Raras
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Distrofia corneana, polimorfa posterior
ORPHA:98973CID-10 · H18.5CID-11 · LA11.5DOENÇA RARA

A distrofia corneana polimorfa posterior (CDPP) é um subtipo leve e raro de distrofia corneana posterior, caracterizada por pequenos agregados de vesículas aparentes delimitadas por uma névoa cinzenta ao nível da membrana de Descemet, geralmente sem efeito na visão.

Mantido por Agente Raras·Colaborar como especialista →

Introdução

O que você precisa saber de cara

📋

A distrofia corneana polimorfa posterior (CDPP) é um subtipo leve e raro de distrofia corneana posterior, caracterizada por pequenos agregados de vesículas aparentes delimitadas por uma névoa cinzenta ao nível da membrana de Descemet, geralmente sem efeito na visão.

Pesquisas ativas
1 ensaio
11 total registrados no ClinicalTrials.gov
Publicações científicas
162 artigos
Último publicado: 2026 Apr

Escala de raridade

CLASSIFICAÇÃO ORPHANET · BRASIL 2024
Unknown
Ultra-rara
<1/50k
Muito rara
1/20k
Rara
1/10k
Pouco freq.
1/5k
Incomum
1/2k
Prevalência
1.0
Czech Republic
Início
Childhood
🏥
SUS: Sem cobertura SUSScore: 0%
CID-10: H18.5
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Sinais e sintomas

O que aparece no corpo e com que frequência cada sintoma acontece

Partes do corpo afetadas

👁️
Olhos
16 sintomas
🫃
Digestivo
1 sintomas
📏
Crescimento
1 sintomas
🫘
Rins
1 sintomas

+ 11 sintomas em outras categorias

Características mais comuns

90%prev.
Morfologia anormal da membrana de Descemet
Muito frequente (99-80%)
90%prev.
Número reduzido de células endoteliais da córnea
Muito frequente (99-80%)
17%prev.
Acuidade visual reduzida
Ocasional (29-5%)
17%prev.
Sinequias anteriores da câmara anterior
Ocasional (29-5%)
17%prev.
Ectrópio uveal
Ocasional (29-5%)
17%prev.
Edema estromal da córnea
Ocasional (29-5%)
30sintomas
Muito frequente (2)
Ocasional (8)
Muito raro (10)
Sem dados (10)

Os sintomas variam de pessoa para pessoa. Abaixo estão as 30 características clínicas mais associadas, ordenadas por frequência.

Morfologia anormal da membrana de DescemetAbnormal Descemet membrane morphology
Muito frequente (99-80%)90%
Número reduzido de células endoteliais da córneaReduced number of corneal endothelial cells
Muito frequente (99-80%)90%
Acuidade visual reduzidaReduced visual acuity
Ocasional (29-5%)17%
Sinequias anteriores da câmara anteriorAnterior synechiae of the anterior chamber
Ocasional (29-5%)17%
Ectrópio uvealUveal ectropion
Ocasional (29-5%)17%

Linha do tempo da pesquisa

Publicações por ano — veja quando o interesse científico cresceu
Anos de pesquisa1desde 2026
Total histórico162PubMed
Últimos 10 anos74publicações
Pico201711 papers
Linha do tempo
2026Hoje · 2026🧪 2008Primeiro ensaio clínico📈 2017Ano de pico
Publicações por ano (últimos 10 anos)

Encontrou um erro ou informação desatualizada? Sugira uma correção →

Genética e causas

O que está alterado no DNA e como passa nas famílias

Genes associados

5 genes identificados com associação a esta condição. Padrão de herança: Autosomal dominant.

VSX1Visual system homeobox 1Disease-causing germline mutation(s) inTolerante
FUNÇÃO

Binds to the 37-bp core of the locus control region (LCR) of the red/green visual pigment gene cluster (PubMed:10903837). May regulate the activity of the LCR and the cone opsin genes at earlier stages of development (PubMed:10903837). Dispensable in early retinal development (By similarity)

LOCALIZAÇÃO

Nucleus

MECANISMO DE DOENÇA

Keratoconus 1

Frequent corneal dystrophy with an incidence that varies from 50 to 230 per 100'000. The cornea assumes a conical shape as a result of a progressive non-inflammatory thinning of the corneal stroma. Keratoconus is most often an isolated sporadic condition with cases of autosomal dominant and autosomal recessive transmission.

