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Retinal pigment epithelial atrophy

MedGen UID:
333564
Concept ID:
C1840457
Finding
Synonym: Loss of retinal pigment epithelium
 
HPO: HP:0007722

Definition

Atrophy (loss or wasting) of the retinal pigment epithelium observed on fundoscopy or fundus imaging. [from HPO]

Term Hierarchy

CClinical test,  RResearch test,  OOMIM,  GGeneReviews,  VClinVar  
  • Retinal pigment epithelial atrophy

Conditions with this feature

Sjögren-Larsson syndrome
MedGen UID:
11443
Concept ID:
C0037231
Disease or Syndrome
Sjogren-Larsson syndrome (SLS) is an autosomal recessive, early childhood-onset disorder characterized by ichthyosis, impaired intellectual development, spastic paraparesis, macular dystrophy, and leukoencephalopathy. It is caused by deficiency of fatty aldehyde dehydrogenase (summary by Lossos et al., 2006).
Retinitis pigmentosa 23
MedGen UID:
238456
Concept ID:
C1419610
Disease or Syndrome
Any retinitis pigmentosa in which the cause of the disease is a mutation in the OFD1 gene.
Retinitis pigmentosa 33
MedGen UID:
332080
Concept ID:
C1835895
Disease or Syndrome
Any retinitis pigmentosa in which the cause of the disease is a mutation in the SNRNP200 gene.
Retinitis pigmentosa 31
MedGen UID:
372159
Concept ID:
C1835923
Disease or Syndrome
Any retinitis pigmentosa in which the cause of the disease is a mutation in the TOPORS gene.
Wagner syndrome
MedGen UID:
326741
Concept ID:
C1840452
Disease or Syndrome
VCAN-related vitreoretinopathy, which includes Wagner syndrome and erosive vitreoretinopathy (ERVR), is characterized by "optically empty vitreous" on slit-lamp examination and avascular vitreous strands and veils, mild or occasionally moderate to severe myopia, presenile cataract, night blindness of variable degree associated with progressive chorioretinal atrophy, retinal traction and retinal detachment in the advanced stages of disease, and reduced visual acuity. Optic nerve inversion as well as uveitis has also been described. Systemic abnormalities are not observed. The first signs usually become apparent during early adolescence, but onset can be as early as age two years.
X-linked cone-rod dystrophy 1
MedGen UID:
336777
Concept ID:
C1844776
Disease or Syndrome
X-linked cone-rod dystrophy is a rare, progressive visual disorder primarily affecting cone photoreceptors (Demirci et al., 2002). Affected individuals, essentially all of whom are males, present with decreased visual acuity, myopia, photophobia, abnormal color vision, full peripheral visual fields, decreased photopic electroretinographic responses, and granularity of the macular retinal pigment epithelium. The degree of rod photoreceptor involvement is variable, with increasing degeneration. Although penetrance appears to be nearly 100%, there is variable expressivity with respect to age at onset, severity of symptoms, and findings (Hong et al., 1994). Genetic Heterogeneity of X-linked Cone-Rod Dystrophy Additional forms of X-linked cone-rod dystrophy include CORDX2 (300085), mapped to chromosome Xq27, and CORDX3 (300476), caused by mutation in the CACNA1F gene (300110) on chromosome Xp11.23. For a discussion of autosomal forms of cone-rod dystrophy, see CORD2 (120970).
Birdshot chorioretinopathy
MedGen UID:
340098
Concept ID:
C1853959
Disease or Syndrome
Multiple cream-yellow colored hypopigmented lesions typically located at the level of the choroid or retinal pigment epithelium; ovoid, cream-colored with indistinct borders. They are between 50 and 1,500 micrometers in size with a characteristic nasal, radial distribution in the postequatorial fundus.
Retinitis pigmentosa 19
MedGen UID:
400996
Concept ID:
C1866422
Disease or Syndrome
Any retinitis pigmentosa in which the cause of the disease is a mutation in the ABCA4 gene.
Isolated microphthalmia 5
MedGen UID:
410021
Concept ID:
C1970236
Disease or Syndrome
Microphthalmia-retinitis pigmentosa-foveoschisis-optic disc drusen syndrome is a rare, genetic, non-syndromic developmental defect of the eye disorder characterized by the association of posterior microphthalmia, retinal dystrophy compatible with retinitis pigmentosa, localized foveal schisis and optic disc drusen. Patients present high hyperopia, usually adult-onset progressive nyctalopia and reduced visual acuity, and, on occasion, acute-angle glaucoma.
Retinitis pigmentosa 56
MedGen UID:
462169
Concept ID:
C3150819
Disease or Syndrome
