5,055 Matching Annotations
  1. Sep 2026
    1. MD-0247ABCA423c.3386G>Tp.Arg1129Leu47c.6410G>Ap.Cys2137Tyr12YesABCR400 + dHPLC + HRMAguirre-Lamban et al. 2009 (8); Aguirre-Lamban et al. 2010 (16)

      Case#: Family MD-0247 Proband, 12yo at onset

      DiseaseAssertion: AR cone rod dystrophy

      FamilyInfo:

      CasePresentingHPOs:

      CaseHPOFreeText: STGD diagnosed based on "bilateral central vision loss; fundus presenting with a beaten-bronze appearance and/or the presence of orange-yellow flecks in the retina from the posterior pole to the mid-periphery; fluorescein angiography showing typical dark choroid; and normal to subnormal electroretinogram (ERGs)." VA loss, VF loss, BCVA=0.05/0.1, cone-pattern on ERG

      CaseNotHPOs:

      CaseNotHPOFreeText:

      PreviouslyPublished: Aguirre-Lamban et al. 2009 (8); PMID: 19959634

      Variant: c.6410G>A (p.Cys2137Tyr); c.3386G>T (p.Arg1129Leu) found by ABCR400 + dHPLC + HRM

      ClinVar: 2202779; 99224

      CAID: CA341277358; CA227116

      SupplementalData:

    1. Table S9. List of unique causative variants detected in 858 STGD probands mmc8.xlsx (19.3KB, xlsx) Table S11. STGD1 cases with at least two (likely) causal ABCA4 variants mmc9.xlsx (39.6KB, xlsx)

      Case#: DNAID 072962/Pat272, male

      DiseaseAssertion: STGD1

      FamilyInfo: n/a

      CasePresentingHPOs:

      CaseHPOFreeText: "In classic STGD1, loss of central vision starts around the second decade of life, but both early- and late-onset subtypes have been extensively described." No patient-specific details provided

      CaseNotHPOs:

      CaseNotHPOFreeText:

      GenotypingMethod: smMIPs sequencing of the complete ABCA4 locus

      PreviouslyPublished: n/a

      Variant: c.6416G>A (p.Arg2139Gln); c.6445C>T (p.Arg2149Ter)

      CAID: CA956878

      SupplementalData: tables s9 and s11

    2. Table S9. List of unique causative variants detected in 858 STGD probands mmc8.xlsx (19.3KB, xlsx) Table S11. STGD1 cases with at least two (likely) causal ABCA4 variants mmc9.xlsx (39.6KB, xlsx)

      Case#: DNAID 072284/Pat191, female

      DiseaseAssertion: STGD1

      FamilyInfo: n/a

      CasePresentingHPOs:

      CaseHPOFreeText: "In classic STGD1, loss of central vision starts around the second decade of life, but both early- and late-onset subtypes have been extensively described." No patient-specific details provided

      CaseNotHPOs:

      CaseNotHPOFreeText:

      GenotypingMethod: smMIPs sequencing of the complete ABCA4 locus

      PreviouslyPublished: n/a

      Variant: c.1519G>T (p.Asp507Tyr); c.4139C>T (p.Pro1380Leu) phase not confirmed

      CAID: CA958508

      SupplementalData: tables s9 and s11

    1. We identified 255 patients (87.9 %) harboring biallelic ABCA4 variants, 27 probands (9.3 %) with two or three variants but lacking familial segregation analysis, and eight patients (2.8 %) with monoallelic ABCA4 variants (Supplemental Table S4). We detected 268 distinct ABCA4 variants, consisting of 114 missense, 35 nonsense, 34 frameshift deletion or insertion, 31 canonical splice variants, 13 noncanonical splice site variants, 9 in-frame deletion or insertion, 9 DIVs, 4 structural variations, and 19 complex variants (Fig. 2).

      Case#: Patient#010633, Chinese, female, 20yo at onset

      DiseaseAssertion: stargardt

      FamilyInfo: n/a

      CasePresentingHPOs: STGD1 diagnosis based on the following criteria: "a bilateral central vision defect; fundus displaying a beaten-bronze appearance and/or orange-yellow flecks in the retina from the macula to the midperiphery; fluorescein angiography presenting with a typical dark choroid; and normal to subnormal ERG results." BCVA=0.05/ 0.05

      CaseHPOFreeText:

      CaseNotHPOs:

      CaseNotHPOFreeText:

      PreviouslyPublished: n/a

      Variant: p.P2097S; c.3468C>G p.(Tyr1156*) phase unknown

      ClinVar: 2202780;

      CAID: CA341277622;

      SupplementalData: supplementary table S4 has phenotype information

    1. In 20 patients (19 STGD and 1 CRD), 18 different genotypes were identified (Table 1). Except p.Arg187His and p.Tyr954Ser variants, the rest of changes were previously reported as disease-associated allele. 14 The p.Arg187His and p.Tyr954Ser variants were not found in 100 ethnically matched control chromosomes. All the mutations identified in the 20 patients except one were detected by HRM for sensitivity of 95%; however, only 16 variants were identified by dHPLC for sensitivity of 80%.  Table 1. View Table Mutations AnalyzedTable 1. Mutations Analyzed Family Exon Genotype Mutation Detected by dHPLC Mutation Detected by HRM Nucleotide Change Amino Acid Change ARDM-167 5 c.560G>A p.Arg187His No Yes ARDM-257 5 c.560G>A p.Arg187His No Yes ARDM-164 6 c.700C>T p.Gln234X Yes Yes ARDM-135 8 c.1029_1030insT p.Asn344fsX Yes No ARDM-240 15 c.2285C>A p.Ala762Glu Yes Yes ARDM-248 19 c.2861A>C p.Tyr954Ser Yes Yes ARDM-90 — IVS21-2A>T — Yes Yes ARDM-40 27 c.3943C>T p.Gln1315X Yes Yes ARDM-158 30 c.4537delC p.Gln1513fsX1525 Yes Yes ARDM-38 33 c.4739delT p.Leu1580fs Yes Yes ARDM-163 36 c.5172G>T p.Trp1724Cys Not Yes ARDM-197 36 c.5172G>T p.Trp1724Cys Yes Yes ARDM-181 — IVS38+5G>A — Yes Yes ARDM-125 40 — p.KNLFA1876dup Yes Yes ARDM-183 43 c.5929G>A(False −) p.Gly1977Ser(False −) Yes Yes ARDM-146 44 c.6140T>A p.lle2047Asn Yes Yes ARDM-174 — IVS44+2T>A — Yes Yes ARDM-247 47 c.6410G>A p.Cys2137Tyr* Yes Yes ARDM-84 47 c.6410G>A p.Cys2137Tyr† No Yes ARDM-225 48 c.6559C>T p.Gln2187X Yes Yes  Previously unreported mutations are shown in bold. *  Mutation in heterozygous. †  Mutation in homozygous. Homozygous sequence alteration (p.Cys2137Tyr) could be identified from wild-type by HRM analyses (Fig. 1). In contrast, dHPLC did not distinguish any homozygous mutation, except when we mixed it, in a 1:1 proportion, with a previously sequenced wild-type sample at the end of each PCR session and before heteroduplex formation.