EXPRESSÃO TECIDUAL(Tecido-específico)
Cérebro - Hemisfério cerebelar
20.9 TPM
Cerebelo
18.0 TPM
Pituitária
3.6 TPM
Hipotálamo
1.7 TPM
Cérebro - Amígdala
1.5 TPM
INTERAÇÕES PROTEICAS (4)
OUTRAS DOENÇAS (3)
keratoconus 1craniofacial anomalies and anterior segment dysgenesis syndromeposterior polymorphous corneal dystrophy
HGNC:12723UniProt:Q9NZR4
GRHL2Grainyhead-like protein 2 homologDisease-causing germline mutation(s) inAltamente restrito
FUNÇÃO

Transcription factor playing an important role in primary neurulation and in epithelial development (PubMed:25152456, PubMed:29309642). Binds directly to the consensus DNA sequence 5'-AACCGGTT-3' acting as an activator and repressor on distinct target genes (By similarity). During embryogenesis, plays unique and cooperative roles with GRHL3 in establishing distinct zones of primary neurulation. Essential for closure 3 (rostral end of the forebrain), functions cooperatively with GRHL3 in closure

LOCALIZAÇÃO

NucleusMembrane

MECANISMO DE DOENÇA

Deafness, autosomal dominant, 28

A form of non-syndromic sensorineural hearing loss. Sensorineural deafness results from damage to the neural receptors of the inner ear, the nerve pathways to the brain, or the area of the brain that receives sound information. DFNA28 is characterized by mild to moderate hearing loss across most frequencies that progresses to severe loss in the higher frequencies by the fifth decade.

EXPRESSÃO TECIDUAL(Tecido-específico)
Skin Not Sun Exposed Suprapubic
41.4 TPM
Skin Sun Exposed Lower leg
39.8 TPM
Próstata
34.7 TPM
Esôfago - Mucosa
33.1 TPM
Glândula salivar
24.8 TPM
INTERAÇÕES PROTEICAS (2)
OUTRAS DOENÇAS (5)
autosomal dominant nonsyndromic hearing loss 28corneal dystrophy, posterior polymorphous, 4nail and teeth abnormalities-marginal palmoplantar keratoderma-oral hyperpigmentation syndromeposterior polymorphous corneal dystrophy
HGNC:2799UniProt:Q6ISB3
COL8A2Collagen alpha-2(VIII) chainDisease-causing germline mutation(s) inTolerante
FUNÇÃO

Macromolecular component of the subendothelium. Major component of the Descemet's membrane (basement membrane) of corneal endothelial cells. Also a component of the endothelia of blood vessels. Necessary for migration and proliferation of vascular smooth muscle cells and thus, has a potential role in the maintenance of vessel wall integrity and structure, in particular in atherogenesis (By similarity)

LOCALIZAÇÃO

Secreted, extracellular space, extracellular matrix, basement membrane

VIAS BIOLÓGICAS (2)
Collagen biosynthesis and modifying enzymesCollagen chain trimerization
MECANISMO DE DOENÇA

Corneal dystrophy, Fuchs endothelial, 1

A corneal disease caused by loss of endothelium of the central cornea. It is characterized by focal wart-like guttata that arise from Descemet membrane and develop in the central cornea, epithelial blisters, reduced vision and pain. Descemet membrane is thickened by abnormal collagenous deposition.

OUTRAS DOENÇAS (4)
corneal dystrophy, Fuchs endothelial, 1posterior polymorphous corneal dystrophy 2posterior polymorphous corneal dystrophyFuchs' endothelial dystrophy
HGNC:2216UniProt:P25067
ZEB1Zinc finger E-box-binding homeobox 1Disease-causing germline mutation(s) inAltamente restrito
FUNÇÃO

Acts as a transcriptional repressor. Inhibits interleukin-2 (IL-2) gene expression. Enhances or represses the promoter activity of the ATP1A1 gene depending on the quantity of cDNA and on the cell type. Represses E-cadherin promoter and induces an epithelial-mesenchymal transition (EMT) by recruiting SMARCA4/BRG1. Represses BCL6 transcription in the presence of the corepressor CTBP1. Positively regulates neuronal differentiation. Represses RCOR1 transcription activation during neurogenesis. Repr