Retinitis pigmentosa-56 (RP56) is an early-onset form of RP with progressive visual-field loss and deterioration of visual acuity (Bandah-Rozenfeld et al., 2010). For a general phenotypic description and a discussion of genetic heterogeneity of retinitis pigmentosa, see 268000.
Cone-rod dystrophy 15
MedGen UID:
462262
Concept ID:
C3150912
Disease or Syndrome
Cone-rod dystrophy-15 (CORD15) is characterized by onset of reduced vision in the third to fifth decades of life. Visual acuity progressively worsens, and most patients exhibit reduced color vision and central scotomas (Cohen et al., 2012; Sobolewska et al., 2023). Retinitis pigmentosa-65 (RP65) is an adult-onset form of RP, with night blindness developing in the second to fourth decades of life. In addition to constriction of visual fields, patients may experience photophobia, reduced visual acuity, and difficulties with color vision (Henderson et al., 2010; Bessette et al., 2018; Dawood et al., 2021). Retinal macular dystrophy-5 (MCDR5) is a late-onset form of macular dystrophy, with most patients noting symptoms in the fourth to sixth decades of life. Symptoms include reduced visual acuity, glare, poor contrast vision, and metamorphopsia; night blindness is uncommon (Stingl et al., 2017; Charbel Issa et al., 2019; Ba-Abbad et al., 2021). Macular atrophy is a characteristic feature in all patients, and early involvement may be observed even in patients with RP who exhibit relatively preserved visual acuity (Malechka et al., 2022). For a general phenotypic description and a discussion of genetic heterogeneity of cone-rod dystrophy, see 120970; for retinitis pigmentosa, see 268000; for retinal macular dystrophy, see 136550. Reviews Bessette et al. (2018) reviewed published reports of patients with disease-causing mutations in the CDHR1 gene. The median age of patients was 36 years, and the majority retained visual acuity of 20/70 or better in at least one eye. Most patients developed symptoms between the first and third decades of life (range, infancy through fourth decade). Night blindness was the most common presenting symptom (54%), followed by photosensitivity (39%) and decreased vision (31%). Macular atrophy was the most common fundus feature reported (96%), followed by vascular attenuation (69%) and peripheral bone spicules (54%). The authors noted significant inter- and intrafamilial phenotypic variability among patients with CDHR1 mutations.
Retinitis pigmentosa 60
MedGen UID:
462784
Concept ID:
C3151434
Disease or Syndrome
Any retinitis pigmentosa in which the cause of the disease is a mutation in the PRPF6 gene.
Cone-rod dystrophy 2
MedGen UID:
483485
Concept ID:
C3489532
Disease or Syndrome
Cone-rod dystrophy (CORD) characteristically leads to early impairment of vision. An initial loss of color vision and of visual acuity is followed by nyctalopia (night blindness) and loss of peripheral visual fields. In extreme cases, these progressive symptoms are accompanied by widespread, advancing retinal pigmentation and chorioretinal atrophy of the central and peripheral retina (Moore, 1992). In many families, perhaps a majority, central and peripheral chorioretinal atrophy is not found (Tzekov, 1998). Genetic Heterogeneity of Autosomal Cone-Rod Dystrophy There are several other autosomal forms of CORD for which the molecular basis is known. CORD3 (604116) is caused by mutation in the ABCA4 gene (601691) on chromosome 1p22. CORD5 (600977) is caused by mutation in the PITPNM3 gene (608921) on chromosome 17p13. CORD6 (601777) is caused by mutation in the GUCY2D gene (600179) on chromosome 17p13.1. CORD9 (612775) is caused by mutation in the ADAM9 gene (602713) on chromosome 8p11. CORD10 (610283) is caused by mutation in the SEMA4A gene (607292) on chromosome 1q22. CORD11 (610381) is caused by mutation in the RAXL1 gene (610362) on chromosome 19p13. CORD12 (612657) is caused by mutation in the PROM1 gene (604365) on chromosome 4p15. CORD13 (608194) is caused by mutation in the RPGRIP1 gene (605446) on chromosome 14q11. CORD14 (see 602093) is caused by mutation in the GUCA1A gene (600364) on chromosome 6p21. CORD15 (613660) is caused by mutation in the CDHR1 gene (609502) on chromosome 10q23. CORD16 (614500) is caused by mutation in the C8ORF37 gene (614477) on chromosome 8q22. CORD18 (615374) is caused by mutation in the RAB28 gene (612994) on chromosome 4p15. CORD19 (615860) is caused by mutation in the TTLL5 gene (612268) on chromosome 14q24. CORD20 (615973) is caused by mutation in the POC1B gene (614784) on chromosome 12q21. CORD21 (616502) is caused by mutation in the DRAM2 gene (613360) on chromosome 1p13. CORD22 (619531) is caused by mutation in the TLCD3B gene (615175) on chromosome 16p11. CORD23 (see 613428) is caused by mutation in the C2ORF71 gene (PCARE; 613425) on chromosome 2p23. CORD24 (620342) is caused by mutation in the UNC119 gene (604011) on chromosome 17q11. A diagnosis of CORD was made in an individual with a mutation in the AIPL1 gene (604392.0004) on chromosome 17p13.1, as well as in an individual with a mutation in the UNC119 gene (604011.0001) on chromosome 17q11.2. Other mapped loci for autosomal CORD include CORD1 (600624) on chromosome 18q21.1-q21.3; CORD7 (603649) on chromosome 6q14; CORD8 (605549) on chromosome 1q12-q24; and CORD17 (615163) on chromosome 10q26. For a discussion of X-linked forms of cone-rod dystrophy, see CORDX1 (304020).
Juvenile retinoschisis
MedGen UID:
811458
Concept ID:
C3714753
Disease or Syndrome
X-linked congenital retinoschisis (XLRS) is characterized by symmetric bilateral macular involvement with onset in the first decade of life, in some cases as early as age three months. Fundus examination shows areas of schisis (splitting of the nerve fiber layer of the retina) in the macula, sometimes giving the impression of a spoke wheel pattern. Schisis of the peripheral retina, predominantly inferotemporally, occurs in approximately 50% of individuals. Affected males typically have 20/60 to 20/120 vision. Visual acuity often deteriorates during the first and second decades of life but then remains relatively stable until the fifth or sixth decade.
Macular dystrophy, retinal, 3
MedGen UID:
854716
Concept ID:
C3888009
Disease or Syndrome
Autosomal recessive bestrophinopathy
MedGen UID:
854806
Concept ID:
C3888198
Disease or Syndrome
Bestrophinopathies, the spectrum of ophthalmic disorders caused by pathogenic variants in BEST1, are typically characterized by retinal degeneration. The four recognized phenotypes are the three autosomal dominant disorders: Best vitelliform macular dystrophy (BVMD), BEST1 adult-onset vitelliform macular dystrophy (AVMD), and autosomal dominant vitreoretinochoroidopathy (ADVIRC); and autosomal recessive bestrophinopathy (ARB). Onset is usually in the first decade (except AVMD in which onset is age 30 to 50 years). Slow visual deterioration is the usual course. Choroidal neovascularization can occur in rare cases. ADVIRC is also associated with panophthalmic involvement including nanophthalmos, microcornea, hyperopia, and narrow anterior chamber angle with angle closure glaucoma.
Retinitis pigmentosa-juvenile cataract-short stature-intellectual disability syndrome
MedGen UID:
863679
Concept ID:
C4015242
Disease or Syndrome
A rare genetic syndromic rod-cone dystrophy disorder with characteristics of psychomotor developmental delay from early childhood, intellectual disability, short stature, mild facial dysmorphism (e.g. upslanted palpebral fissures, hypoplastic alae nasi, malar hypoplasia, attached earlobes), excessive dental spacing and malocclusion, juvenile cataract and ophthalmologic findings of atypical retinitis pigmentosa (i.e. salt-and-pepper retinopathy, attenuated retinal arterioles, generalised rod-cone dysfunction, mottled macula, peripapillary sparing of retinal pigment epithelium).
Retinal dystrophy and obesity
MedGen UID:
863861
Concept ID:
C4015424
Disease or Syndrome
Retinitis pigmentosa and erythrocytic microcytosis
MedGen UID:
934743
Concept ID:
C4310776
Disease or Syndrome
Features that occur less commonly in people with TRNT1 deficiency include hearing loss caused by abnormalities of the inner ear (sensorineural hearing loss), recurrent seizures (epilepsy), and problems with the kidneys or heart.\n\nNeurological problems are also frequent in TRNT1 deficiency. Many affected individuals have delayed development of speech and motor skills, such as sitting, standing, and walking, and some have low muscle tone (hypotonia).\n\nTRNT1 deficiency encompasses what was first thought to be two separate disorders, a severe disorder called sideroblastic anemia with B-cell immunodeficiency, periodic fevers, and developmental delay (SIFD) and a milder disorder called retinitis pigmentosa with erythrocytic microcytosis (RPEM), each named for its most common features. SIFD begins in infancy, and affected individuals usually do not survive past childhood. RPEM, on the other hand, is recognized in early adulthood, and the microcytosis usually does not cause any health problems. However, it has since been recognized that some individuals have a combination of features that fall between these two ends of the severity spectrum. All of these cases are now considered part of TRNT1 deficiency.