      Case#: Family MD-0247/ARDM-247 Proband, 12yo at onset

      DiseaseAssertion: AR cone rod dystrophy

      FamilyInfo:

      CasePresentingHPOs:

      CaseHPOFreeText: STGD diagnosed based on "bilateral central vision loss; fundus presenting with a beaten-bronze appearance and/or the presence of orange-yellow flecks in the retina from the posterior pole to the mid-periphery; fluorescein angiography showing typical dark choroid; and normal to subnormal electroretinogram (ERGs)." VA loss, VF loss, BCVA=0.05/0.1, cone-pattern on ERG

      CaseNotHPOs:

      CaseNotHPOFreeText:

      PreviouslyPublished: PMID: 19028736

      Variant: c.6410G>A (p.Cys2137Tyr); c.3386G>T (p.Arg1129Leu) found by ABCR400 + dHPLC + HRM

      ClinVar: 2202779

      CAID: CA341277358

      SupplementalData: n/a

    1. 5137 Mo 25 3/10 / FC ND / c.32T>C(1) ND/p.Leu11Pro

      Case#: Maia-Lopes Family 17 Proband 5137, Portuguese, 25yo at onset

      DiseaseAssertion: STGD

      FamilyInfo: Family 17

      CasePresentingHPOs:

      CaseHPOFreeText: moderate central fundus changes, vision: 3/10 / FC

      CaseNotHPOs:

      CaseNotHPOFreeText:

      GenotypingMethod: ABCR400 microarray, dHPLC

      PreviouslyPublished: n/a

      Variant: ND / c.32T>C(1); ND/p.Leu11Pro

      ClinVar: 99217

      CAID: CA227106

      SupplementalData: n/a

    1. Supplementary data. bjophthalmol-2018-312064supp004.pdf

      This variant is found on pg 2 in proband 11019. Compound heterozygous for c.4532C>A, (p.Pro1511His). JHU institute (US). Said to have Stargardt based on the following criteria: "(1) patients (at least 6 years old) with at least two ABCA4 variants or one ABCA4 variant associated with a typical STGD1 phenotype and (2) presence of a well-defined atrophic lesion with/without flecks at the most recent visit of at least 300 µm in diameter (the total area of all lesions <12 mm2)." No additional details provided

    2. Supplementary data. bjophthalmol-2018-312064supp004.pdf

      This variant is found on pg 21 in proband 13047. Compound heterozygous for c.5882G>A p.Gly1961Glu. Said to have Stargardt based on the following criteria: "(1) patients (at least 6 years old) with at least two ABCA4 variants or one ABCA4 variant associated with a typical STGD1 phenotype and (2) presence of a well-defined atrophic lesion with/without flecks at the most recent visit of at least 300 µm in diameter (the total area of all lesions <12 mm2)." No additional details provided

    1. 13/8 35 0.017 163 0 – 3 – 3 4 L541P R1098C

      Case#: Patient 13, 35yo

      DiseaseAssertion: STGD

      FamilyInfo: Family 8

      CasePresentingHPOs:

      CaseHPOFreeText: Visual acuity=0.017. OCT ft (μm)=163. MP (dB)=0. Fundus=3(extensive atrophic-appearing RPE changes). ERG=3(abnormal responses involving both rods and cones). mfERG=4(subnormal mfERG in the entire test field (0°–30°) plus pathologic Ganzfeld ERG).

      CaseNotHPOs:

      CaseNotHPOFreeText:

      GenotypingMethod: PCR of coding regions, intron/exon boundaries, and 5′ and 3′ regions of ABCA4; Standard cycle-sequencing reactions with BigDye Terminator

      PreviouslyPublished:

      Variant: L541P; R1098C

      CAID: CA226911;

      SupplementalData: n/a

    1. 48-year-old man

      Case#:48-year old man, onset at 13-years old

      DiseaseAssertion: STGD1

      FamilyInfo: n/a

      CasePresentingHPOs: HP:0003621, HP:0025147, HP:0011507, HP:0030329, HP:0030610, HP:0007722, HP:0007703, HP:0007663

      CaseHPOFreeText: BCVA was 20/200 bilaterally and refractive error was OD: −1.50/+0.50 × 149° and OS: −1.50/+0.25 × 161°. Hyperautofluorescent transitional zone in each eye more pronounced in right eye. The left eye showed a complete defect of the RPE-Bruch membrane complex with herniation of the outer retina. Maximum horizontal diameter of this RPE-Bruch membrane complex defect was 266um.

      CaseNotHPOs: HP:0000510, HP:0000548, HP:0007984

      CaseNotHPOFreeText: No defect observed in the RPE and Bruch membrane in right eye. Patient had normal cone and rod responses on ERG

      Genotyping Method: ABCR 600 micro-array chip

      PreviouslyPublished: n/a

      Variant: NM_000350.3(ABCA4):c.4216C>T (p.His1406Tyr), NM_000350.3(ABCA4):c.5882G>A (p.Gly1961Glu)

      ClinVar: 99259, 7888

      SupplementalData: n/a

    1. Seventy eyes (38 patients), of which 46 (66%) were female and 24 (34%) male, with RPE atrophy secondary to ABCA4 -related retinopathy (age [years], 45.51 ± 16.70; range 14–78) were included in the study ( Table 1 and see Table, Supplemental Digital Content 2 , http://links.lww.com/IAE/B170 , which shows the individual baseline and progression data of all included eyes).

      Case#: Patient #33, female, 64yo at baseline visit, "late" age of onset

      DiseaseAssertion: ABCA4-related retinopathy with secondary RPE atrophy

      FamilyInfo:

      CasePresentingHPOs:

      CaseHPOFreeText: Inclusion criteria were defined as 1) presence of at least one mutated allele in ABCA4 (NM_000350.2) in Sanger sequencing with multiplex ligation-dependent probe amplification analysis or next-generation sequencing,9 2) a compatible phenotype with flecks at the level of the RPE consistent with ABCA4 -related Stargardt disease,9 3) presence of RPE atrophy, and 4) serial examinations with an interval of at least 6 months. RPE atrophy to the end-stage (i.e., demarcated lesions with ≥90% darkness of the optic disc under short-wavelength excitation light, DDAF) that previously showed highest interreader agreement.7 The size of DDAF has to be at least 0.05 mm 2 (each single atrophic area in cases of multifocality), and the entire lesion must be completely visualized on the AF image at each visit to be advanced for analysis. Self-reported symptom onset into early-onset (≤10 years), intermediate-onset (11–44 years), and late-onset (≥45 years). ff-ERG based Category: Group 1 contained eyes with normal scotopic and photopic responses; Group 2, eyes with normal scotopic responses, but reduced (over 2 SDs) photopic B-wave and 30-Hz flicker amplitudes; and Group 3, eyes with impairment of both rod- and cone-driven responses. BCVA: OD=0.4, OS=1.1 [LogMAR] .

      CaseNotHPOs:

      CaseNotHPOFreeText: Insufficient pupil dilation, additional retinal pathology, previous retinal treatment, or other ocular comorbidities substantially affecting image quality led to exclusion from the study

      GenotypingMethod: Sanger sequencing with multiplex ligation-dependent probe amplification analysis or next-generation sequencing

      PreviouslyPublished: possible since Birtel is an author on this paper and the probands both have the same second variant as in PMID: 29555955

      Variant: allele 1: c.3468C>G p.(Tyr1156*) allele 2: c.5059A>T p.(Ile1687Phe); c.4297G>A p.(Val1433Ile)

      ClinVar: n/a

      CAID: CA341290648

      SupplementalData: The supplemental table linked here contains genotype and phenotype information.

    1. 3 39 6/6 1 RCD Val552Ile 6/6

      Case#: Case 3, 39yo

      DiseaseAssertion: BEM, RCD

      FamilyInfo: n/a

      CasePresentingHPOs:

      CaseHPOFreeText: a ring of increased AF surrounding decreased foveal AF, visual acuity= 6/6, 6/6

      CaseNotHPOs:

      CaseNotHPOFreeText: acquired toxic aetiology

      GenotypingMethod: The entire coding sequence (50 exons), including exon–intron boundaries, of the ABCA4 gene of each patient was screened using single‐stranded conformational polymorphism (SSCP) analysis and direct sequencing.

      PreviouslyPublished: n/a

      Variant: Val552Ile heterozygous

      CAID: CA239745

      SupplementalData: n/a

    1. Disease-causing or likely disease-causing mutations were identified in 185 out of 251 patients (74%) with MD/CCRD (Supplementary Table 1).