LOCALIZAÇÃO

Nucleus

VIAS BIOLÓGICAS (3)
Negative Regulation of CDH1 Gene TranscriptionRegulation of MITF-M-dependent genes involved in extracellular matrix, focal adhesion and epithelial-to-mesenchymal transitionInterleukin-4 and Interleukin-13 signaling
MECANISMO DE DOENÇA

Corneal dystrophy, posterior polymorphous, 3

A subtype of posterior corneal dystrophy, a disease characterized by alterations of Descemet membrane presenting as vesicles, opacities or band-like lesions on slit-lamp examination and specular microscopy. Affected patient typically are asymptomatic.

EXPRESSÃO TECIDUAL(Ubíquo)
Cólon sigmoide
79.8 TPM
Fibroblastos
78.6 TPM
Aorta
65.9 TPM
Útero
65.5 TPM
Cervix Ectocervix
63.3 TPM
OUTRAS DOENÇAS (4)
posterior polymorphous corneal dystrophy 3corneal dystrophy, Fuchs endothelial, 6posterior polymorphous corneal dystrophyFuchs' endothelial dystrophy
HGNC:11642UniProt:P37275
OVOL2Transcription factor Ovo-like 2Disease-causing germline mutation(s) inTolerante
FUNÇÃO

Zinc-finger transcription repressor factor (PubMed:19700410). Plays a critical role in maintaining the identity of epithelial lineages by suppressing epithelial-to mesenchymal transition (EMT) mainly through the repression of ZEB1, an EMT inducer (By similarity). Positively regulates neuronal differentiation (By similarity). Suppresses cell cycling and terminal differentiation of keratinocytes by directly repressing MYC and NOTCH1 (PubMed:19700410). Important for the correct development of primo

LOCALIZAÇÃO

Nucleus

MECANISMO DE DOENÇA

Corneal dystrophy, posterior polymorphous, 1

A rare corneal disorder characterized by small aggregates of apparent vesicles bordered by a gray haze at the level of Descemet membrane, an altered corneal endothelial cell structure, and an unusual proliferation of endothelial cells. Symptoms can range from very aggressive to asymptomatic and non-progressive, even within the same family.

EXPRESSÃO TECIDUAL(Tecido-específico)
Glândula salivar
15.6 TPM
Testículo
13.0 TPM
Skin Sun Exposed Lower leg
12.6 TPM
Skin Not Sun Exposed Suprapubic
11.6 TPM
Próstata
11.0 TPM
INTERAÇÕES PROTEICAS (1)
OUTRAS DOENÇAS (2)
posterior polymorphous corneal dystrophy 1posterior polymorphous corneal dystrophy
HGNC:15804UniProt:Q9BRP0

Variantes genéticas (ClinVar)

91 variantes patogênicas registradas no ClinVar.

🧬 OVOL2: NC_000020.10:g.(?_17603729)_(18541384_?)del ()
🧬 OVOL2: NC_000020.10:g.16400000_24400000del ()
🧬 OVOL2: GRCh37/hg19 20p13-11.21(chr20:68351-23860313)x3 ()
🧬 OVOL2: GRCh38/hg38 20p13-11.21(chr20:87153-23635465)x3 ()
🧬 OVOL2: NC_000020.10:g.(?_17587682)_(18168103_?)del ()
Ver todas no ClinVar

Classificação de variantes (ClinVar)

Distribuição de 87 variantes classificadas pelo ClinVar.

30
35
22
Patogênica (34.5%)
VUS (40.2%)
Benigna (25.3%)
VARIANTES MAIS SIGNIFICATIVAS
ZEB1: NM_001174096.2(ZEB1):c.1448del (p.Pro483fs) [Likely pathogenic]
ZEB1: NM_001174096.2(ZEB1):c.1691C>A (p.Ala564Glu) [Conflicting classifications of pathogenicity]
ZEB1: NM_001174096.2(ZEB1):c.692_693del (p.His231fs) [Pathogenic/Likely pathogenic]
LOC130003630: NM_001174096.2(ZEB1):c.1A>C (p.Met1Leu) [Pathogenic]
ZEB1: NM_001174096.2(ZEB1):c.2252C>A (p.Ser751Ter) [Pathogenic]

Diagnóstico

Os sinais que médicos procuram e os exames que confirmam

Carregando...