\n\nEye abnormalities, often involving the light-sensing tissue at the back of the eye (the retina), can occur in people with TRNT1 deficiency. Some of these individuals have a condition called retinitis pigmentosa, in which the light-sensing cells of the retina gradually deteriorate. Eye problems in TRNT1 deficiency can lead to vision loss.\n\nIn addition, many individuals with TRNT1 deficiency have recurrent fevers that are not caused by an infection. These fever episodes are often one of the earliest recognized symptoms of TRNT1 deficiency, usually beginning in infancy. The fever episodes are typically accompanied by poor feeding, vomiting, and diarrhea, and can lead to hospitalization. In many affected individuals, the episodes occur regularly, arising approximately every 2 to 4 weeks and lasting 5 to 7 days, although the frequency can decrease with age.\n\nMany people with TRNT1 deficiency have an immune system disorder (immunodeficiency) that can lead to recurrent bacterial infections. Repeated infections can cause life-threatening damage to internal organs. The immunodeficiency is characterized by low numbers of immune system cells called B cells, which normally help fight infections by producing immune proteins called antibodies (or immunoglobulins). These proteins target foreign invaders such as bacteria and viruses and mark them for destruction. In many individuals with TRNT1 deficiency, the amount of immunoglobulins is also low (hypogammaglobulinemia).\n\nA common feature of TRNT1 deficiency is a blood condition called sideroblastic anemia, which is characterized by a shortage of red blood cells (anemia). In TRNT1 deficiency, the red blood cells that are present are unusually small (erythrocytic microcytosis). In addition, developing red blood cells in the bone marrow (erythroblasts) can have an abnormal buildup of iron that appears as a ring of blue staining in the cell after treatment in the lab with certain dyes. These abnormal cells are called ring sideroblasts.\n\nTRNT1 deficiency is a condition that affects many body systems. Its signs and symptoms can involve blood cells, the immune system, the eyes, and the nervous system. The severity of the signs and symptoms vary widely.
Retinitis pigmentosa 81
MedGen UID:
1637738
Concept ID:
C4693443
Disease or Syndrome
Retinal macular dystrophy type 2
MedGen UID:
1666864
Concept ID:
C4749334
Disease or Syndrome
A rare, genetic macular dystrophy disorder characterised by slowly progressive bull''s eye maculopathy associated, in most cases, with mild decrease in visual acuity and central scotomata. Usually, only the central retina is involved, however some cases of more widespread rod and cone anomalies have been reported. Rare additional features include empty sella turcica, impaired olfaction, renal infections, haematuria and recurrent miscarriages. Caused by mutation in the prominin-1 gene (PROM1).
Retinitis pigmentosa 86
MedGen UID:
1684789
Concept ID:
C5231428
Disease or Syndrome
Retinitis pigmentosa-86 (RP86) is characterized by night blindness followed by progressive narrowing of visual fields and decline in visual acuity, with typical findings of RP on fundus examination, including attenuated retinal vessels, waxy pallor of the optic disc, and bone spicule-like pigmentation (de Bruijn et al., 2018). For a general phenotypic description and a discussion of genetic heterogeneity of retinitis pigmentosa, see 268000.
Retinitis pigmentosa 90
MedGen UID:
1733837
Concept ID:
C5436588
Disease or Syndrome
Retinitis pigmentosa-90 (RP90) is characterized by early-onset night blindness, within the first decade of life. Patients exhibit other typical features of RP, including retinal vessel attenuation, optic disc pallor, and retinal pigment epithelium (RPE) atrophy and pigmentation abnormalities. Macular pseudocoloboma and cystoid macular edema have also been observed (Pierrache et al., 2017). For a discussion of genetic heterogeneity of RP, see 268000.
Cone-rod dystrophy 22
MedGen UID:
1794199
Concept ID:
C5561989
Disease or Syndrome
Cone-rod dystrophy-22 (CORD22) is a retinal dystrophy characterized by loss of central vision due to cone photoreceptor degeneration, with onset of symptoms ranging from the first to fifth decades of life. There is significant degeneration of the macula, as well as generalized cone system involvement that predominates over rod system dysfunction, including in the peripheral retina (Bertrand et al., 2021). For a general phenotypic description and discussion of genetic heterogeneity of CORD, see CORD2 (120970).

