mice, the role of tumor necrosis factor (TNF)-α receptors was evaluated [108]. CNV was induced in TNF-α receptor 1a and 1b (?/?) mice and the expression of TNF-α in the RPE, and the choroid was determined using western blot analysis. In this experiment, it was observed that TNF-α levels were elevated in the chorioretinal tissue in mice with CNV. The absence of TNF-α receptors increased endothelial cell apoptosis and led to a reduced inflammatory cellular response [108]. This experiment provides a preclinical evidence of the use of anti-TNF-α agents in the management of i-CNV. In a murine model of laser-induced i-CNVs, the anti-TNF-α agents (etanercept and infliximab) were shown to be effective in decreasing the CNV size and leakage on fluorescein angiography compared to the control group [109]. These experiments support the role of immunosuppressive agents such as TNF-α in the management of i-CNVs. At optimal doses, intravitreal injection of infliximab (an anti-TNF-α agent) in experimentally induced CNV has been demonstrated to reduce the area of CNV and decrease the levels of VEGF (by ELISA and immunofluorescence testing) without any cytotoxic effects on the RPE [110].
Systemic immunosuppressive therapy Systemic immunosuppressive therapy can result in resolution of i-CNV. A case report published in 1998 by Kilmartin et al. demonstrates a case of a 3-year-old boy with sympathetic ophthalmia who developed i-CNV resulting in the worsening of visual acuity. Systemic cyclosporin resulted in the stabilization of the lesion with resolution of associated edema and hemorrhage [111]. In a series by Dees et al., 14 patients (17 eyes) with i-CNV and posterior uveitis were enrolled, of which 3 had extrafoveal CNV, 6 had juxtafoveal CNV, and 8 had subfoveal CNV. Of the 11 patients that received systemic immunosuppressive therapy with agents such as cyclosporin, CNV resolved in most eyes [112]. Neri et al. performed a prospective open-label interventional study evaluating the efficacy of systemic corticosteroids and mycophenolate mofetil for controlling juxta/sub-foveal i-CNV, unresponsive to traditional immunosuppressive therapy. Of the 12 eyes (9 patients), all patients showed stable or reduced lesion size at 12 months [113]. Ganesh et al. studied a large series of 49 eyes (43 patients) with i-CNV. The authors managed 17 eyes with systemic immunosuppressive therapy with favorable results [114].
Immunosuppressive therapy may also be combined with other forms of therapy such as PDT. In a retrospective study by Hogan et al., of the 6 patients, 2 with subfoveal i-CNV were treated with systemic immunosuppression (oral mycophenolate mofetil). This approach was effective in decreasing the fluorescein angiographic leakage from i-CNVs. The authors showed that combination PDT and systemic immunosuppression was a useful therapeutic option [115]. Systemic methotrexate has also been used in combination with intravitreal ranibizumab in a patient with VKH disease complicated by i-CNV [116]
Advantages and limitations of the use of immunosuppressive agents Knowledge of the use of immunosuppressive agents for i-CNVs is increasing with passing time. However, there are no clear guidelines on the use of these agents, nor on the choice of agents for managing i-CNVs. The exact mechanisms by which immunosuppressive therapies act on the CNV is not yet clear. Therefore, further studies that evaluate the efficacy of immunosuppressive therapies (systemic and/or local) that highlight the choice of the agent, timing and number of injections, and outcome measures are necessary.
Since there are no guidelines on the use of anti-VEGF, corticosteroid or immunosuppressive therapies for i-CNV, a randomized clinical trial is necessary. In the context of uveitic macular edema, where a similar dilemma exists, the National Eye Institute (NEI) is currently recruiting patients in a multicenter clinical trial, Macular Edema Ranibizumab versus Intravitreal Anti-inflammatory Therapy Trial (MERIT), to evaluate the relative efficacy and safety of intravitreal methotrexate, intravitreal ranibizumab, and the intravitreal dexamethasone implant [118]. A similar approach is needed for the management of i-CNVs.
Other therapeutic strategies Other various therapeutic strategies have been used in the literature in the management of i-CNVs. These have been summarized in the following sections.