Tratamento e manejo

Remédios, cuidados de apoio e o que precisa acompanhar

Pipeline de tratamentos
Pipeline regulatório — de medicamentos já aprovados a drogas em pesquisa exploratória.
·Pré-clínico2
Medicamentos catalogadosEnsaios clínicos· 0 medicamentos · 2 ensaios
Carregando informações de tratamento...

Onde tratar no SUS

Hospitais de referência no Brasil e o protocolo oficial do SUS (PCDT)

🇧🇷 Atendimento SUS — Distrofia corneana, polimorfa posterior

🗺️

Selecione um estado ou use sua localização para ver resultados.

Dados de DATASUS/CNES, SBGM, ABNeuro e Ministério da Saúde. Sempre confirme a disponibilidade diretamente com o estabelecimento.

Pesquisa ativa

Ensaios clínicos abertos e novidades científicas recentes

🟢 Recrutando agora

1 pesquisa recrutando participantes. Converse com seu médico sobre a possibilidade de participar.

Outros ensaios clínicos

11 ensaios clínicos encontrados, 1 ativos.

Distribuição por fase
Ver todos no ClinicalTrials.gov
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Publicações mais relevantes

Timeline de publicações
78 papers (10 anos)
#1

Generation of a Novel Col8a2P2A-CreERT2 Mouse Line Enables Targeted Genetic Manipulation of Corneal Endothelial Cells and Modeling of Endothelial Decompensation.

Genesis (New York, N.Y. : 2000)2026 Apr

The corneal endothelium is a monolayer of specialized cells that maintains stromal deturgescence and transparency, functions essential for vision. Despite its clinical importance, the developmental origins and homeostatic programs of the endothelium remain poorly understood, in part due to the lack of a lineage-specific genetic driver. To overcome this limitation, we generated a Col8a2P2A-CreERT2 knock-in mouse line that enables selective genetic manipulations of corneal endothelial cells. Cre activity was validated with reporter alleles and functional importance was assessed by conditional ablation of Col8a2+ cells in adulthood, with phenotypic outcomes evaluated by histology, immunofluorescence, and in vivo imaging. We found that Col8a2P2A-CreERT2 drives robust and specific recombination in corneal endothelial cells. Functional assays demonstrated that Col8a2+ cells contribute continuously to Descemet's membrane synthesis and are essential for maintaining endothelial integrity. Ablation disrupted endothelial density and barrier function, resulting in phenotypes resembling human endothelial dystrophies, including features of Fuchs' endothelial corneal dystrophy and posterior polymorphous corneal dystrophy. These findings identify Col8a2+ cells as indispensable regulators of endothelial development, homeostasis, and disease pathogenesis. The Col8a2P2A-CreERT2 line provides the first corneal endothelium-specific genetic driver, establishing a platform for mechanistic investigation and therapeutic discovery in endothelial disorders.

#2

Outcomes of descemet's membrane endothelial keratoplasty in patients under thirty years old.

European journal of ophthalmology2026 Jan 22

BackgroundEvidence for Descemet's membrane endothelial keratoplasty (DMEK) in patients under 30 years old remains limited, although understanding outcomes in this demographic is important given the requirement for decades of graft function and concerns about long-term DMEK survival.MethodsWe conducted a retrospective case series at Moorfields Eye Hospital of consecutive patients under 30 years undergoing DMEK between 2015 and 2022. Primary outcome was change in best-corrected visual acuity (BCVA). Secondary outcomes included change in central corneal thickness (CCT), graft failure rates, and post-operative complications.Results18 eyes of 17 patients underwent DMEK surgery (mean age 22.7 ± 5.1) over a mean follow-up of 1072.1 ± 869.8 days. Mean BCVA improvement was 0.36 logMAR from pre-operative to final follow-up (p > 0.05), though significant improvements occurred at 1-month and 12-month intervals (p < 0.001 and p < 0.01, respectively). CCT improved significantly from baseline by 111.3 μm (95% CI, 64.3-158.2 μm, p < 0.0001). At final follow-up, 22.2% of eyes achieved BCVA ≤ 0.3 logMAR (n = 4). No patient achieved BCVA ≤ 0.1 logMAR. Rebubbling was performed 9 times (50%) in 8 eyes and was similar between both SF6 and air (p > 0.05). Post-operative complications occurred in 11.1% (n = 2) with no rejection episodes, although secondary graft failure occurred in 22.2% (n = 4), all within 12 months.ConclusionsDMEK effectively improves visual and anatomical outcomes in patients under 30, though with higher complication rates than older populations. The complex pathology and longer follow-up requirements in this demographic necessitate careful patient selection and realistic expectations. Larger prospective studies are needed to establish definitive guidelines for this population.