      Case#: Patient #42, female, 31yo at onset, German

      DiseaseAssertion: macular dystrophy or cone-rod dystrophy

      FamilyInfo: phase not confirmed, but assumed in case of parental consanguinity or if only siblings were affected

      CasePresentingHPOs: HP:0012508

      CaseHPOFreeText:

      CaseNotHPOs:

      CaseNotHPOFreeText: syndromic retinal disease, age-related macular degeneration, central serous retinopathy, autoimmune retinopathy, retinal vascular disease, achromatopsia, X-linked retinoschisis, North Carolina macular dystrophy

      PreviouslyPublished: n/a

      Variant: c.3468C>G (p.Tyr1156Ter); c.5059A>T (p.Ile1687Phe) Sanger sequencing of ABCA4

      ClinVar: n/a

      CAID: CA341290648

      SupplementalData: Supplementary table 1

    1. Family 1ABCA4c.[1957C>T];[4604dup]M7.06.0PV, PP0.200.15MA, TPOD, ARAMA, TPOD, ARANormalReduced

      Case#: Family 1 proband, male, 6yo at onset, Chinese

      DiseaseAssertion: CORD

      FamilyInfo: heterozygous unaffected parents

      CasePresentingHPOs: HP:0000613, HP:0000505, HP:0007401, HP:0012511, HP:0008043, HP:0000512

      CaseHPOFreeText:  ERG responses from cones reduced, BVA=0.20/0.15

      CaseNotHPOs:

      CaseNotHPOFreeText:

      PreviouslyPublished: n/a

      Variant: c.[1957C>T];[4604dup] phase confirmed

      ClinVar: n/a

      CAID: CA645372205

      SupplementalData:

    1. 024 m Caucasian STGD ABCA4 NM_000350.2 c.[6601_6602delAG];[=], c.[4253+43G>A];[=] p.Arg2201fs* p.Ile1377Hisfs*3 Not found 0.004694 AR Pathogenic Pathogenic 2 [36] [19]

      Case#: Patient 24, male, Caucasian, onset at 50yo, Germany

      DiseaseAssertion: STGD

      FamilyInfo: co-segregation of variant in 2 family members (siblings) but they do not appear to be affected based on pedigree

      CasePresentingHPOs: HP:0030528, HP:0000505, HP:0012508, HP:0001105, HP:0025148

      CaseHPOFreeText: progressive paracentral scotoma OU, progressive visual impairment OU (blurry vision). BCVA: OD-0.1, OS-0.22. Tension: 13mmHg/14mmHg. FAF: bilateral hyperautofluorescent macular and peripapillary spots, few spots of paracentral retinal atrophy (foveal sparing). Autofluorescence and deposits (severity): deposits medium, atrophy low. OCT: hyperreflective spots, partially invading into the outer retina, partly confluent lesions of cRORA, foveal sparing, degenerative intraretinal fluid. Central macular thickness: 328µm/322µm. Macular volume: 9.31mm³/9.00mm³. mfERG: bilateral amplitudes in normal range, slight relative reduction in the paracentral areas. Fluorescein angiography: bilateral dark choroid, mild paracentral dye pooling in the late phase. Color vision: Inconspicuous. Clinical examination: pattern-like distribution of the lesions.

      CaseNotHPOs: n/a

      CaseNotHPOFreeText: n/a

      GenotypingMethod: WES, in-house RD-associated gene panel including 619 candidates and disease-associated genes

      PreviouslyPublished: n/a

      Variant: ABCA4 NM_000350.2 c.[6601_6602delAG] (p.Arg2201fs);[=], c.[4253+43G>A] p.Ile1377Hisfs3;[=]

      CAID: CA227421; CA227172

      SupplementalData: phenotype and segregation info in supplemental data (table s1, figure s1)

    1. F17-003

      Case#: Patient 225, Female, age of onset 7 y.o, Poland

      DiseaseAssertion: STGD-1

      FamilyInfo: no given family information.

      CasePresentingHPOs: HP:0007722, HP:0000608, HP:0025158

      CaseHPOFreeText: RPE atrophy, macular degeneration, central hyper-autofluorescence in fundus autofluorescence

      CaseNotHPOs: n/a

      CaseNotHPOFreeText: n/a, non-proband identified HPO's mentioned, but not assignable to individual proband.

      Genotyping Method: DNA isolated from peripheral blood from patients and relatives via MagNA Pure 24, samples screened with MIPs targeting 108 genes involved in pathogensis of IRD's. PCR completed on library, analysed with NGS fragment analysis kit.

      PreviouslyPublished: yes

      Variant: c.[1622T>C;3113C>T]

      ClinVar: 99067, 7894

      CAID: n/a

      gnomeAD 0.0001266 allele frequency

      SupplementalData: Fig1: List of families displaying pseudo-dominant inheritance. Fig2: Number of alleles for most common variants.

    1. Mutation scanning and direct DNA sequencing of all 50 exons of ABCR were completed for 150 families segregating recessive Stargardt disease (STGD1). ABCR variations were identified in 173 (57%) disease chromosomes, the majority of which represent missense amino acid substitutions. These ABCR variants were not found in 220 unaffected control individuals (440 chromosomes) but do cosegregate with the disease in these families with STGD1, and many occur in conserved functional domains. Missense amino acid substitutions located in the amino terminal one-third of the protein appear to be associated with earlier onset of the disease and may represent misfolding alleles. The two most common mutant alleles, G1961E and A1038V, each identified in 16 of 173 disease chromosomes, composed 18.5% of mutations identified. G1961E has been associated previously, at a statistically significant level in the heterozygous state, with age-related macular degeneration (AMD). Clinical evaluation of these 150 families with STGD1 revealed a high frequency of AMD in first- and second-degree relatives. These findings support the hypothesis that compound heterozygous ABCR mutations are responsible for STGD1 and that some heterozygous ABCR mutations may enhance susceptibility to AMD.

      Annotating here since the full text is a PDF.

      Case#: Family AR321 proband, US, 6yo at onset

      DiseaseAssertion: Stargardt

      FamilyInfo: proband and two other siblings are affected

      CasePresentingHPOs: The essential and defining features of STGD were (1) pedigrees with at least one living affected individual compatible with autosomal recessive inheritance; (2) an ophthalmoscopically characteristic retinal disorder in families with both parents living; (3) bilateral central visual loss with both “beaten metal” elliptical foveal dystrophy and temporal pallor of the optic discs, documented by retinal color photography, with or without yellow-pigment epithelial flecks in the macular and/or retinal “near periphery”; and (4) the characteristic fluorescein angiographic feature of a dark choroid (Blacharski 1988).

      CaseHPOFreeText:

      CaseNotHPOs:

      CaseNotHPOFreeText: (1) evidence of autosomal dominant inheritance; (2) any history of night blindness, loss of peripheral vision, or "retinitis pigmentosa"; (3) cataracta complicata or cells in the vitreous; (4) substantially abnormal electroretinographic or electrooculographic responses; (5) no fluorescein angiography performed or no dark choroid documented; (6) neurological disease (including loss of cognition or seizures); 7) drug exposures (especially to antimalarial and agents known to cause crystalline retinopathies); or (8) any "atypical" maculopathies in which a unique diagnosis of STGD could not be established.

      PreviouslyPublished: PMID: 8533764

      Variant: c.3113C>T p.A1038V; c.1715G>C p.R572P . Heteroduplex and SSCP analyses were used to screen the 50 exons of ABCA4. Linkage analysis and haplotype analysis were previously performed

      ClinVar: 99073

      CAID: CA226919

      SupplementalData: n/a

    1. JB260 Stargardt ABCA4 c.6119G>A p.Arg2040Gln rs148460146 Zernant et al (2014)50 c.2879del p.Ala960Aspfs*17 N/A

      Case#: Bryant Subject JB260, US

      DiseaseAssertion: Stargardt

      FamilyInfo:

      CasePresentingHPOs: "Stargardt disease is a childhood-onset macular degeneration and is most commonly caused by mutations in ABCA4. Characteristic yellow flecks are typically seen under the macula during a fundus exam."

      CaseHPOFreeText:

      CaseNotHPOs:

      CaseNotHPOFreeText:

      GenotypingMethod: WES; previously screened using arrayed primer extension (APEX) multigene panels for the relevant disease and no disease-causing variants had been identified; PCR and Sanger for verification

      PreviouslyPublished: n/a

      Variant: c.6119G>A p.Arg2040Gln; c.2879del p.Ala960Aspfs*17

      CAID: CA232815

      SupplementalData:

    1. See Supplementary Table S2 for a complete genotypic glossary of the cohort.

      Case#: Patients were identified from the inherited retinal disease (IRD) database at UC San Diego (UCSD).

