# Macular Telangiectasia Type 2: The Role of Optical Coherence Tomography and Management Options

**Authors:** David-Ionuț Beuran, Ioana Ruxandra Boca, Cătălin Cornăcel, Călin Petru Tătaru, Cătălina Ioana Tătaru, Maria-Emilia Cerghedean-Florea, Cosmin Adrian Teodoru

PMC · DOI: 10.3390/jcm15041327 · Journal of Clinical Medicine · 2026-02-07

## TL;DR

This review discusses how optical coherence tomography helps diagnose and monitor Macular Telangiectasia Type 2, a rare eye disease, and explores treatment options based on disease stage.

## Contribution

The paper systematically reviews OCT findings and management strategies for MacTel type 2, emphasizing stage-specific treatment approaches.

## Key findings

- OCT reveals foveal cavitation, ellipsoid zone disruption, and retinal pigment clumps in MacTel type 2.
- Central macular thickness reduction on OCT correlates with visual acuity decline.
- CNTF implants and anti-VEGF therapies show promise for non-proliferative and proliferative stages, respectively.

## Abstract

Background/Objectives: Macular Telangiectasia Type 2 (MacTel type 2) is a rare, progressive retinal disease that can lead to central vision loss. Optical coherence tomography (OCT) plays a crucial role in the early diagnosis, monitoring, and prognostic assessment of this condition. This narrative review aims to summarize the clinical features, OCT findings, and current management strategies for MacTel type 2. Methods: A literature search of PubMed, MEDLINE, and Google Scholar was performed for articles published from October 1993 to September 2025 using keywords related to MacTel type 2, OCT, clinical features, and treatment. All relevant clinical studies, including observational studies, clinical trials, and case series, were considered. The literature was screened independently by two authors, and a total of 69 articles were included. Results: Characteristic OCT findings include foveal cavitation, hyperreflective middle retinal layers, inner and outer retinal cavities, ellipsoid zone disruption, and retinal pigment clumps. Central macular thickness is consistently reduced, and structural biomarkers identified on OCT correlate with visual acuity decline. Treatment strategies vary by disease stage: non-proliferative MacTel type 2 currently has no universally effective therapy, although neuroprotective interventions such as ciliary neurotrophic factor (CNTF) show promising results. Proliferative MacTel type 2 is primarily managed with anti-vascular endothelial growth factor therapy (anti-VEGF), demonstrating functional and anatomical improvements. Conclusions: OCT provides essential structural evaluation for monitoring MacTel type 2, while treatment approaches remain stage-dependent. Emerging therapies, including CNTF implants and novel anti-VEGF agents, hold potential for improving outcomes.

## Linked entities

- **Proteins:** CNTF (ciliary neurotrophic factor)
- **Diseases:** Macular Telangiectasia Type 2 (MONDO:1010183)

## Full-text entities

- **Genes:** PSAT1 (phosphoserine aminotransferase 1) [NCBI Gene 29968] {aka EPIP, NLS2, PSA, PSAT, PSATD}, PHGDH (phosphoglycerate dehydrogenase) [NCBI Gene 26227] {aka 3-PGDH, 3PGDH, HEL-S-113, NLS, NLS1, PDG}, CNTF (ciliary neurotrophic factor) [NCBI Gene 1270] {aka HCNTF}, PLXNA2 (plexin A2) [NCBI Gene 5362] {aka OCT, PLXN2}, VEGFA (vascular endothelial growth factor A) [NCBI Gene 7422] {aka L-VEGF, MVCD1, VEGF, VPF}
- **Diseases:** injury to (MESH:D014947), scotomas (MESH:D012607), EZ loss (MESH:D016388), intraretinal pigment (MESH:D006949), fibrosis (MESH:D005355), retinal vein or branch occlusion (MESH:D012170), MacTel (MESH:D013684), hypertension (MESH:D006973), capillary occlusion (MESH:D001157), hyperplastic retinal pigment epithelium (MESH:C536309), blurred (MESH:D014786), capillary obstruction (OMIM:163000), neovascularization (MESH:D016510), cystoid macular edema (MESH:D008269), vascular abnormalities (MESH:D014652), juvenile familial idiopathic retinal telangiectasias (MESH:D012173), diabetes (MESH:D003920), Type 1 macular telangiectasia (MESH:D013683), diabetic retinopathy (MESH:D003930), pigmentation (MESH:D010859), CMT (MESH:D008268), central nervous system impairment (MESH:D002493), atrophy (MESH:D001284), MacTel type 2 (MESH:D003924), ILM (MESH:D015433), photoreceptor degeneration (MESH:D009410), obese (MESH:D009765), subretinal hemorrhage (MESH:D006470), MacTel Type 2 (MESH:C537139), retinopathy (MESH:D058437), coronary artery disease (MESH:D003324), retinal disease (MESH:D012164), choroidal neovascularization (MESH:D020256), vascular anomalies (MESH:D020785), hyperplasia (MESH:D006965), Coats disease (MESH:D058456), macular hole (MESH:D012167), radiation retinopathy (MESH:D011832), Systemic Diseases (MESH:D034721), FAF (MESH:C535828)
- **Chemicals:** ENCELTO (-), Faricimab (MESH:C000723200), fenofibrate (MESH:D011345), Fluorescein (MESH:D019793), serine (MESH:D012694), carotenoids (MESH:D002338), steroids (MESH:D013256), glycine (MESH:D005998), argon (MESH:D001128)
- **Species:** Homo sapiens (human, species) [taxon 9606]
- **Cell lines:** RPE — Homo sapiens (Human), Spontaneously immortalized cell line (CVCL_0145)

## Full text

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## Figures

2 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12941054/full.md

## References

69 references — full list in the complete paper: https://tomesphere.com/paper/PMC12941054/full.md

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Source: https://tomesphere.com/paper/PMC12941054