#3

[Endothelial dystrophies and degenerations of the cornea].

Klinische Monatsblatter fur Augenheilkunde2026 Feb

The corneal endothelium is the innermost layer of the human cornea and it acts as a barrier between the aqueous humor and the corneal stroma, thus maintaining the hydration of the cornea. Both congenital dystrophies including (1) Fuchs' endothelial corneal dystrophy (FECD), (2) posterior polymorphous corneal dystrophy (PPCD), (3) congenital hereditary endothelial dystrophy (CHED), (4) X-linked endothelial corneal dystrophy (XECD) and age-related degenerations like (5) pseudoexfoliation-related (PEX) keratopathy, (6) pseudophakic bullous keratopathy (PBK), (7) iridocorneal endothelial (ICE) syndromes and endothelial graft rejection after keratoplasty can impair this function and are described in this review article.

#4

Pentacam-based corneal densitometry in posterior polymorphous corneal dystrophy.

BMJ case reports2025 Apr 15
#5

Polymorphous corneal dystrophy subtype 3 and keratoconus aggravation after corneal refractive surgery in a three-generation family carrying both ZEB1 and ZNF469 pathogenic variant.

Frontiers in genetics2025

This study reports a three-generation Chinese family with polymorphous corneal dystrophy subtype 3 (PPCD3) and keratoconus (KC) aggravation induced by corneal refractive surgery, specifically small incision lenticule extraction (SMILE), in the context of genetic variations. The history of illnesses and blood samples of all family members were collected. One hundred healthy individuals served as normal controls. We conducted whole exome sequencing on genomic DNA and sanger sequencing to verify the variants between all controls and family members. Three family members were previously diagnosed with subclinical keratoconus (III1 and III2 preoperatively, and II2). Both the proband (III1) and her younger brother (III2) underwent SMILE to correct refractive errors. One year later, visual acuity of III1 decreased significantly with KC aggravation and corneal opacification. The KC of III2 progressed significantly 6 months after surgery. Both were subsequently diagnosed with PPCD3. We detected both Zinc finger E-box-binding homeobox 1 (ZEB1) gene and zinc finger protein 469 (ZNF469) gene pathogenic variant in the proband and another two patients in this family, including a heterozygous missense variation c.13C>G (p.P5A, rs753301298) in the ZEB1 gene, and a heterozygous non-frameshift variant c. 3093_3104del (p.D1035_K1038del) in the ZNF469 gene. The variants including c.13C>G in ZEB1 and c.3093_3104del in ZNF469 were speculated to be pathogenic or a variant of uncertain significance by online prediction software. This study demonstrated the importance of a thorough ocular examination, especially the cornea, and a gene screening before SMILE.

Publicações recentes

Ver todas no PubMed

📚 EuropePMC94 artigos no totalmostrando 74

2026

Generation of a Novel Col8a2P2A-CreERT2 Mouse Line Enables Targeted Genetic Manipulation of Corneal Endothelial Cells and Modeling of Endothelial Decompensation.

Genesis (New York, N.Y. : 2000)
2026

Outcomes of descemet's membrane endothelial keratoplasty in patients under thirty years old.

European journal of ophthalmology
2026

[Endothelial dystrophies and degenerations of the cornea].

Klinische Monatsblatter fur Augenheilkunde
2025

Polymorphous corneal dystrophy subtype 3 and keratoconus aggravation after corneal refractive surgery in a three-generation family carrying both ZEB1 and ZNF469 pathogenic variant.

Frontiers in genetics
2025

Pentacam-based corneal densitometry in posterior polymorphous corneal dystrophy.