      DiseaseAssertion: RP with macular edema

      FamilyInfo:

      CasePresentingHPOs:

      CaseHPOFreeText: Dx of RP based on "a history of progressive peripheral vision loss or nyctalopia, and ocular examination findings of RP including bone spicule pigmentation, disc pallor and attenuated vessels and genetic confirmation."

      CaseNotHPOs:

      CaseNotHPOFreeText:

      GenotypingMethod: Next-generation sequencing (NGS), exome sequencing, and/or targeted Sanger sequencing were the primary genetic testing approaches.

      PreviouslyPublished: PMID:10206579 is referenced but it seems a reference to the variant and not the proband

      Variant: c.6383A>G (p.His2128Arg); c.3G>T (p.Met1?). phase unknown

      ClinVar: 99455

      CAID: CA227399

      SupplementalData: Variant is found in table S2

  2. Jul 2026
    1. F17-003

      Case#: Patient 225, Female, age of onset 7 y.o, Poland

      DiseaseAssertion: STGD-1

      FamilyInfo: no given family information.

      CasePresentingHPOs: HP:0007722, HP:0000608, HP:0025158

      CaseHPOFreeText: RPE atrophy, macular degeneration, central hyper-autofluorescence in fundus autofluorescence

      CaseNotHPOs: n/a

      CaseNotHPOFreeText: n/a, non-proband identified HPO's mentioned, but not assignable to individual proband.

      Genotyping Method: DNA isolated from peripheral blood from patients and relatives via MagNA Pure 24, samples screened with MIPs targeting 108 genes involved in pathogensis of IRD's. PCR completed on library, analysed with NGS fragment analysis kit.

      PreviouslyPublished: yes

      Variant: c.[1622T>C;3113C>T]

      ClinVar: 99067, 7894

      CAID: n/a

      gnomeAD 0.0001266 allele frequency

      SupplementalData: Fig1: List of families displaying pseudo-dominant inheritance. Fig2: Number of alleles for most common variants.

    1. Sixty-six individuals representing 54 families were studied (Supplementary Material, Table S1). All individuals were found to harbor two ABCA4 variants likely to cause the retinal disease (18,20–26). In 40 families (74%), independent segregation of the two alleles was demonstrated. The ages at the time of their first visit ranged from 9 to 74 years (mean = 35.9, median = 35.2 years); in the majority of individuals (36/66=55%), data were available from a second visit that occurred on average 8.7 years (range=2–20 years, median = 6.9 years) after the first visit.

      Case#: Patient #35, male, 35yo at report, 14yo at onset,

      DiseaseAssertion: STGD

      FamilyInfo: family 30, segregation was noted as "yes" but no other details provided

      CasePresentingHPOs:

      CaseHPOFreeText:

      CaseNotHPOs:

      CaseNotHPOFreeText:

      GenotypingMethod:

      PreviouslyPublished: n/a

      Variant: allele 1: A1038V;L541P allele 2: G818E

      ClinVar: 99135

      CAID: CA227000

      SupplementalData: supplemental table 1

    1. STGD87 2588G→C Q1750X Yes

      Case#: STGD87, 10-14yo at onset, German

      DiseaseAssertion: STGD

      FamilyInfo: segregation in family

      CasePresentingHPOs:

      CaseHPOFreeText: "The diagnosis of STGD was based on the demonstration of bilateral impairment of central vision and the appearance of perimacular and/or peripheral yellow-white flecks, with or without atrophy of the central retinal-pigment epithelium and a normal or only mildly abnormal flash electroretinogram when recorded in early stages of the disease."

      CaseNotHPOs:

      CaseNotHPOFreeText:

      GenotypingMethod: denaturing gradient gel electrophoresis, dHPLC, and SSCP analysis, PCR amplification of individual coding exons and flanking intron sequences, direct DNA sequencing

      PreviouslyPublished: n/a

      Variant: Q1750X; 2588G→C in trans "Correct segregation of disease alleles was demonstrated in all 39 cases in which family samples were available for study"

      ClinVar: 7879

      CAID: CA119128

      SupplementalData: n/a

    2. STGD47/164 IVS13+1G→A 2588G→C Yes

      Case#: STGD47/164, 10-14yo at onset, German

      DiseaseAssertion: STGD

      FamilyInfo: segregation in family

      CasePresentingHPOs:

      CaseHPOFreeText: "The diagnosis of STGD was based on the demonstration of bilateral impairment of central vision and the appearance of perimacular and/or peripheral yellow-white flecks, with or without atrophy of the central retinal-pigment epithelium and a normal or only mildly abnormal flash electroretinogram when recorded in early stages of the disease."

      CaseNotHPOs:

      CaseNotHPOFreeText:

      GenotypingMethod: denaturing gradient gel electrophoresis, dHPLC, and SSCP analysis, PCR amplification of individual coding exons and flanking intron sequences, direct DNA sequencing

      PreviouslyPublished: n/a

      Variant: IVS13+1G→A; 2588G→C in trans "Correct segregation of disease alleles was demonstrated in all 39 cases in which family samples were available for study"

      ClinVar: 7879

      CAID: CA119128

      SupplementalData: n/a

    1. Case 4A 52-year-old male was examined for declining vision OS over the past few months. He was previously clinically diagnosed with STGD 7 years before presentation. Family history was not significant for ocular disease. Best-corrected visual acuity measured 20/100 OD and 20/70 OS. Spherical refractive error measured −3.00 OD and −3.25 OS. Anterior segment examination was unremarkable and applanation tonometry measured 17 mmHg OD and 14 mmHg OS. Posterior segment examination was significant for central atrophy and classic peripheral pisciform flecks sparing the peripapillary regions OU (Figure 4, A and B). Autofluorescence imaging demonstrated inner atrophic flecks and outer hyperautofluorescent flecks. Moderate peripapillary hypoautofluorescence, but not atrophy, was present, likely secondary to the patient’s myopia (Figure 4, C and D). Genotyping revealed two heterozygous ABCA4 mutations, P1380L and S1696N.Open in a separate windowFig. 4Case 4. STGD mutation IVS40 + 5G>A. A, Color Photo OU. B, Red-Free Photo OU reveal central atrophy and classic peripheral pisciform flecks sparing the peripapillary regions OU. C, Autofluorescence OD. D, Autofluorescence OS show that the innermost flecks are hypoautofluorescent, consistent with atrophy, whereas the outermost flecks are hyperautofluorescent, demonstrating excess lipofuscin. There is moderate peripapillary hypoautofluorescence that is not as dark as this patient’s central atrophy or the peripapillary atrophy of Case 1. This finding may thus be due to the patient’s myopia.

      Case#: Hwang Case 4, male, 52yo at report, 45yo at onset

      DiseaseAssertion: Stargardt

      FamilyInfo: Family history was not significant for ocular disease.

      CasePresentingHPOs: HP:0000545

      CaseHPOFreeText: declining vision OS, BCVA was 20/100 OD and 20/70 OS. Spherical refractive error measured −3.00 OD and −3.25 OS. Posterior segment examination was significant for central atrophy and classic peripheral pisciform flecks sparing the peripapillary regions OU (Figure 4, A and B). Autofluorescence imaging demonstrated inner atrophic flecks and outer hyperautofluorescent flecks. Moderate peripapillary hypoautofluorescence, but not atrophy, was present (Figure 4, C and D).

      CaseNotHPOs: HP:0500087

      CaseNotHPOFreeText:

      GenotypingMethod: Genotyping was performed by the ABCR400 microarray followed by direct sequencing to confirm identified variants.