Professional guidelines

PubMed

Fukuyama H, Komuku Y, Gomi F
Jpn J Ophthalmol 2021 May;65(3):372-379. Epub 2021 Feb 3 doi: 10.1007/s10384-021-00815-x. PMID: 33532933
Kim M, Kim ES, Seo KH, Yu SY, Kwak HW
Indian J Ophthalmol 2016 Jun;64(6):427-33. doi: 10.4103/0301-4738.187659. PMID: 27488150Free PMC Article
Young M, Chui L, Fallah N, Or C, Merkur AB, Kirker AW, Albiani DA, Forooghian F
Retina 2014 Jul;34(7):1308-15. doi: 10.1097/IAE.0000000000000081. PMID: 24451923

Recent clinical studies

Etiology

Rohart C, Le HM, Estrada-Walker J, Giocanti-Auregan A, Cohen SY
Retina 2023 Jun 1;43(6):882-887. doi: 10.1097/IAE.0000000000003746. PMID: 36727798
Shroff D, Agarwal A, Saha I, Aggarwal K, Grover S, Gupta V, Shroff C, Querques G
Retin Cases Brief Rep 2022 May 1;16(3):275-279. Epub 2020 Jan 22 doi: 10.1097/ICB.0000000000000972. PMID: 31977927
Cho HJ, Kim K, Lim SH, Kang DH, Kim JW
Br J Ophthalmol 2020 Oct;104(10):1443-1447. Epub 2020 Jan 2 doi: 10.1136/bjophthalmol-2019-315496. PMID: 31896542
Baek J, Lee JH, Lee WK
Graefes Arch Clin Exp Ophthalmol 2019 Sep;257(9):1863-1871. Epub 2019 Jun 20 doi: 10.1007/s00417-019-04388-x. PMID: 31222406
Kuroda Y, Yamashiro K, Tsujikawa A, Ooto S, Tamura H, Oishi A, Nakanishi H, Miyake M, Yoshikawa M, Yoshimura N
Am J Ophthalmol 2016 Jan;161:94-103.e1. Epub 2015 Oct 1 doi: 10.1016/j.ajo.2015.09.032. PMID: 26432927

Diagnosis

Liu W, Liu S, Li P, Yao K
Int J Mol Sci 2022 Apr 28;23(9) doi: 10.3390/ijms23094883. PMID: 35563274Free PMC Article
Cho HJ, Kim K, Lim SH, Kang DH, Kim JW
Br J Ophthalmol 2020 Oct;104(10):1443-1447. Epub 2020 Jan 2 doi: 10.1136/bjophthalmol-2019-315496. PMID: 31896542
Baek J, Lee JH, Lee WK
Graefes Arch Clin Exp Ophthalmol 2019 Sep;257(9):1863-1871. Epub 2019 Jun 20 doi: 10.1007/s00417-019-04388-x. PMID: 31222406
Kuroda Y, Yamashiro K, Tsujikawa A, Ooto S, Tamura H, Oishi A, Nakanishi H, Miyake M, Yoshikawa M, Yoshimura N
Am J Ophthalmol 2016 Jan;161:94-103.e1. Epub 2015 Oct 1 doi: 10.1016/j.ajo.2015.09.032. PMID: 26432927
Bird AC
Br J Ophthalmol 1975 Apr;59(4):177-99. doi: 10.1136/bjo.59.4.177. PMID: 1138842Free PMC Article