BMJ case reports
2025

Familial Steep Corneas in Posterior Polymorphous Corneal Dystrophy 3 Due to a Novel ZEB1 Gene Mutation.

Cornea
2024

Poor intraoperative visibility and postoperative astigmatism associated with trabecular micro-bypass stent for corneal dystrophy: A case report.

Medicine
2024

[Alport syndrome presenting as posterior polymorphous corneal dystrophy: Case report].

Journal francais d'ophtalmologie
2024

Unusual finding in a patient with unilateral posterior polymorphous corneal dystrophy: A case report.

Journal francais d'ophtalmologie
2024

Corneal pseudoectasia: a case series.

International ophthalmology
2024

Ovol2 promoter mutations in mice and human illuminate species-specific phenotypic divergence.

Human molecular genetics
2024

Loss-of-function variants in ZEB1 cause dominant anomalies of the corpus callosum with favourable cognitive prognosis.

Journal of medical genetics
2023

Systematic review of SLC4A11, ZEB1, LOXHD1, and AGBL1 variants in the development of Fuchs' endothelial corneal dystrophy.

Frontiers in medicine
2023

Posterior Polymorphous Corneal Dystrophy: Clinical-Pathologic Correlation.

Ophthalmology
2023

Posterior corneal vesicle syndrome or posterior polymorphous corneal dystrophy? A case report of a heterozygous intronic variant in the COL4A3 gene.

Journal francais d'ophtalmologie
2022

Posterior Polymorphous Corneal Dystrophy in a Patient with a Novel ZEB1 Gene Mutation.

International journal of molecular sciences
2022

Unilateral posterior polymorphous corneal dystrophy due to a novel ZEB1 gene mutation in a Korean girl.

Ophthalmic genetics
2024

Descemet Membrane Endothelial Keratoplasty (DMEK) for Severe Verrucous Posterior Polymorphous Corneal Dystrophy with Uncommon Clinical and Ultrastructural Findings.

Klinische Monatsblatter fur Augenheilkunde
2022

Update on the genetics of corneal endothelial dystrophies.

Indian journal of ophthalmology
2022

Bilateral posterior lamellar corneal transplant surgery in an infant of 17 weeks old: Surgical challenges and the added value of intraoperative optical coherence tomography.

Clinical case reports
2022

Posterior corneal vesicles are not associated with the genetic variants that cause posterior polymorphous corneal dystrophy.

Acta ophthalmologica
2022

[Imaging features of posterior polymorphous corneal dystrophy observed by in vivo confocal microscopy].

[Zhonghua yan ke za zhi] Chinese journal of ophthalmology
2021

Maculopathy, Fundus Changes and Anterior Lenticonus in Alport Syndrome.

Beyoglu eye journal
2022

Posterior Polymorphous Corneal Dystrophy in a Pediatric Population.

Cornea
2022

c.-61G>A in OVOL2 is a Pathogenic 5' Untranslated Region Variant Causing Posterior Polymorphous Corneal Dystrophy 1.

Cornea
2021

Clearing the Haze: Navigating Corneal Refractive Surgery in Patients with Posterior Polymorphous Corneal Dystrophy.

Ophthalmology and therapy
2021

Corneal ectasia associated with posterior lamellar opacification.

Ophthalmic genetics
2021

Non-Penetrance for Ocular Phenotype in Two Individuals Carrying Heterozygous Loss-of-Function ZEB1 Alleles.

Genes
2021

Expression and Function of ZEB1 in the Cornea.

Cells
2021

Corneal cross-linking for treatment of progressive keratoconus in a patient with Alport syndrome: A case report.

European journal of ophthalmology
2021

Endothelial cell density in children with posterior polymorphous corneal dystrophy: a longitudinal case-control study.

Eye (London, England)
2021

Diseases of the corneal endothelium.

Experimental eye research
2021

Laser refractive surgery in corneal dystrophies.

Journal of cataract and refractive surgery
2021

Case Series of Urrets-Zavalia Syndrome After Descemet Membrane Endothelial Keratoplasty.

Cornea
2020

Successful pediatric DMEK facilitated by intracameral tissue plasminogen activator to mitigate anterior chamber fibrin reaction.

American journal of ophthalmology case reports
2020

Corneal endothelial cell abnormalities in X-linked Alport syndrome.