      PreviouslyPublished: n/a

      Variant: P1380L and S1696N

      ClinVar: 7904

      CAID: CA129033

      SupplementalData: n/a

    2. Case 1A 55-year-old male was examined for long-standing central visual impairment since age 18. Family history was not significant for ocular disease. His best-corrected visual acuity of 20/350 OD and 20/200 OS was consistent with measurements over the last 20 years. Spherical refractive error measured −3.5 OD and −2.0 OS. Anterior segment examination was unremarkable and applanation tonometry measured 17 mmHg OD and 14 mmHg OS. Posterior segment examination and autofluorescence imaging were significant for sharply demarcated central and peripapillary zones of atrophy and the absence of fleck lesions (Figure 1, A–D). Humphrey visual fields demonstrated bilateral central scotomas with eccentric fixation at the inferior border. ERG examination was subnormal and similar to results obtained 22 years ago.Open in a separate windowFig. 1Case 1. STGD with peripapillary atrophy and mutations P1380L and IVS40 + 5G>A. A, Autofluorescence OD. B, Color Photo OD. C, Autofluorescence OS. D, Color Photo OS. All show marked peripapillary and macular atrophy with a sharply demarcated zone of sparing between them. These characteristics caused initial diagnostic confusion with choroidal sclerosis.Genetic testing was employed for further diagnostic information and two heterozygous ABCA4 mutations, P1380L and IVS40 + 5G>A, were identified and classified as disease-causing alleles, thereby confirming the diagnosis of STGD.

      Case#: Hwang Case 1, US, male, 55yo at report, 18yo at onset

      DiseaseAssertion: Stargardt disease

      FamilyInfo: Family history was not significant for ocular disease

      CasePresentingHPOs: HP:0007663, HP:0500087, HP:0000603, HP:0000512

      CaseHPOFreeText: BCVA of 20/350 OD and 20/200 OS. Spherical refractive error measured −3.5 OD and −2.0 OS. Posterior segment examination and autofluorescence imaging were significant for sharply demarcated central and peripapillary zones of atrophy and the absence of fleck lesions (Figure 1, A–D). Humphrey visual fields demonstrated bilateral central scotomas with eccentric fixation at the inferior border.

      CaseNotHPOs:

      CaseNotHPOFreeText:

      GenotypingMethod: Genotyping was performed by the ABCR400 microarray followed by direct sequencing to confirm identified variants.

      PreviouslyPublished: n/a

      Variant: P1380L and IVS40 + 5G>A

      ClinVar: 7904

      CAID: CA129033

      SupplementalData: n/a

    1. 13/8 35 0.017 163 0 – 3 – 3 4 L541P R1098C

      Case#: Patient 13, 35yo

      DiseaseAssertion: STGD

      FamilyInfo: Family 8

      CasePresentingHPOs:

      CaseHPOFreeText: Visual acuity=0.017. OCT ft (μm)=163. MP (dB)=0. Fundus=3(extensive atrophic-appearing RPE changes). ERG=3(abnormal responses involving both rods and cones). mfERG=4(subnormal mfERG in the entire test field (0°–30°) plus pathologic Ganzfeld ERG).

      CaseNotHPOs:

      CaseNotHPOFreeText:

      GenotypingMethod: PCR of coding regions, intron/exon boundaries, and 5′ and 3′ regions of ABCA4; Standard cycle-sequencing reactions with BigDye Terminator

      PreviouslyPublished:

      Variant: L541P; R1098C

      CAID: CA226911;

      SupplementalData: n/a

    1. 3 39 6/6 1 RCD Val552Ile 6/6

      Case#: Case 3, 39yo

      DiseaseAssertion: BEM, RCD

      FamilyInfo: n/a

      CasePresentingHPOs:

      CaseHPOFreeText: a ring of increased AF surrounding decreased foveal AF, visual acuity= 6/6, 6/6

      CaseNotHPOs:

      CaseNotHPOFreeText: acquired toxic aetiology

      GenotypingMethod: The entire coding sequence (50 exons), including exon–intron boundaries, of the ABCA4 gene of each patient was screened using single‐stranded conformational polymorphism (SSCP) analysis and direct sequencing.

      PreviouslyPublished: n/a

      Variant: Val552Ile heterozygous

      CAID: CA239745

      SupplementalData: n/a

    1. Mutation scanning and direct DNA sequencing of all 50 exons of ABCR were completed for 150 families segregating recessive Stargardt disease (STGD1). ABCR variations were identified in 173 (57%) disease chromosomes, the majority of which represent missense amino acid substitutions. These ABCR variants were not found in 220 unaffected control individuals (440 chromosomes) but do cosegregate with the disease in these families with STGD1, and many occur in conserved functional domains. Missense amino acid substitutions located in the amino terminal one-third of the protein appear to be associated with earlier onset of the disease and may represent misfolding alleles. The two most common mutant alleles, G1961E and A1038V, each identified in 16 of 173 disease chromosomes, composed 18.5% of mutations identified. G1961E has been associated previously, at a statistically significant level in the heterozygous state, with age-related macular degeneration (AMD). Clinical evaluation of these 150 families with STGD1 revealed a high frequency of AMD in first- and second-degree relatives. These findings support the hypothesis that compound heterozygous ABCR mutations are responsible for STGD1 and that some heterozygous ABCR mutations may enhance susceptibility to AMD.

      Annotating here since the full text is a PDF.

      Case#: Family AR321 proband, US, 6yo at onset

      DiseaseAssertion: Stargardt

      FamilyInfo: proband and two other siblings are affected

      CasePresentingHPOs: The essential and defining features of STGD were (1) pedigrees with at least one living affected individual compatible with autosomal recessive inheritance; (2) an ophthalmoscopically characteristic retinal disorder in families with both parents living; (3) bilateral central visual loss with both “beaten metal” elliptical foveal dystrophy and temporal pallor of the optic discs, documented by retinal color photography, with or without yellow-pigment epithelial flecks in the macular and/or retinal “near periphery”; and (4) the characteristic fluorescein angiographic feature of a dark choroid (Blacharski 1988).

      CaseHPOFreeText:

      CaseNotHPOs:

      CaseNotHPOFreeText: (1) evidence of autosomal dominant inheritance; (2) any history of night blindness, loss of peripheral vision, or "retinitis pigmentosa"; (3) cataracta complicata or cells in the vitreous; (4) substantially abnormal electroretinographic or electrooculographic responses; (5) no fluorescein angiography performed or no dark choroid documented; (6) neurological disease (including loss of cognition or seizures); 7) drug exposures (especially to antimalarial and agents known to cause crystalline retinopathies); or (8) any "atypical" maculopathies in which a unique diagnosis of STGD could not be established.

      PreviouslyPublished: PMID: 8533764

      Variant: c.3113C>T p.A1038V; c.1715G>C p.R572P . Heteroduplex and SSCP analyses were used to screen the 50 exons of ABCA4. Linkage analysis and haplotype analysis were previously performed

      ClinVar: 99073

      CAID: CA226919

      SupplementalData: n/a

    1. JB260 Stargardt ABCA4 c.6119G>A p.Arg2040Gln rs148460146 Zernant et al (2014)50 c.2879del p.Ala960Aspfs*17 N/A

      Case#: Bryant Subject JB260, US

      DiseaseAssertion: Stargardt

      FamilyInfo:

      CasePresentingHPOs: "Stargardt disease is a childhood-onset macular degeneration and is most commonly caused by mutations in ABCA4. Characteristic yellow flecks are typically seen under the macula during a fundus exam."

      CaseHPOFreeText:

      CaseNotHPOs:

      CaseNotHPOFreeText:

      GenotypingMethod: WES; previously screened using arrayed primer extension (APEX) multigene panels for the relevant disease and no disease-causing variants had been identified; PCR and Sanger for verification

      PreviouslyPublished: n/a

      Variant: c.6119G>A p.Arg2040Gln; c.2879del p.Ala960Aspfs*17

      CAID: CA232815

      SupplementalData:

    1. See Supplementary Table S2 for a complete genotypic glossary of the cohort.

      Case#: Patients were identified from the inherited retinal disease (IRD) database at UC San Diego (UCSD).

      DiseaseAssertion: RP with macular edema

      FamilyInfo:

      CasePresentingHPOs:

      CaseHPOFreeText: Dx of RP based on "a history of progressive peripheral vision loss or nyctalopia, and ocular examination findings of RP including bone spicule pigmentation, disc pallor and attenuated vessels and genetic confirmation."