Therapy

Shroff D, Agarwal A, Saha I, Aggarwal K, Grover S, Gupta V, Shroff C, Querques G
Retin Cases Brief Rep 2022 May 1;16(3):275-279. Epub 2020 Jan 22 doi: 10.1097/ICB.0000000000000972. PMID: 31977927
Cho HJ, Kim K, Lim SH, Kang DH, Kim JW
Br J Ophthalmol 2020 Oct;104(10):1443-1447. Epub 2020 Jan 2 doi: 10.1136/bjophthalmol-2019-315496. PMID: 31896542
Kuroda Y, Yamashiro K, Tsujikawa A, Ooto S, Tamura H, Oishi A, Nakanishi H, Miyake M, Yoshikawa M, Yoshimura N
Am J Ophthalmol 2016 Jan;161:94-103.e1. Epub 2015 Oct 1 doi: 10.1016/j.ajo.2015.09.032. PMID: 26432927
Ferrucci S, Anderson SF, Townsend JC
Optom Vis Sci 1998 Aug;75(8):560-70. doi: 10.1097/00006324-199808000-00021. PMID: 9734800
Roberts TV, Francis IC, Kappagoda MB, Dick AD
Eye (Lond) 1995;9 ( Pt 5):594-8. doi: 10.1038/eye.1995.146. PMID: 8543079

Prognosis

Rohart C, Le HM, Estrada-Walker J, Giocanti-Auregan A, Cohen SY
Retina 2023 Jun 1;43(6):882-887. doi: 10.1097/IAE.0000000000003746. PMID: 36727798
Cho HJ, Kim K, Lim SH, Kang DH, Kim JW
Br J Ophthalmol 2020 Oct;104(10):1443-1447. Epub 2020 Jan 2 doi: 10.1136/bjophthalmol-2019-315496. PMID: 31896542
Baek J, Lee JH, Lee WK
Graefes Arch Clin Exp Ophthalmol 2019 Sep;257(9):1863-1871. Epub 2019 Jun 20 doi: 10.1007/s00417-019-04388-x. PMID: 31222406
Hata M, Yamashiro K, Oishi A, Ooto S, Tamura H, Miyata M, Ueda-Arakawa N, Kuroda Y, Takahashi A, Tsujikawa A, Yoshimura N
Retina 2017 Nov;37(11):2069-2077. doi: 10.1097/IAE.0000000000001457. PMID: 28085772
Ferrucci S, Anderson SF, Townsend JC
Optom Vis Sci 1998 Aug;75(8):560-70. doi: 10.1097/00006324-199808000-00021. PMID: 9734800

Clinical prediction guides

Fukuyama H, Komuku Y, Gomi F
Jpn J Ophthalmol 2021 May;65(3):372-379. Epub 2021 Feb 3 doi: 10.1007/s10384-021-00815-x. PMID: 33532933
Baek J, Lee JH, Lee WK
Graefes Arch Clin Exp Ophthalmol 2019 Sep;257(9):1863-1871. Epub 2019 Jun 20 doi: 10.1007/s00417-019-04388-x. PMID: 31222406
Kuroda Y, Yamashiro K, Ooto S, Tamura H, Oishi A, Nakanishi H, Miyata M, Hata M, Takahashi A, Wakazono T, Yoshimura N, Tsujikawa A
Retina 2018 Sep;38(9):1743-1750. doi: 10.1097/IAE.0000000000001765. PMID: 28691937
Kim M, Kim ES, Seo KH, Yu SY, Kwak HW
Indian J Ophthalmol 2016 Jun;64(6):427-33. doi: 10.4103/0301-4738.187659. PMID: 27488150Free PMC Article
Hikichi T, Kitamei H, Shioya S
BMC Ophthalmol 2016 May 16;16(1):55. doi: 10.1186/s12886-016-0237-x. PMID: 27184489Free PMC Article

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