Ophthalmic genetics
2019

A Mutation in ZNF143 as a Novel Candidate Gene for Endothelial Corneal Dystrophy.

Journal of clinical medicine
2019

Alterations in GRHL2-OVOL2-ZEB1 axis and aberrant activation of Wnt signaling lead to altered gene transcription in posterior polymorphous corneal dystrophy.

Experimental eye research
2020

CUGC for posterior polymorphous corneal dystrophy (PPCD).

European journal of human genetics : EJHG
2019

ZEB1 insufficiency causes corneal endothelial cell state transition and altered cellular processing.

PloS one
2019

Descemet membrane endothelial keratoplasty in iridocorneal endothelial syndrome and posterior polymorphous corneal dystrophy.

Canadian journal of ophthalmology. Journal canadien d'ophtalmologie
2019

Coincidental Occurrence of Schnyder Corneal Dystrophy and Posterior Polymorphous Corneal Dystrophy Type 3.

Cornea
2019

Alport Patients without Classic Ocular Symptoms Have Smaller Lens Diameter.

Medical science monitor : international medical journal of experimental and clinical research
2019

The utility of massively parallel sequencing for posterior polymorphous corneal dystrophy type 3 molecular diagnosis.

Experimental eye research
2018

Investigating the Pathogenicity of VSX1 Missense Mutations and Their Association With Corneal Disease.

Investigative ophthalmology &amp; visual science
2018

Genetic Aspects of Keratoconus: A Literature Review Exploring Potential Genetic Contributions and Possible Genetic Relationships with Comorbidities.

Ophthalmology and therapy
2018

Clinical findings observed by in-vivo confocal microscopy of posterior polymorphous corneal dystrophy.

Journal francais d'ophtalmologie
2018

Effect of Posterior Corneal Vesicles on Corneal Endothelial Cell Density and Anisometropic Amblyopia.

Cornea
2018

Ectopic GRHL2 Expression Due to Non-coding Mutations Promotes Cell State Transition and Causes Posterior Polymorphous Corneal Dystrophy 4.

American journal of human genetics
2017

Endothelial keratoplasty for posterior polymorphous corneal dystrophy in a 4-month-old infant.

American journal of ophthalmology case reports
2017

Elucidating the molecular basis of PPCD: Effects of decreased ZEB1 expression on corneal endothelial cell function.

Molecular vision
2017

Retinal pathology in the PPCD1 mouse.

PloS one
2017

Agenesis of the corpus callosum, developmental delay, autism spectrum disorder, facial dysmorphism, and posterior polymorphous corneal dystrophy associated with ZEB1 gene deletion.

American journal of medical genetics. Part A
2017

Transcriptomic Profiling of Posterior Polymorphous Corneal Dystrophy.

Investigative ophthalmology &amp; visual science
2017

Unilateral Posterior Polymorphous Corneal Dystrophy Presented as Anisometropic Astigmatism: 3 Case Reports.

Case reports in ophthalmology
2017

Active transforming growth factor-β2 in the aqueous humor of posterior polymorphous corneal dystrophy patients.

PloS one
2017

Thick keratoconic cornea associated with posterior polymorphous corneal dystrophy.

Journal francais d'ophtalmologie
2017

Confirmation of the OVOL2 Promoter Mutation c.-307T>C in Posterior Polymorphous Corneal Dystrophy 1.

PloS one
2017

Clinical Features in Children with Posterior Polymorphous Corneal Dystrophy.

Optometry and vision science : official publication of the American Academy of Optometry
2016

In vivo confocal microscopic observations of eyes diagnosed with posterior corneal vesicles.

Japanese journal of ophthalmology
2017

Clinical characterization of posterior polymorphous corneal dystrophy in patients of Indian ethnicity.

International ophthalmology
2016

Investigating the Molecular Basis of PPCD3: Characterization of ZEB1 Regulation of COL4A3 Expression.

Investigative ophthalmology &amp; visual science
2016

Identification of Potentially Pathogenic Variants in the Posterior Polymorphous Corneal Dystrophy 1 Locus.

PloS one
2016

Association of a Chromosomal Rearrangement Event with Mouse Posterior Polymorphous Corneal Dystrophy and Alterations in Csrp2bp, Dzank1, and Ovol2 Gene Expression.

PloS one
2016

Contact lens fitting in a patient with Alport syndrome and posterior polymorphous corneal dystrophy: a case report.

Arquivos brasileiros de oftalmologia
2016

Autosomal-Dominant Corneal Endothelial Dystrophies CHED1 and PPCD1 Are Allelic Disorders Caused by Non-coding Mutations in the Promoter of OVOL2.

American journal of human genetics
2016

Mutational spectrum of Korean patients with corneal dystrophy.

Clinical genetics
2016

Congenital Corneal Endothelial Dystrophies Resulting From Novel De Novo Mutations.

Cornea
2016

Heterozygous deletions at the ZEB1 locus verify haploinsufficiency as the mechanism of disease for posterior polymorphous corneal dystrophy type 3.

European journal of human genetics : EJHG
2015

Posterior Corneal Steepening in Posterior Polymorphous Corneal Dystrophy.

Optometry and vision science : official publication of the American Academy of Optometry
2015

Long-Term Observation of Coexistence of Posterior Polymorphous Corneal Dystrophy, Resultant High Myopia and Nonkeratoconic Developing Corneal Astigmatism: A Case Report of 7-Year Tracking in a Chinese Boy.

Medicine
2015

[The revised newest IC³D classification of corneal dystrophies].

Klinische Monatsblatter fur Augenheilkunde
2015

Ocular features in Alport syndrome: pathogenesis and clinical significance.

Clinical journal of the American Society of Nephrology : CJASN
2015

IC3D classification of corneal dystrophies--edition 2.

Cornea
Ver todos os 94 no EuropePMC

Associações

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Comunidades

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Doenças relacionadas

Doenças com sintomas parecidos — ajudam quem ainda está buscando diagnóstico

Referências e fontes

Bases de dados externas citadas neste artigo

Publicações científicas

Artigos indexados no PubMed ligados a esta doença no grafo RarasNet — título, periódico e PMID direto da fonte, sem intermediação de IA.

  1. Generation of a Novel Col8a2P2A-CreERT2 Mouse Line Enables Targeted Genetic Manipulation of Corneal Endothelial Cells and Modeling of Endothelial Decompensation.
    Genesis (New York, N.Y. : 2000)· 2026· PMID 41840915mais citado
  2. Outcomes of descemet's membrane endothelial keratoplasty in patients under thirty years old.
    European journal of ophthalmology· 2026· PMID 41569999mais citado
  3. [Endothelial dystrophies and degenerations of the cornea].
    Klinische Monatsblatter fur Augenheilkunde· 2026· PMID 41248687mais citado
  4. Pentacam-based corneal densitometry in posterior polymorphous corneal dystrophy.
    BMJ case reports· 2025· PMID 40234074mais citado
  5. Polymorphous corneal dystrophy subtype 3 and keratoconus aggravation after corneal refractive surgery in a three-generation family carrying both ZEB1 and ZNF469 pathogenic variant.
    Frontiers in genetics· 2025· PMID 40547359mais citado

Bases de dados e fontes oficiais

Identificadores e referências canônicas usadas para montar este verbete.

  1. ORPHA:98973(Orphanet)
  2. MONDO:0020364(MONDO)
  3. GARD:16882(GARD (NIH))
  4. Variantes catalogadas(ClinVar)
  5. Busca completa no PubMed(PubMed)
  6. Q4183965(Wikidata)

Dados compilados pelo RarasNet a partir de fontes abertas (Orphanet, OMIM, MONDO, PubMed/EuropePMC, ClinicalTrials.gov, DATASUS, PCDT/MS). Este conteúdo é informativo e não substitui avaliação médica.

Conteúdo mantido por Agente Raras · Médicos e pesquisadores podem colaborar

Distrofia corneana, polimorfa posterior
Compêndio · Raras BR

Distrofia corneana, polimorfa posterior

ORPHA:98973 · MONDO:0020364
Prevalência
Unknown
Herança
Autosomal dominant
CID-10
H18.5 · Distrofias hereditárias da córnea
CID-11
Ensaios
1 ativos
Início
Childhood
Prevalência
1.0 (Czech Republic)
MedGen
UMLS
C0339284
EuropePMC
Wikidata
Papers 10a
DiscussaoAtiva

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