      CaseNotHPOs:

      CaseNotHPOFreeText:

      GenotypingMethod: Next-generation sequencing (NGS), exome sequencing, and/or targeted Sanger sequencing were the primary genetic testing approaches.

      PreviouslyPublished: PMID:10206579 is referenced but it seems a reference to the variant and not the proband

      Variant: c.6383A>G (p.His2128Arg); c.3G>T (p.Met1?). phase unknown

      ClinVar: 99455

      CAID: CA227399

      SupplementalData: Variant is found in table S2

  3. Apr 2026
    1. patients

      Case#: Patient 2 is a 24-year-old Japanese man. Birth weight was 1900 g (~4.2 lbs) and mental and motor development were both normal. He had graduated from high school. Physical examination demonstrated a height of 157.0 cm, body weight of 45.3 kg.

      DiseaseAssertion: MPS1-S

      FamilyInfo: He was born from nonconsanguineous, young and healthy parents. He had a healthy elder brother and an affected twin brother (Patient 1).

      CasePresentingHPOs: Inguinal hernia, bronchial asthma, systolic ejection heart murmur, umbilical hernia, joint contractures, spastic gait, hypoesthesia, positive Romberg sign, Babinski signs, mild aortic valve stenosis (HP:0000023, HP:0002099, HP:0031664, HP:0001537, HP:0002828, HP:0002064, HP:0033748, HP:0002403, HP:0003487, HP:0001650)

      CaseHPOFreeText: Admitted to the hospital due to a 3-month history of progressive gait disturbance, onset was 6 months after the development of gait disturbance in Patient 1. Exaggeration of deep tendon reflexes was slight in the upper extremities, and marked in the lower extremities. Radiographies of chest and cervical spine showed similar findings to those in Patient 1. CSF examinations demonstrated an elevated protein level (342 mg/dL) without pleocytosis. WAIS-III demonstrated an overall IQ of 75, verbal IQ of 67 and performance IQ of 90.

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CaseEnzymeAssay: The patient showed IDUA activity from peripheral leukocytes < 0.9 nmol/mg protein/h (normal range; 29.8–89.8 nmol/mg protein/h), and that of their mother showed 19.9 nmol/mg protein/h.

      CaseUrineGAGs: Urine chemistry examination demonstrated increased excretion of uronic acid (51.7 mg/g creatinine).

      CaseERT: Yes, with laronidase

      CaseBMT: N/A

      Variant1: c.164dup (p.Leu56AlafsTer7) (c.252insC - in paper but nomenclature is not current)

      Variant1ClinVarID: 855487

      Variant1CAID: CA355945969

      Variant2: c.1121C>A (p.Thr374Asn) (c.1209C>A - in paper but nomenclature is not current)

      Variant2ClinVarID: 4078984

      Variant2CAID: CA355963378

      AdditionalVariants: N/A

      ParentalGenotype: Mother: c.164dup; Father: c.1121C>A

      PreviouslyPublished N/A

    2. twins

      Case#: Patient 1 is a 24-year-old Japanese man. His birth weight was 2300 g (~5 lbs) and he had graduated from a vocational school. Physical examination demonstrated a height of 156.6 cm (mean height of Japanese male at age 24 is 170.9 ± 6.0 (SD) cm, body weight of 45.8 kg (mean body weight of Japanese male at age 24 is 62.6 ± 9.8 (SD) kg according to the National Health and Nutrition Survey in Japan, 2006). He demonstrated overall intelligence quotient (IQ) of 101, verbal IQ of 93 and performance IQ of 112.

      DiseaseAssertion: MPS1-S

      FamilyInfo: He was born from nonconsanguineous, young and healthy parents. He had a healthy elder brother and an affected twin brother (Patient 2).

      CasePresentingHPOs: Inguinal hernia (treated by surgical repair in childhood and again at age 20), systolic ejection heart murmur, umbilical hernia, scissor gait, Babinski sign, mild aortic valve stenosis, severe cervical cord compression (HP:0000023, HP:0031664, HP:0001537, HP:0012407, HP:0003487, HP:0001650, HP:0002341)

      CaseHPOFreeText: Admitted to the hospital due to a 6-month history of progressive gait disturbance. Mental and motor development were normal. Past medical histories included Kawasaki disease at age 6 months. Deep tendon reflexes were mildly exaggerated in the upper extremities, and markedly exaggerated in the lower extremities with bilateral Babinski signs. Radiography of the chest demonstrated mild thoracic deformity and that of cervical spine demonstrated hypoplasia of vertebral body and spinous process. Brain MRI demonstrated enlarged perivascular space and small hyperintense lesions on fluid attenuated inversion recovery image. Cerebrospinal fluid (CSF) examinations demonstrated an elevated protein level (440 mg/dL; normal range 10–40 mg/dL), which would be resulted from CSF circulatory disturbance caused by severe spinal canal stenosis, without pleocytosis.

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CaseEnzymeAssay: The patient showed IDUA activity from peripheral leukocytes < 0.9 nmol/mg protein/h (normal range; 29.8–89.8 nmol/mg protein/h), and that of their mother showed 19.9 nmol/mg protein/h.

      CaseUrineGAGs: Urine chemistry examination demonstrated increased excretion of uronic acid (63.1 mg/g creatinine; normal range 8.3–12.3 mg/g creatinine).

      CaseERT: Yes, with laronidase

      CaseBMT: N/A

      Variant1: c.164dup (p.Leu56AlafsTer7) (c.252insC - in paper but nomenclature is not current)

      Variant1ClinVarID: 855487

      Variant1CAID: CA355945969

      Variant2: c.1121C>A (p.Thr374Asn) (c.1209C>A - in paper but nomenclature is not current)

      Variant2ClinVarID: 4078984

      Variant2CAID: CA355963378

      AdditionalVariants: N/A

      ParentalGenotype: Mother: c.164dup; Father: c.1121C>A

      PreviouslyPublished N/A

  4. Feb 2026
    1. c.371A>G (p.Y124C)

      Case: 16 years diagnosis, Chinese

      DiseaseAssertion: Charcot-Marie-Tooth disease

      FamilyInfo: Mother(mild Pes Cavus); Brother(Amyotrophy, Pes Cavus and so forth)

      CasePresentingHPOs: HP:0001761, HP:0033526, HP:0001265

      GenotypingMethod: Genomic DNA was extracted from the peripheral blood of the family members of a pedigree with autosomal dominant CMT disease, and 65 candidate genes of the proband were screened using target exon capture and the next generation sequencing, and the suspicious genes were verified using Sanger sequencing.

      Variant: NM_018972.4:c.371A>G (p.Tyr124Cys)

      CAID: CA371548535

      gnomAD: NOT in gnomAD

  5. Aug 2025
    1. A 55-year-old male

      Case#: 55-year-old man

      DiseaseAssertion: single coronary artery (SCA) and presented with dilated cardiomyopathy (DCM)

      FamilyInfo: Unremarkable

      ParentalTesting: NR

      CasePresentingHPOs: HP:0002094, HP:0031352, HP:0001638, HP:0001644, HP:0010741

      CaseHPOFreeText: chest tightness and dyspnoea after activity lasting for 2 months. CTCA showed congenital absence of the right coronary artery. TTE revealed enlargement of the left heart and cardiomyopathy. CMR revealed DCM. oedema of both lower limbs. Laboratory data in Table 1.

      CaseNotHPOs: NR

      CaseNotHPOFreeText: Stenosis

      CasePreviousTesting: See NGS results in Supplementary Table 1

      Genotyping Method: Genetic screening (NGS results in Supplementary Table 1) with confirmation by Sanger

      FunctionalAnalysis: NR

      Variant: c.1858C>T (p.Arg620Cys)

      ClinVar: 67694

      CAID: CA015449

      gnomAD: v4.1.0 GrpMax FAF: 0.00002033 (European non-Finnish)

      AdditionalInfo: The patient also has APOA5:c.990_993delAACA (p. Asp332Valfs*5) (P/LP in ClinVar with 2 stars)

  6. Oct 2022
    1. V-3

      Case#: V3, Pakistan, female, 23 years old (report),

      DiseaseAssertion: GAMT deficiency

      FamilyInfo: Patient V3 is a sister of V1. Consanguineous family.