Photodynamic therapy As mentioned in the preceding sections, PDT has been variably used in the management of CNV associated with uveitis, often combining it with anti-VEGF therapy or corticosteroids. The consensus of the use of PDT alone is that it can stabilize but can rarely improve the visual acuity. PDT with verteporfin has been used in the monotherapy of CNV associated with serpiginous choroiditis, POHS, and PIC [119–121]. In a prospective pilot study of 19 patients with i-CNV, standard PDT with verteporfin was performed for patients with diagnoses of PIC, POHS, and multifocal choroiditis. The authors suggested that PDT may perform better in CNV due to ocular inflammation compared to AMD over a period of 1 year [122]. However, the exact reasons for this is not clear.
Long-term results of PDT have been extensively studied in CNV lesions occurring in association with toxoplasma retinochoroiditis. In a study of 8 patients, classic or predominantly classic CNV was treated using PDT. Persistent CNV regression was achieved in all the patients at 2 years [123]. Neri et al. evaluated the long-term (4-year) outcome of PDT in CNV lesions associated with toxoplasmosis in 9 patients. The authors observed stable/improved visual acuity and stabilized CNV diameters after PDT at 4 years’ follow-up [124]. In other case reports, PDT has been combined with either bevacizumab or with intravitreal triamcinolone acetonide in the treatment of CNV associated with toxoplasmosis [125, 126].
PDT has also been employed in the management of CNV lesions associated with other pathologies such as VKH disease [127, 128]. Nowilaty et al. performed PDT in six eyes of 6 patients with VKH disease who developed CNV. Three eyes showed the development of submacular fibrosis. All the eyes showed stabilization of visual acuity and CNV lesions [127]. However, in another case report, retinal pigment epithelial alterations raised concerns following PDT for CNV associated with VKH disease [128].
Among patients with multifocal choroiditis, PDT has been performed either as a monotherapy [129] or in combination with immunosuppression [115] or anti-VEGF agents [130]. In all these series, PDT was associated with stabilization of CNV and visual acuity. In summary, PDT is rarely used as monotherapy for managing i-CNV in the present times.
Surgical excision Surgical excision of CNV lesions was a historical treatment modality that has gone out of favor in the modern era. This treatment option was selected by ophthalmologists when the sole alternative therapy was laser photocoagulation, which often resulted in visual loss. In a series of 43 eyes of 40 patients with CNV not to related AMD by Benson et al., surgical excision of the subfoveal CNV lesions was performed. In this series, 79% patients showed either improved or unchanged visual acuity following surgery. Recurrence of CNV was noted in 23% eyes for whom repeat surgery was performed [131]. CNV lesions in toxoplasma retinochoroiditis [132] and candida endophthalmitis [133, 134] have been also treated using submacular surgery.
In the era of anti-VEGF therapy, submacular surgery has not found popularity. Thus, this treatment option is no longer preferred and very rarely, if ever, employed in present-day clinical practice.
Many treatment modalities are available in the management of i-CNV associated with uveitis. The general principle of treatment is to limit the inflammatory response with corticosteroids and/or immunosuppressive agents. If the inflammation is unilateral, local therapies such as intravitreal dexamethasone implant, methotrexate, or triamcinolone acetonide can be considered, which can also help to reduce the size of the CNV lesion. Anti-VEGF agents are highly efficacious and are usually employed as the first-line agents for treating CNV associated with uveitis, keeping in mind that the inflammation needs to be controlled for the best outcome and reduction of recurrences. PDT is uncommonly used in the anti-VEGF era due to its limitations in improving visual acuity and potential adverse effects. In the future, novel anti-inflammatory agents and immunosuppressive agents, including intravitreal injections, may become available for the management of i-CNV.
上面內容來自【7】
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Features of inflammatory choroidal neovascularization (CNV) commonly associated with infectious uveitis（炎癥性脈絡膜新生血管（CNV）的特征通常與感染性葡萄膜炎有關）
| Prevalence | Frequent; present in majority cases | Estimated between 0.3–19% | Uncommon; prevalence not known | Only few cases (<?5) reported |
| Location of CNV | CNV is seen at the edge of a pre-existing scar in the macular or peripapillary region | CNV typically grows close to the edge of an atrophic chorioretinal scar | CNV is typically adjacent to the healed choroidal granuloma or to a healed choroiditis scar | CNV is adjacent to chorioretinal scars |
| Morphology of CNV | Active lesions have a disciform appearance at the macula, with a green-gray subretinal lacy discoloration and surrounding pigment. Inactive CNV appears as a white disciform scar with fibrovascular tissue | Active CNV appears as an outer retinal lesion close to the scar with associated hemorrhages and intra- or subretinal fluid. | CNV may present as a subretinal lesion with hemorrhages and intra- or subretinal fluid. Rarely, type 1 CNV may be detected only using imaging | CNV presents as a chorioretinal lesion with subretinal fluid and area of retinal hemorrhage |
| Associated inflammatory lesions | The triad of POHS includes the presence of peripapillary atrophy or pigmentation, histo spots (focal round-shaped chorioretinal lesions), and absence of overlying vitritis | Recurrent disease appears as an oval or circular whitish focal area of retinochoroiditis in the periphery of old atrophic lesions; dense overlying vitritis (headlight-in-fog); perivasculitis with diffuse venous sheathing; segmental arteriolar plaques | Choroiditis may have amoeboid lesions with central healing and active margins (serpiginous choroiditis) or it may present with choroidal granulomas | There is multifocal chorioretinitis with vitritis; multiple active chorioretinal lesions have the appearance of deep, creamy lesions and are 200–1000?μm in size. Inactive lesions are partly atrophic and partly pigmented with a “target-like appearance.” |
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Features of inflammatory choroidal neovascularization (CNV) commonly associated with non-infectious uveitis（炎癥性脈絡膜新生血管（CNV）的特征通常與非感染性葡萄膜炎相關）
| Prevalence | 33–50% cases | 76–100% cases | 10–25% cases | 9–15% |
| Location of CNV | Associated with inflammatory lesions in the subfoveal or extrafoveal region | Highly focal; associated with inflammatory lesions in the macula | CNV is located near chorioretinal lesions in peripapillary, subfoveal, or extrafoveal areas | Usually extrafoveal; can be subfoveal and associated with chorioretinal scar |
| Morphology of CNV | CNV appear as subretinal elevations and subretinal fluid with or without associated hemorrhage, closely resembling inflammatory lesions | CNV appear as subretinal elevations and subretinal fluid with or without hemorrhage, closely resembling inflammatory lesions | CNV lesions are deep with associated chorioretinal atrophy, subretinal fibrosis, and pigment clumping | CNV lesions are deep, associated with subretinal or intraretinal fluid, with hemorrhage and exudation. |
| Associated inflammatory lesions | Multifocal choroiditis present with minimal vitreous inflammation with multiple punched-out, white-yellow lesions (50–200?μm) in the peripapillary, mid-peripheral, and anteriorly to the equator | The lesions are characterized by multiple, small (50–300?μm in diameter), yellow or white, opaque, round lesions scattered throughout the posterior pole, rarely extending to mid-periphery; absence of vitritis | Active lesions appear as gray-white lesions that progress in a geographic manner in the posterior fundus | VKH presents with granulomatous anterior uveitis, posterior synechiae, iris nodules, and stromal atrophy; multiple pockets of subretinal fluid with exudative detachments; sunset glow fundus in the chronic disease. |
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【2】隱匿型CNV分為:
①PED型CNV
②無PED型CNV
Reference：
【1】Response to Aflibercept Therapy in Three Types of Choroidal Neovascular Membrane in Neovascular Age-Related Macular Degeneration: Real-Life Evidence in the Czech Republic
【2】Types of choroidal neovascularisation in newly diagnosed exudative age-related macular degeneration
【3】
J. J. Jung, C. Y. Chen, S. Mrejen et al., “The incidence of neovascular subtypes in newly diagnosed neovascular age-related macular degeneration,”?American Journal of Ophthalmology, vol. 158, no. 4, pp. 769.e2–779.e2, 2014.
【4】
M. Marsiglia, S. Boddu, C. Y. Chen et al., “Correlation between neovascular lesion type and clinical characteristics of nonneovascular fellow eyes in patients with unilateral, neovascular age-related macular degeneration,”?Retina, vol. 35, no. 5, pp. 966–974, 2015
【5】Topical administration of the kappa opioid receptor agonist nalfurafine suppresses corneal neovascularization and inflammation?
【6】Inflammatory Choroidal Neovascular Membranes: Clinical Profile, Treatment Effectiveness, and Visual Prognosis - PMC
【7】An update on inflammatory choroidal neovascularization: epidemiology, multimodal imaging, and management - PMC?
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