      CasePresentingHPOs: HP:0010864, HP:0001250, HP:0001257, HP:0003487, HP:0001251, HP:0001761 (severe intellectual disability, seizure, spasticity, Babinski sign, ataxia, pes cavus)

      CaseHPOFreeText: Neonatal onset of seizures, Spasticity in upper and lower limbs, Peripheral neuropathy probably present, sitting delayed, standing delayed, walking delayed, never developed speech

      CaseNotHPOs: HP:0001347 (hyperreflexia)

      CaseNotHPOFreeText: Bed ridden, recurrent bone fractures

      Biochemical analyte testing:

      Brain Magnetic Resonance Spectroscopy (MRS): N/A

      GAMT activity assay: N/A

      Zygosity: Homozygous / compound heterozygous.

      Variant 1: c.134G > A (p.Trp45)

      ClinVarID: N/A

      CAID: N/A

      gnomAD: N/A

      Variant 2: N/A

      ClinVarID: N/A

      CAID: N/A

      gnomAD: N/A

      ParentalGenotypes: Both parents confirmed to be heterozygous for c.134G > A

      AlsoPublished: N/A

    2. V-1

      Case#: V1, Pakistan, male, 25 years old (report),

      DiseaseAssertion: GAMT deficiency

      FamilyInfo: Patient V1 is a brother of V3. Consanguineous family.

      CasePresentingHPOs: HP:0010864, HP:0001250, HP:0001347, HP:0001257, HP:0003487, HP:0001251, HP:0001761 (severe intellectual disability, seizure, hyperreflexia, spasticity, Babinski sign, ataxia, pes cavus)

      CaseHPOFreeText: Neonatal onset of seizures, Spasticity in upper and lower limbs, Peripheral neuropathy probably present, sitting delayed, standing delayed, walking delayed, never developed speech, bed ridden since age 17, recurrent bone fractures

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      Biochemical analyte testing: GAA: 13.7 μmol/L, creatine: 2 μmol/L

      Brain Magnetic Resonance Spectroscopy (MRS): N/A

      GAMT activity assay: N/A

      Zygosity: Homozygous

      Variant 1: c.134G > A (p.Trp45)

      ClinVarID: N/A

      CAID: N/A

      gnomAD: N/A

      Variant 2: N/A

      ClinVarID: N/A

      CAID: N/A

      gnomAD: N/A

      ParentalGenotypes: Both parents confirmed to be heterozygous for c.134G > A

      AlsoPublished: N/A

  7. Sep 2022
    1. 2

      Case#: Subject number 2, 37 years

      DiseaseAssertion: Late Onset Pompe disease

      FamilyInfo: N/A

      CasePresentingHPOs: HP:0008994 (proximal muscle weakness in lower limbs), HP:0003325 (limb-girdle muscle weakness), HP:0003701 (proximal muscle weakness), HP:0003691 (scapular winging), HP:0002355 (difficulty walking).

      CaseHPOFreeText: N/A

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: Serum creatin kinase was 7.7 μkat/l

      glucosidase activity: Whole uncoagulated blood samples used for leukocyte and DNA isolations.

      GAA activity (w/o acarbose) 35 nmol.h.mg–1 (control 37±14).

      8 nmol.h.mg–1 (with acarbose) (control 16±6).

      Ratio of with/w/o acarbose is 0.24 (control 0.42±0.08).

      Variant 1: NM_000152.5(GAA):c.-32-13T>G

      Variant 1 ClinVarID: 4027

      Variant 1 CAid: CA116606

      Variant 2: NM_000152.5(GAA):c.1456G>C

      Variant 2 ClinVarID: N/A

      Variant 2 CAid: CA401366835

      Zygosity: compund heterozygous

      ParentalGenotype: N/A

      PreviouslyPublished: N/A

  8. Aug 2022
    1. 1

      Case#: Subject number 1, 18 years

      DiseaseAssertion: Late Onset Pompe disease

      FamilyInfo: N/A

      CasePresentingHPOs: HP:0003325 (limb-girdle muscle weakness), HP:0008994 (proximal muscle weakness in lower limbs), HP:0008968 (muscle hypertrophy of the lower extremities), HP:0007340 (lower limb muscle weakness), HP:0003797 (limb-girdle muscle atrophy), HP:0002515 (waddling gait), HP:0003691 (scapular winging).

      CaseHPOFreeText: Positive Trendelenburg sign

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: Serum creatin kinase was 19. 9 μkat/l

      glucosidase activity: Whole uncoagulated blood samples used for leukocyte and DNA isolations.

      GAA activity (w/o acarbose) 29 nmol.h.mg–1 (control 37±14).

      3 nmol.h.mg–1 (with acarbose) (control 16±6).

      Ratio of with/w/o acarbose is 0.10 (control 0.42±0.08).

      Variant 1: NM_000152.5(GAA):c.-32-13T>G

      Variant 1 ClinVarID: 4027

      Variant 1 CAid: CA116606

      Variant 2: NM_000152.5(GAA):c.-32-13T>G

      Variant 2 ClinVarID: 4027

      Variant 2 CAid: CA116606

      Zygosity: homozygous

      ParentalGenotype: N/A

      PreviouslyPublished: N/A

  9. Jul 2022
    1. mutations in the α-sarcoglycan gene (SGCA)

      PMID: 30989758

      Gene: SGCA

      HGNCID: 10805

      Case: 8 year old boy, Chinese.

      DiseaseAssertion: LGMD

      FamilyInfo: Family members denied relevant family history

      CasePresentingHPOs: HP:0006785, HP:0003551, HP:0003391, HP:0003560

      MotorAchievement: Noticed around 7 years old that he had trouble climbing stairs and standing up when crouching and had slower activity than other peers.

      CreatineKinase: Creatine kinase CK 15550U/L, MB fraction 276 U/L

      CasePreviousTesting:430 genes associated with muscular dystrophy were captured with a liquid catch kit.

      GenotypingMethod: NGS

      PreviouslyPublished: NA

      SupplementalData: NA

      Variant: NM_000023c.218 C>T

      ClinVarID: Unregistered varient

      CAID: Unregistered varient

      gnomAD: https://gnomad.broadinstitute.org/variant/17-48245003-C-T?dataset=gnomad_r2_1

      "0.000 Allele Frequency - East Asian

  10. May 2021
  11. Mar 2021
    1. affected boy (IV-1; 11 years)

      Case#: IV-1, male, 11 y.o, Pakistani

      DiseaseAssertion: Limb-girdle muscular dystrophy (LGMD2F), sarcoglycanopathy

      FamilyInfo: Consanguineous parents, both described as healthy and showing no abnormality. Three unaffected siblings were also reported: IV-2 (male, 10 y.o), IV-4 (male, 7 y.o), and IV-5 (female, 1.5 y.o). A deceased sister is included on the pedigree, but no details about this individual were reported. See Figure 1.

      CasePresentingHPOs: HP:0001288, HP:0002650, HP:0003547, HP:0003749, HP:0001655

      CaseHPOFreeText: Reduced weight gain noted at 3-4 y.o. Mild cardiac hypertrophy observed on cardiac review (additional echocardiography results reported in "Echocardiography" section). Additional phenotypic information reported in Supplementary Table 1.

      CaseNotHPOs: HP:0009077, HP:0000703, HP:0001382, HP:0000365, HP:0001510, HP:0001249, HP:0000478, HP:0030148, HP:0011675

      CaseNotHPOFreeText: Extensor muscles of the wrist, toes flexors, and hip abductors noted to be relatively normal. Additional phenotypic information reported in Supplementary Table 1.

      MotorAchievement: Sat without assistance at 8 months of age, walked at 15 months of age, ran at 1.5 months of age. Never jumped or hopped. Frequent falls noted, as well as difficulty in walking and climbing stairs since 3 y.o.

      CreatineKinase: 18SU (normal: 20SU for children, 10SU for adults) (see Supplementary Table 1). No assertion was made by the authors regarding whether this represents a normal or decreased CK level.

      PreviousTesting: Thyroid stimulating hormone: 2.3mU/L (normal: <0.6mU/L); Serum VZV IgG: 286mlU/ml (normal: >150mlU/ml); IGF-1:186 ng/μl (normal: 102-520 ng/μl for males, 14 y.o); PRL: 202 ng/dl (normal: 42.5-414 ng/dl for males); Vitamin D: 47nmol/L (normal: 25-50 nmol/L); Free T4: 17.0 pmol/L (normal:10.8-19.0 pmol/L) (see Supplementary Table 1)

      GenotypingMethod: (1) Targeted next generation sequencing of 31 genes associated with LGMD from proband genomic DNA extracted from peripheral blood sample; (2) Sanger sequencing of genomic DNA extracted from peripheral blood samples to confirm SGCD variant of interest in proband and three family members (III-3, III-4, IV-4). Variant was identified in homozygosity in the proband, in heterozygosity in each of the parents, and was not present in the unaffected sibling (IV-4).

      Variant: NM_000337.5:c.289C>T (p.Arg97Ter)

      CAID: CA3530549

      gnomAD: Not reported

  12. Jan 2021
    1. AJV

      CaseAJV: 17 years diagnosis, Australia

      DiseaseAssertion: Hypertrophic Cardiomyopathy

      FamilyInfo: Father (index case) died awaiting cardiac transplant (carried both variants). Two possibly affected relatives.

      CasePresentingHPOs: HP:0001639, HP:0006536

      (Hypertrophic cardiomyopathy, Obstructive lung disease)

      HPOsFreeText: Maximum left ventricular hypertrophy at 17 mm, Sudden cardiac death event at 17 years, Maximal wall thickness at 22mm,

      CaseNotHPOs: N/A

      NotHPOsFreeText: N/A

      CasePreviousTesting: See Table 1

      CaseGenotypingMethod: DNA was isolated from peripheral blood. Most participants underwent testing from the Illumina Cardiomyopathy Sequencing Panel, which includes 46 cardiomyopathy related genes. For others, whole exome sequencing or Sanger squencing was used. After the results were returned, variants were filtered for pathogenicity and rarity.

      Variant:NM_000257.3:c.1954A>G (p.Arg652Gly)

      ClinVarID:177626 https://www.ncbi.nlm.nih.gov/clinvar/variation/177626/

      gnomAD: Not in gnomAD

      Multiple Gene Variants:

      MYBPC3 Variant

      Variant: NM_000256.3:c.2980C>T (p.Leu994Phe)

      ClinVarID:180992 https://www.ncbi.nlm.nih.gov/clinvar/variation/180992/

      gnomAD: European (Non-Finnish) 1.624e-4, Overall 8.461e-5 https://gnomad.broadinstitute.org/variant/11-47355487-G-A

  13. Sep 2019
    1. I 1

      CaseI1-2: Case I1 is the asymptomatic paternal grandfather of proband 2 in family 2. The heterozygous Thr295Ile substitution was found in this individual.

      CasePresentingHPOs: HP:0005543, (Reduced protein C activity)

      HPOsFreeText: Protein C activity was reduced: Normal range = 70-140% (actual = 39%). Patient also had reduced protein C antigen: Normal range = 70-130% (Actual=36%).

      CaseNotHPOs:

      NotHPOsFreeText:

      CaseAddInfo: This individual was asymptomatic.

      CasePMIDs:

    2. grandmother (I3) of Proband 2

      CaseI3-2: Case I3 is the asymptomatic grandmother of proband 2 in family 2. The heterozygous Leu-34Pro substitution was found in this individual.

      CasePresentingHPOs: HP:0005543, (Reduced protein C activity)

      HPOsFreeText: Protein C activity was reduced: Normal range = 70-140% (actual = 48%). Patient also had reduced protein C antigen: Normal range = 70-130% (Actual=36%).

      CaseNotHPOs:

      NotHPOsFreeText:

      CaseAddInfo: This individual was asymptomatic.

      CasePMIDs:

    3. asymptomaticmother (II4

      CaseII4-2: Case II4 is the asymptomatic mother of proband 2 in family 2. The heterozygous Leu-34Pro substitution was found in this individual.

      CasePresentingHPOs: HP:0005543, (Reduced protein C activity)

      HPOsFreeText: Protein C activity was reduced: Normal range = 70-140% (actual = 55%). Patient also had reduced protein C antigen: Normal range = 70-130% (Actual=34%).

      CaseNotHPOs:

      NotHPOsFreeText:

      CaseAddInfo: This individual was asymptomatic.

      CasePMIDs:

    4. paternal relatives II2

      CaseII2-2: Case II2 is the asymptomatic paternal uncle of proband 2 in family 2. The Thr295Ile substitution was found in this individual.

      CasePresentingHPOs: HP:0005543, (Reduced protein C activity)

      HPOsFreeText: Protein C activity was reduced: Normal range = 70-140% (actual = 44%). Patient also had reduced protein C antigen: Normal range = 70-130% (Actual=33%).

      CaseNotHPOs:

      NotHPOsFreeText:

      CaseAddInfo: This individual was completely asymptomatic.

      CasePMIDs:

    5. he asymptomatic fatherof Proband 2 (II3)

      CaseII3-2: Case II3 is the clinically asymptomatic father of proband 2 in family 2. The Thr295Ile substitution was found in this individual.

      CasePresentingHPOs: HP:0005543, (Reduced protein C activity)

      HPOsFreeText: Protein C activity was reduced: Normal range = 70-140% (actual = 43%). Patient also had reduced protein C antigen: Normal range = 70-130% (Actual=34%).

      CaseNotHPOs:

      NotHPOsFreeText:

      CaseAddInfo: This individual was completely asymptomatic.

      CasePMIDs:

    6. Proband 2

      CaseIII1-2: Proband 2 (Case III 1 family 2) was a 19 year old male diagnosed with deep vein thrombosis in both legs since the age of 16. The family of this individual was asymptomatic with respect to thrombolytic disease and was non-consanguineous.

      CasePresentingHPOs: HP:0002625, HP:0005543, HP:0004936, (Deep venous thrombosis), (Protein C deficiency), (Venous thrombosis),

      HPOsFreeText: Deep vein thrombosis was in both legs since age of 16. This patient also had low protein C antigen.

      CaseNotHPOs:

      NotHPOsFreeText:

      CaseAddInfo: This Case (Case III1-2) was designated as Proband 2.

      CasePMIDs:

    7. the father (I1) of Proband 1

      CaseI1-1: Case I1-1 is a 54 year-old male from Family 1. This individual has a heterozygous Asp255His mutation and is the father of the proband (II1-1). This individual was asymptomatic and lab results were within normal ranges.

      CasePresentingHPOs:

      HPOsFreeText:

      CaseNotHPOs:

      NotHPOsFreeText: Patient was completely asymptomatic.

      CaseAddInfo:

      CasePMIDs:

    8. Proband 1

      CaseIII1-1: Proband 1 (Case II1 Family 1) was a 28 year male admitted to the medical facility for deep vein thrombosis (DVT) and mesenteric vein thrombosis. This patient had a history of DVT and pulmonary embolism before admission. The mutation was compound heterozygous.

      CasePresentingHPOs: HP:0030780, HP:0002625, HP:0002204, HP:0005543, HP:0004936, (Abnormality of the protein C anticoagulant pathway), (Deep venous thrombosis), (Pulmonary embolism), (Reduced protein C activity), (Venous thrombosis),

      HPOsFreeText: Patient had mesenteric vein thrombosis (no HPO# found). The patient also had reduced protein C antigen.

      CaseNotHPOs:

      NotHPOsFreeText:

      CaseAddInfo: This case (II1 family 1) is designated as proband 1. Proband 1 was also given heparin and warfarin (together) in an attempt to control clotting. Doses for this treatment regimen were not included. All other members of the family were asymptomatic with respect to thrombolytic disease and non-consanguineous. CasePMIDs: