632 Matching Annotations
  1. Last 7 days
    1. GT31

      Case30: (GT31) Gender, age and ethnicity are not specified

      DiseaseAssertion: Glanzmann thrombasthenia

      FamilyInfo: N/A

      ParentalGenotype: N/A

      CasePresentingHPOs: N/A

      CaseHPOFreeText: Inclusion criteria were patients with a history of mucocutaneous bleeding (Figure 1 shows a bar diagram of all the clinical manifestations in the patient cohort in this article)

      CaseNotHPOs: N/A

      ProteinExpression: Platelet receptor alphaIIbbeta3 protein was analyzed by flow cytometry followed by western blotting

      Platelet Aggregation: Inclusion criteria for probands was absent or reduced platelet aggregation with agonists such as ADP, adrenaline, arachidonic acid, and collagen (no mention of ristocetin here-- this article does not tell us the specific aggregation for each proband in the paper)

      CasePreviousTesting: For mutation analysis of ITGA2B and ITGB3 genes, DNA extraction from whole blood, PCR, heteroduplex PCR followed by CSGE and DNA sequencing were performed. All 30 exons of ITGA2B and 15 exons of ITGB3, as well as their promoters, were analyzed by CSGE following heteroduplex PCR.

      Gene: ITGB3

      Variant: NM_000212.2:c.887_901del

      LegacyVariant: N/A

      ClinVar: N/A

      CAiD: CA626379036

      gnomAD MAF in the South Asian population is 0.00003266 https://gnomad.broadinstitute.org/variant/17-45364541-AATGACGGGCAGTGTC-A

    2. GT12

      Case6: (GT12) Gender, age and ethnicity not specified

      DiseaseAssertion: Glanzmann thrombasthenia

      FamilyInfo: N/A

      ParentalGenotype: N/A

      CasePresentingHPOs: N/A

      CaseHPOFreeText: Inclusion criteria were patients with a history of mucocutaneous bleeding (Figure 1 shows a bar diagram of all the clinical manifestations in the patient cohort in this article)

      CaseNotHPOs: N/A

      ProteinExpression: Platelet receptor alphaIIbbeta3 protein was analyzed by flow cytometry followed by western blotting

      Platelet Aggregation: Inclusion criteria for probands was absent or reduced platelet aggregation with agonists such as ADP, adrenaline, arachidonic acid, and collagen (no mention of ristocetin here-- this article does not tell us the specific aggregation for each proband in the paper)

      CasePreviousTesting: For mutation analysis of ITGA2B and ITGB3 genes, DNA extraction from whole blood, PCR, heteroduplex PCR followed by CSGE and DNA sequencing were performed. All 30 exons of ITGA2B and 15 exons of ITGB3, as well as their promoters, were analyzed by CSGE following heteroduplex PCR.

      Gene: ITGA2B

      Variant: NM_000419.3:c.641T>C (p.Leu214Pro)

      LegacyVariant: N/A

      ClinVar: 2901

      CAiD: CA115848

      gnomAD N/A

    3. GT14

      Case35: (GT14) Gender, age and ethnicity are not specified

      DiseaseAssertion: Glanzmann thrombasthenia

      FamilyInfo: N/A

      ParentalGenotype: N/A

      CasePresentingHPOs: N/A

      CaseHPOFreeText: Inclusion criteria were patients with a history of mucocutaneous bleeding (Figure 1 shows a bar diagram of all the clinical manifestations in the patient cohort in this article)

      CaseNotHPOs: N/A

      ProteinExpression: Platelet receptor alphaIIbbeta3 protein was analyzed by flow cytometry followed by western blotting

      Platelet Aggregation: Inclusion criteria for probands was absent or reduced platelet aggregation with agonists such as ADP, adrenaline, arachidonic acid, and collagen (no mention of ristocetin here-- this article does not tell us the specific aggregation for each proband in the paper)

      CasePreviousTesting: For mutation analysis of ITGA2B and ITGB3 genes, DNA extraction from whole blood, PCR, heteroduplex PCR followed by CSGE and DNA sequencing were performed. All 30 exons of ITGA2B and 15 exons of ITGB3, as well as their promoters, were analyzed by CSGE following heteroduplex PCR.

      Gene:

      Variant: NM_000419.3:c.188+8del

      LegacyVariant: N/A

      ClinVar: N/A

      CAiD: CA8603523

      gnomAD MAF in the South Asian population is 0.0002613 https://gnomad.broadinstitute.org/variant/17-42466645-AC-A

    1. 1.

      Case1: Male, now deceased

      DiseaseAssertion: Glanzmann thrombasthenia type I

      FamilyInfo: N/A

      ParentalGenotype: N/A

      CasePresentingHPOs: HP:0002239

      (Gastrointestinal bleeding)

      CaseHPOFreeText: Severe bleeding when young

      CaseNotHPOs: N/A

      CaseNotHPOsFreeText: N/A

      ProteinExpression: N/A

      PlateletAggregation: Minimal information, not specific at all

      CasePreviousTesting: Sanger sequencing identified disease-causing variants in 18 out of 20 patients (Probands 6 and 14 excluded) with istoantibodies to αIIbβ3. The mutations were evenly distributed between ITGB3 and ITGA2B.

      Gene: ITGA2B

      Variant: NM_000419.3:c.1413C>G (p.Tyr471Ter) Codon change confirmed from PMID: 20492470 and NM_000419.3:c.1882C>T (p.Arg628Ter)

      LegacyVariant: N/A

      ClinVar: N/A

      CAiD: CA290950376 and CA399801310

      gnomAD: MAF in European non Finnish population 0.000008791 http://gnomad.broadinstitute.org/variant/17-42457994-G-C and MAF in Latino population 0.00003983 http://gnomad.broadinstitute.org/variant/17-42456075-G-A

    2. 22.

      Case22: Female, age not specified

      DiseaseAssertion: Glanzmann thrombasthenia

      FamilyInfo: N/A

      ParentalGenotype: N/A

      CasePresentingHPOs: N/A

      CaseHPOFreeText: N/A

      CaseNotHPOs: N/A

      CaseNotHPOsFreeText: N/A

      ProteinExpression: N/A

      PlateletAggregation: Minimal information, not specific enough

      CasePreviousTesting: Sanger sequencing identified disease-causing variants in 18 out of 20 patients (Probands 6 and 14 excluded) with istoantibodies to αIIbβ3. The mutations were evenly distributed between ITGB3 and ITGA2B.

      Gene: ITGB3

      Variant: NM_000212.2:c.166-2A>G (IVS2-2A>G)

      LegacyVariant: N/A

      ClinVar: N/A

      CAiD: CA291224483

      gnomAD: N/A

    3. 21

      Case21: Male, age not specified

      DiseaseAssertion: Glanzmann thrombasthenia

      FamilyInfo: N/A

      ParentalGenotype: N/A

      CasePresentingHPOs: N/A

      CaseHPOFreeText: Mild bleeding tendency (See Table 1 for Clinical and Biological data for selected genotyped patients

      CaseNotHPOs: N/A

      CaseNotHPOsFreeText: N/A

      ProteinExpression: N/A

      PlateletAggregation: Minimal information, not specific enough

      CasePreviousTesting: Sanger sequencing identified disease-causing variants in 18 out of 20 patients (Probands 6 and 14 excluded) with istoantibodies to αIIbβ3. The mutations were evenly distributed between ITGB3 and ITGA2B.

      Gene: ITGA2B

      Variant: NM_000419.3:c.2421G>A (p.Trp807Ter)

      LegacyVariant: N/A

      ClinVar: N/A

      CAiD: CA399796017

      gnomAD: N/A

    4. 13.

      Case13: Female, African, age not specified

      DiseaseAssertion: Glanzmann thrombasthenia

      FamilyInfo: N/A

      ParentalGenotype: N/A

      CasePresentingHPOs: N/A

      CaseHPOFreeText: N/A

      CaseNotHPOs: N/A

      CaseNotHPOsFreeText: N/A

      ProteinExpression: N/A

      PlateletAggregation: Minimal information, not specific enough

      CasePreviousTesting: Sanger sequencing identified disease-causing variants in 18 out of 20 patients (Probands 6 and 14 excluded) with istoantibodies to αIIbβ3. The mutations were evenly distributed between ITGB3 and ITGA2B.

      Gene: ITGA2B

      Variant: NM_000419.3:c.1357C>T (p.Arg453Ter)

      LegacyVariant: N/A

      ClinVar: 631773

      CAiD: CA399803529

      gnomAD: N/A

    1. 7

      Case7: Male, 1.5 years old, Indian

      DiseaseAssertion: Glanzmann thrombasthenia

      FamilyInfo: N/A

      ParentalGenotype: N/A

      CasePresentingHPOs: HP:0031364, HP:0000421 (Ecchymosis, epistaxis)

      CaseHPOFreeText: N/A

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      ProteinExpression: Diagnosis of GT was made on the basis of quantitive determination of receptor count by flow cytometric analysis of GPIIb-IIIa

      PlateletAggregation: Diagnosis of GT was made on the basis of impaired platelet aggregation (platelet aggregation was tested against ristocetin, ADP, collagen, epinephrine and arachidonic acid)

      CasePreviousTesting: Multiplex PCR by using GPIIb primers and CSGE analysis were performed

      Gene: ITGA2B

      Variant: NM_000419.3:c.2315C>G (p.Pro772Arg)

      LegacyVariant: (p.Pro741Arg)

      ClinVar: N/A

      CAiD: CA8602740

      gnomAD: MAF in the South Asian population is 0.0002613 https://gnomad.broadinstitute.org/variant/17-42453709-G-C

    2. 6

      Case6: Female, 7 years old, Indian

      DiseaseAssertion: Glanzmann thrombasthenia

      FamilyInfo: N/A

      ParentalGenotype: N/A

      CasePresentingHPOs: HP:0000225 (Gingival bleeding)

      CaseHPOFreeText: N/A

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      ProteinExpression: Diagnosis of GT was made on the basis of quantitive determination of receptor count by flow cytometric analysis of GPIIb-IIIa

      PlateletAggregation: Diagnosis of GT was made on the basis of impaired platelet aggregation (platelet aggregation was tested against ristocetin, ADP, collagen, epinephrine and arachidonic acid)

      CasePreviousTesting: Multiplex PCR by using GPIIb primers and CSGE analysis were performed

      Gene: ITGA2B

      Variant: NM_000419.3:c.1374C>G (p.Ile458Met)

      LegacyVariant: (p.Ile427Met)

      ClinVar: N/A

      CAiD: CA8603157

      gnomAD: MAF in the South Asian population is 0.003658 https://gnomad.broadinstitute.org/variant/17-42458266-G-C

    3. 5

      Case5: Female, 3 years old, Indian

      DiseaseAssertion: Glanzmann thrombasthenia

      FamilyInfo: N/A

      ParentalGenotype: N/A

      CasePresentingHPOs: HP:0000421, HP:0000225

      (Epistaxis, gingival bleeding)

      CaseHPOFreeText: Severe epistaxis and mild gum bleeding

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      ProteinExpression: Diagnosis of GT was made on the basis of quantitive determination of receptor count by flow cytometric analysis of GPIIb-IIIa

      PlateletAggregation: Diagnosis of GT was made on the basis of impaired platelet aggregation (platelet aggregation was tested against ristocetin, ADP, collagen, epinephrine and arachidonic acid)

      CasePreviousTesting: Multiplex PCR by using GPIIb primers and CSGE analysis were performed

      Gene: ITGA2B

      Variant: NM_000419.3:c.859G>C (p.Gly287Arg)

      LegacyVariant: (p.Gly256Arg)

      ClinVar: N/A

      CAiD: CA399805008

      gnomAD: N/A

    4. 4

      Case4: Female, 18 years old, Indian

      DiseaseAssertion: Glanzmann thrombasthenia

      FamilyInfo: N/A

      ParentalGenotype: N/A

      CasePresentingHPOs: HP:0000225, HP:0000132

      (Gingival bleeding, menorrhagia)

      CaseHPOFreeText: Menorrhagia only during puberty

      CaseNotHPOs: N/A

      CaseNotHPOFreeText:N/A

      ProteinExpression: Diagnosis of GT was made on the basis of quantitive determination of receptor count by flow cytometric analysis of GPIIb-IIIa

      PlateletAggregation: Diagnosis of GT was made on the basis of impaired platelet aggregation (platelet aggregation was tested against ristocetin, ADP, collagen, epinephrine and arachidonic acid)

      CasePreviousTesting: Multiplex PCR by using GPIIb primers and CSGE analysis were performed

      Gene: ITGA2B

      Variant: NM_000419.3:c.2264G>C (p.Arg755Pro)

      LegacyVariant: (p.Arg724Pro)

      ClinVar: N/A

      CAiD: CA8602772

      gnomAD: MAF in the European (non-Finnish) population is 0.00001060 https://gnomad.broadinstitute.org/variant/17-42454380-C-G

    5. 3

      Case3: Male, 40 years old, Indian

      DiseaseAssertion: Glanzmann thrombasthenia

      FamilyInfo: N/A

      ParentalGenotype: N/A

      CasePresentingHPOs: HP:0000421, HP:0002239, HP:0002248

      (Epistaxis, GI bleeding, hematemesis)

      CaseHPOFreeText: N/A

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      ProteinExpression: Diagnosis of GT was made on the basis of quantitive determination of receptor count by flow cytometric analysis of GPIIb-IIIa

      PlateletAggregation: Diagnosis of GT was made on the basis of impaired platelet aggregation (platelet aggregation was tested against ristocetin, ADP, collagen, epinephrine and arachidonic acid)

      CasePreviousTesting: Multiplex PCR by using GPIIb primers and CSGE analysis were performed

      Gene: ITGA2B

      Variant: NM_000419.3:c.310+1G>A (IVS2(+1)G>A)

      LegacyVariant: N/A

      ClinVar: N/A

      CAiD: CA8603502

      gnomAD: MAF in the European (non-Finnish) population is 0.00001771 https://gnomad.broadinstitute.org/variant/17-42463377-C-T

    6. 2

      Case2: Male, 3 years old, Indian

      DiseaseAssertion: Glanzmann thrombasthenia

      FamilyInfo: N/A

      ParentalGenotype: N/A

      CasePresentingHPOs: HP:0030137 (Prolonged bleeding following circumcision)

      CaseHPOFreeText: N/A

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      ProteinExpression: Diagnosis of GT was made on the basis of quantitive determination of receptor count by flow cytometric analysis of GPIIb-IIIa

      PlateletAggregation: Diagnosis of GT was made on the basis of impaired platelet aggregation (platelet aggregation was tested against ristocetin, ADP, collagen, epinephrine and arachidonic acid)

      CasePreviousTesting: Multiplex PCR by using GPIIb primers and CSGE analysis were performed

      Gene: ITGA2B

      Variant: NM_000419.3:c.1652G>A (p.Arg551Gln)

      LegacyVariant: (p.Arg520Gln)

      ClinVar: N/A

      CAiD: CA8602986

      gnomAD: MAF in the South Asian population is 0.00006536 https://gnomad.broadinstitute.org/variant/17-42457470-C-T

    7. 10

      Case10: Female, 7 years old, Indian

      DiseaseAssertion: Glanzmann thrombasthenia

      FamilyInfo: N/A

      ParentalGenotype: N/A

      CasePresentingHPOs: HP:0000421, HP:0000790 (Epistaxis, hematuria)

      CaseHPOFreeText: N/A

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      ProteinExpression: Diagnosis of GT was made on the basis of quantitive determination of receptor count by flow cytometric analysis of GPIIb-IIIa

      PlateletAggregation: Diagnosis of GT was made on the basis of impaired platelet aggregation (platelet aggregation was tested against ristocetin, ADP, collagen, epinephrine and arachidonic acid)

      CasePreviousTesting: Multiplex PCR by using GPIIb primers and CSGE analysis were performed

      Gene: ITGA2B

      Variant: NM_000419.3:c.2415del

      LegacyVariant: N/A

      ClinVar: N/A

      CAiD: CA915940581

      gnomAD: N/A

    1. 56-year-old Algerian woman

      Case1: Female, 56 years old, Algerian

      DiseaseAssertion: Glanzmann thrombasthenia

      FamilyInfo: N/A

      ParentalGenotype: N/A

      CasePresentingHPOs: HP:0004406, HP:0000132

      (Recurrent epistaxis, menorrhagia)

      CaseHPOFreeText: N/A

      CaseNotHPOs: N/A

      CaseNotHPOsFreeText: N/A

      ProteinExpression: No platelet αIIbβ3 expression (mentioned briefly in abstract)

      PlateletAggregation: The patient shows all the typical signs of GT with no platelet aggregation in response to physiologic agonists and an absence of clot retraction. No mention of ristocetin

      CasePreviousTesting: N/A

      Gene: ITGA2B

      Variant: NM_000419.3:c.1063G>A (p.Glu355Lys)

      LegacyVariant: p.Glu324Lys

      ClinVar: 2899

      CAiD: CA115844

      gnomAD: MAF in European (non-Finnish population 0.00001978 http://gnomad.broadinstitute.org/variant/17-42461008-C-T

      PreviouslyPublished: Proband 9 in PMID: 2180491

    1. GT 07

      Case16: GT07, Male, India, age of onset is 3 years old

      DiseaseAssertion: Glanzmann thrombasthenia

      FamilyInfo: N/A

      ParentalGenotype: N/A

      CasePresentingHPOs: N/A

      CaseHPOFreeText: Patients were recruited as they presented consecutively from 1996 to 1998 for evaluation of a mucocutaneous bleeding disorder

      CaseNotHPOs: N/A

      CaseNotHPOsFreeText: N/A

      ProteinExpression: N/A

      PlateletAggregation: All patients examined had defective ADP, epinephrine, and collagen induced aggregation and normal ristocetin induced aggregation

      CasePreviousTesting: Mutations were detected by the method of single strand conformation polymorphism (SSCP) analysis, followed by nucleotide sequencing and confirmation by restriction fragment length polymorphism (RFLP) assays. The sequences of the primers employed and the reaction conditions for PCR amplification of the exons, adjacent intronic regions, and 50 and 30 untranslated regions of the aIIb and b3 gene

      Gene: ITGB3

      Variant: NM_000212.2:c.153del (p.Trp51CysfsTer5)

      LegacyVariant: N/A

      ClinVar: N/A

      CAiD: CA915940728

      gnomAD: N/A

    2. GT 55

      Case34: GT55, Male, India, age of onset is 21 years old

      DiseaseAssertion: Glanzmann thrombasthenia

      FamilyInfo: N/A

      ParentalGenotype: N/A

      CasePresentingHPOs: N/A

      CaseHPOFreeText: Patients were recruited as they presented consecutively from 1996 to 1998 for evaluation of a mucocutaneous bleeding disorder

      CaseNotHPOs: N/A

      CaseNotHPOsFreeText: N/A

      ProteinExpression: N/A

      PlateletAggregation: All patients examined had defective ADP, epinephrine, and collagen induced aggregation and normal ristocetin induced aggregation

      CasePreviousTesting: Mutations were detected by the method of single strand conformation polymorphism (SSCP) analysis, followed by nucleotide sequencing and confirmation by restriction fragment length polymorphism (RFLP) assays. The sequences of the primers employed and the reaction conditions for PCR amplification of the exons, adjacent intronic regions, and 50 and 30 untranslated regions of the aIIb and b3 gene

      Gene: ITGB3

      Variant: NM_000212.2:c.921C>A (p.Tyr307Ter)

      LegacyVariant: N/A

      ClinVar: N/A

      CAiD: CA400025209

      gnomAD: N/A

    3. GT 24

      Case6: GT24, Male, India, age of onset is 10 years old

      DiseaseAssertion: Glanzmann thrombasthenia

      FamilyInfo: N/A

      ParentalGenotype: N/A

      CasePresentingHPOs: N/A

      CaseHPOFreeText: Patients were recruited as they presented consecutively from 1996 to 1998 for evaluation of a mucocutaneous bleeding disorder

      CaseNotHPOs: N/A

      CaseNotHPOsFreeText: N/A

      ProteinExpression: N/A

      PlateletAggregation: All patients examined had defective ADP, epinephrine, and collagen induced aggregation and normal ristocetin induced aggregation

      CasePreviousTesting: Mutations were detected by the method of single strand conformation polymorphism (SSCP) analysis, followed by nucleotide sequencing and confirmation by restriction fragment length polymorphism (RFLP) assays. The sequences of the primers employed and the reaction conditions for PCR amplification of the exons, adjacent intronic regions, and 50 and 30 untranslated regions of the aIIb and b3 gene

      Gene: ITGA2B

      Variant: NM_000419.3:c.2898_2902dup

      LegacyVariant: N/A

      ClinVar: N/A

      CAiD: CA915940725

      gnomAD: N/A

    4. GT 40

      Case29: GT40, Female, India, age of onset is 6 years old

      DiseaseAssertion: Glanzmann thrombasthenia

      FamilyInfo: N/A

      ParentalGenotype: N/A

      CasePresentingHPOs: N/A

      CaseHPOFreeText: Patients were recruited as they presented consecutively from 1996 to 1998 for evaluation of a mucocutaneous bleeding disorder

      CaseNotHPOs: N/A

      CaseNotHPOsFreeText: N/A

      ProteinExpression: N/A

      PlateletAggregation: All patients examined had defective ADP, epinephrine, and collagen induced aggregation and normal ristocetin induced aggregation

      CasePreviousTesting: Mutations were detected by the method of single strand conformation polymorphism (SSCP) analysis, followed by nucleotide sequencing and confirmation by restriction fragment length polymorphism (RFLP) assays. The sequences of the primers employed and the reaction conditions for PCR amplification of the exons, adjacent intronic regions, and 50 and 30 untranslated regions of the aIIb and b3 gene

      Gene: ITGB3

      Variant: NM_000212.2:c.428T>G (p.Leu143Trp)

      LegacyVariant: N/A

      ClinVar: 13567

      CAiD: CA123252

      gnomAD: MAF in the Other population is 0.0001629 https://gnomad.broadinstitute.org/variant/17-45361875-T-G)

    1. Case 1

      Case#: 11 yo, Female

      DiseaseAssertion: GT

      FamilyInfo: No family hx. No pedigree.

      CasePresentingHPOs: (HP:0002249) Melena; (HP:0000421) Epistaxis; (HP:0000225) Gingival bleeding; (HP:0100769) Synovitis; (HP:0005261) Joint hemorrhage, right ankle; (HP:0001891) Iron deficiency anemia;

      PlateletAggregation: Prothrombin time: 11, Partial thromboplastin time: 26, Platelet function analyzer-100: >300

      CaseHPOFreeText: stable intestinal angiodysplasia

      ProteinExpression: Flow cytometry: CD41 and 61 <50%

      CasePreviousTesting: Molecular sequencing, Patients’ information was obtained from the medical record system of the Madinah Hereditary Blood Disorders Center, Maternity and Children Hospital, King Fahd Hospital, Al Madinah, Saudi Arabia.

      Gene: ITGB3

      HGVS: NM_000212.3:c.2111_2112del

      ClinVar:

      CAID: CA3062865178

      gnomAD:

    1. GT2

      Case2: (GT2) Male, 76 years old, French

      DiseaseAssertion: Glanzmann thrombasthenia

      FamilyInfo: N/A

      ParentalGenotype: N/A

      CasePresentingHPOs: N/A

      CaseHPOFreeText: Mucocutaneous bleeding

      CaseNotHPOs: N/A

      ProteinExpression: <5% surface expression levels of αIIbβ3

      Platelet Aggregation: Absent platelet aggregation to all agonists (no mention for which agonists or response to ristocetin)

      CasePreviousTesting: All the information we are given is "mutation screening of the ITGA2B and ITGB3 genes" the method for sequencing etc. was not stated

      Gene: ITGB3

      Variant: NM_000212.2:c.1260G>A

      LegacyVariant: N/A

      ClinVar: N/A

      CAiD: CA8623200

      gnomAD MAF in the African population is 0.00004005 https://gnomad.broadinstitute.org/variant/17-45368454-G-A

    2. GT6

      Case6: (GT6), Male, 82 years old, French

      DiseaseAssertion: Glanzmann thrombasthenia

      FamilyInfo: N/A

      ParentalGenotype: N/A

      CasePresentingHPOs: N/A

      CaseHPOFreeText: Mucocutaneous bleeding

      CaseNotHPOs: N/A

      ProteinExpression: 40-55% surface expression levels of αIIbβ3

      Platelet Aggregation: Absent platelet aggregation to all agonists (no mention for which agonists or response to ristocetin)

      CasePreviousTesting: All the information we are given is "mutation screening of the ITGA2B and ITGB3 genes" the method for sequencing etc. was not stated

      Gene: ITGB3

      Variant: NM_000212.2:c.665T>C (p.Leu222Pro) and NM_000212.2:c.1871G>A (p.Cys592Tyr)

      LegacyVariant: (p.Leu196Pro) and (p.Cys624Tyr) (The paper gives legacy and current nomenclature)

      ClinVar: N/A

      CAiD: CA291224887 and CA400032726

      gnomAD MAF in the European (non-Finnish) population is 0.00006482 https://gnomad.broadinstitute.org/variant/17-45363676-T-C

    1. Case1: Male, 61 years old, Iraqi-Jewish origin

      DiseaseAssertion: Glanzmann thrombasthenia

      FamilyInfo: His sister is the other proband in this article

      ParentalGenotype: N/A

      CasePresentingHPOs: HP:0000225, HP:0000225, HP:0031364, HP:0002249

      (Gingival bleeding, epistaxis, ecchymosis, melena)

      CaseHPOFreeText: N/A

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      ProteinExpression: Surface expression GPIIb/IIIa was 9% of normal

      PlateletAggregation: Platelet aggregation in response to thrombin, collagen, ADP and epinephrine was absent, whereas ristocetin induced aggregation was normal

      CasePreviousTesting: DNA fragments containing exons and flanking intronic regions of the GPIIb gene were amplified by PCR

      Gene: ITGA2B

      Variant: NM_000419.3:c.1947-2A>G

      LegacyVariant: N/A

      ClinVar: N/A

      CAiD: CA399801096

      gnomAD: N/A

  2. Sep 2026
    1. 32-year-old woman

      Case#: 32-year old woman, onset in early twenties

      DiseaseAssertion: STGD1

      FamilyInfo: n/a

      CasePresentingHPOs: HP:0011462, HP:0011507, HP:0000505, HP:0007722, HP:0030500, HP:0030329, HP:0030610, HP:0000575, HP:0030602

      CaseHPOFreeText: Patient’s best-corrected visual acuity was OD: 20/200 and OS: 20/40. Refractive error was OD: −5.25/−0.75 × 4° and OS: −5.75/−0.50 × 133°. Flecks in macular area extended anterior to the vascular arcades and the optic disc in both eyes. Atrophic lesion in the macula with flecks observed across the posterior pole. IS/OS junction loss central macular area bilaterally. Absolute scotoma in left eye (ie total deviation −20 dB). Defect in the RPE/Bruch membrane complex was observed on SD-OCT in both eyes in the central macula. The defects in the RPE-Bruch membrane complex measured OD: 332 um and OS: 266 um in maximum horizontal diameter. Herniation of the retina through these defects into the sub-RPE/choroidal space. Abnormal thickening of the RPE in the parafoveal region. Normal amplitudes and implicit times in both rod and cone photoreceptor systems were detected by ERG.

      CaseNotHPOs: HP:0000510, HP:0007984

      CaseNotHPOFreeText: Normal amplitudes and implicit times in both rod and cone photoreceptor systems were detected by ERG. There was no evidence of sub-RPE choroidal neovascularization (CNV), pigment epithelial defects (PED) or subretinal fluid.

      Genotyping Method: ABCR 600 micro-array chip

      PreviouslyPublished: n/a

      Variant: NM_000350.3(ABCA4):c.5714+5G>A

      ClinVar: 99403

      SupplementalData: n/a

    1. A 25-year-old White man presented with bilateral central vision loss due to foveal lesions consisting of vitelliform fluid.

      Case#: Patient 1, male, Caucasian, onset at 20yo, USA

      DiseaseAssertion: ABCA4

      FamilyInfo: No family history of retinal disease.

      CasePresentingHPOs: HP:0007677, HP:0030603, HP:0030500, HP:0030636, HP:0004328, HP:0012372

      CaseHPOFreeText: Bilateral central vision loss, progressive decline in visual acuity (20/60 both eyes), foveomacular vitelliform lesions with fluid accumulation, optical gap lesions progressing to cavitated appearance after fluid resorption, thinning and abnormal reflectivity of photoreceptor layers, near-infrared autofluorescence abnormalities in lesion-adjacent regions

      CaseNotHPOs: HP:0000510, HP:0000511

      CaseNotHPOFreeText: No generalized rod or cone dysfunction on full-field electroretinogram, EOG findings not consistent with bestrophinopathy (Arden ratio 1.62)

      Genotyping Method: Exome sequencing

      PreviouslyPublished: None

      Variant: NM_000350.3(ABCA4):c.5882G>A (p.Gly1961Glu), NM_000350.3(ABCA4):c.4139C>T (p.Pro1380Leu)

      ClinVar: ClinVarID:7888, ClinVarID:7904

      CAID: N/A

      SupplementalData: N/A

    1. Case 3

      Case#:3, 34–year-old woman

      DiseaseAssertion:NR

      FamilyInfo: no family history of an ocular disease

      CasePresentingHPOs: HP:0007663, HP:0030506, HP:0030528, HP:0000603

      CaseHPOFreeText:bilateral markedly decreased vision (logMar BCVA OD:0.93, OS:0.95), bilateral atrophic lesions of the macula accompanied by yellow-white stellate flecks at the level of the retinal pigment epithelium, Atrophic lesions and flecks were also extending to the mid-periphery of both retinae, bilateral absolute central scotoma and relative paracentral scotomas as well in both eyes, PERG was significantly reduced, while scotopic and photopic amplitudes were also lower than normal.

      CaseNotHPOs:

      CaseNotHPOFreeText:NR

      Genotyping Method: “Analysis of the ABCA4 gene”

      PreviouslyPublished: No

      Variant: NM_000350.3:c.5882G>A, NM_000350.3:c.6709dup

      ClinVar: ​​7888, 99485

      CAID: CA119132, CA227437

      SupplementalData:

  3. Jul 2026
    1. Patient 1

      Case:Patient 1, Male, 4 y/o, German and Thai

      DiseaseAssertion:FOXG1 syndrome

      FamilyInfo: Non-consanguineous parents. De novo. Patient 1 has maternally inherited duplications at 15q21.12(47292250-47309868)x3 and Xp22.31(6451676-8115124)x3 of unknown clinical significance.

      ParentalGenotype:Not provided

      CasePresentingHPOs:HP:0002197, HP:0005484, HP:0011344, HP:0001252, HP:0020045,HP:0000540, HP:0010808, HP:0002019, HP:0003781, HP:0012741, HP:0002421, HP:0000748, HP:0003763, HP:5200017, HP:0025112, HP:0000957

      CaseHPOFreeText: At 19 months, could not sit independently and no speech development. Stereotypic hand and head movements. High pain tolerance. X-ray at age 2 showed broad ribs. Improved head control by age 4.

      CaseNotHPO:HP:0410263, HP:0002376

      CaseNotHPOFreeText:Dysmorphic features. breathing abnormalities

      CasePreviousTesting:No previous testing

      PreviouslyPublished:Not previously published

      GenotypingMethod:Mate-pair sequencing, Sanger sequencing

      Gene:FOXG1

      Variant:46,XY,t(9;14)(q22.3;q11.2)dn

      HGVS:Not provided

      ClinVarID:426096

      gnomAD:Not provided

    2. Patient 3

      Case:Patient 3, Male, 1 y/o, Brazilian

      DiseaseAssertion: FOXG1 syndrome

      FamilyInfo: Non-consanguineous parents

      ParentalGenotype: No family testing mentioned.

      CasePresentingHPOs: HP:0000252, HP:0001252, HP:0000486

      CaseHPOFreeText: Developed microcephaly within 1 year. Developmental delay, unable to sit without assistance at 1 year old. Central Nervous System (CNS) MRI showed a volumetric reduction of the cerebral parenchyma, hypomyelination, and hypoplasia of corpus callosum mainly involving the anterior part and prominent lateral ventricles

      CaseNotHPO: HP:0030917

      CaseNotHPOFreeText: Normal length, weight, HC at birth. No retinal abnormalities.

      CasePreviousTesting: Not asserted.

      PreviouslyPublished: Not previously published.

      GenotypingMethod: Sanger sequencing, mate-pair sequencing

      Gene: FOXG1

      Variant: 46,XY,t(2;14)(q37;q11.2)dn

      HGVS: Not provided.

      ClinVarID:426094

      gnomAD:Not provided

    3. Patient 2

      Case:Patient 2, Female, 5 y/o, Brazilian

      DiseaseAssertion:quadriplegic cerebral palsy with axial hypotonia and distal spasticity

      FamilyInfo: Non-consanguineous parents. Parents had normal karyotypes. Older sister was clinically normal.

      ParentalGenotype: Normal karyotypes for both parents.

      CasePresentingHPOs: HP:0002098, HP:0010959, HP:0008755, HP:0002090, HP:0032661, HP:0001274, HP:0011344, HP:0001249, HP:0001344, HP:0000748, HP:0034435, HP:0000486, HP:0000483, HP:0200136

      CaseHPOFreeText: Dilated superficial blood vessels seen on brain MRI.

      CaseNotHPO:N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: Not asserted

      PreviouslyPublished: Not previously published

      GenotypingMethod:Mate-pair sequencing, Sanger sequencing, chromosome analysis

      Gene: FOXG1

      Variant: 46,XX,t(4;14)(q27;q13)dn

      HGVS: Not provided

      ClinVarID: 426095

      gnomAD: Not provided

    1. Case  1

      Case: Patient 1, female, 2 years old

      DiseaseAssertion: Rett Syndrome

      FamilyInfo: DeNovo. Patient 1 was the second child of a nonconsanguineous Chinese couple. Patient 1 was born at full term with a birth weight of 3.83 kg.

      ParentalGenotype(s):Not provided

      CasePresentingHPOs:HP:0011344, HP:0001250, HP:0001252, HP:0000252, HP:0000748, HP:0003763, HP:0005469, HP:0000486, HP:0012171.

      CaseHPOFreeRext:Patient 1 presents with severe global developmental delay, epilepsy, and hypotonia. The Patient History contains all of Patient 1's phenotypes along with the progression of her condition.

      Patient History

      @ 3 months - Patient 1 had microcephaly (head circumference was less than 3rd percentile with a body weight and body height at 75th percentile). Patient 1 had hypotonia.

      Patient 1 was given a metabolic screening, a muscle enzyme, and a brain tomography with normal results.

      @ 6 months - Patient 1 had microcephaly, flat occiput, right divergent squint, and hypotonia. No syndromal diagnosis could be ascertained at that time.

      @ 2 years - Patient 1 had epilepsy.

      Patient 1 had severe global development delay.

      Patient 1 was given an EEG which showed nonspecific background slowing, but no epileptiform abnormalities. Patient 1 was also given a brain MRI which showed mild thinning of corpus callosum without major structural defect. Patient 1 had no developmental regression but she developed stereotypical hand movements, bruxism, and occasional outburst of laughter.

      Based on these phenotypes, Angelman/Rett Syndrome was suspected.

      CaseNOTHPOs: HP:0002353.

      CaseNOTHPOFreeText: Patient 1 was given an EEG which detected no epileptic abnormalites.

      CasePreviousTesting: Genetic investigations (including methylation-specific multiplex ligation-dependent probe amplification (MS-MLLPA)) was conducted for Angelman Syndrome, UBE3A gene, MECP gene, and array CGH. These studies were negative. A FOXG1 related disease was suspected

      PreviouslyPublished:Not previously published

      GenotypingMethod: A FOXG1 gene test showed a de novo frameshift pathogenic mutation FOXG1 {NM_005249.3} c. 396_397ins26; FOXG1{NP_005240.3} :(p. Gly133TRPfs*68) which confirmed the diagnosis of a FOXG1 related congenital variant of Rett Syndrome.

      Gene:FOXG1

      Variant: (NM_005249.3) c. 396_397ins26 (p. Gly133Trpfs*68)

      HGVS:Not provided

      ClinVarID:Not found

      CAID:Not found

      gnomAD:Not found

    2. Case  2

      Case:Patient 2, female, Chinese

      DiseaseAssertion:Global delay

      FamilyInfo:Patient 2 was the first child of nonconsanguineous Chinese couple born at 38-week gestation. The mother had gestational diabetes mellitus that required insulin therapy.

      ParentalGenotype:Not provided

      CasePresentingHPOs:HP:0000365, HP:0020049, HP:0000252, HP:0001263, HP:0012171, HP:0000154, HP:0000708, HP:0003763, HP:0002376, HP:0012433.

      CaseHPOFreeText:

      Patient History

      @ birth - Patient 2 presented with mild grade bilateral hearing impairment and left divergent squint diagnosed at birth.

      @ Follow-up visit - Patient 2 had microbrachycephaly and global developmental delay. Brain MRI, metabolic screening and array CGH were normal.

      @ 1 year - Patient 2 had stereotypical handwashing movement.

      There was no clinical or electrical seizure.

      Patient 2 has craniofacial features like microbrachycephaly, wide mouth, divergent squint, and behavioral phenotype.

      @ 1.5 years - Patient 2 had bruxism and developmental regression. Patient 2 also had loss of some motor and social skills.

      CaseNotHPOs:HP:0001250

      CaseNotHPOFreeText:Patient 2 has no seizures.

      CasePreviousTesting:Not provided

      PreviouslyPublished:Not previously published

      GenotypingMethod:Not provided

      Gene:MECP2 (MN_004992.3) (NP_004983.1)

      Variant:c. 808C>T (p. Arg270*)

      HGVS:Not provided

      ClinVarID:Not found

      CAID:CA172577

      gnomAD:Not found

      MultipleGeneVariants:NA

    1. Patient 2

      Case:Patient 2, female, 2.5 years old

      DiseaseAssertion:CDKL5 Disorder

      FamilyInfo:De Novo with an unremarkable family history.

      ParentalGenotype:Not provided

      CasePresentingHPOs:HP:0032792, HP:0007359, HP:0011154, HP:0002194, HP:0010862, HP:0000750, HP:0012434, HP:0000710, HP:0100023, HP:0000252, HP:0009062, HP:0010845, HP:0020174, HP:0010841.

      CaseHPOFreeText:

      Patient history

      @ 2 months to 2.5 years - Patient 2 experienced tonic and focal seizures with autonomic symptoms.

      @ 2 years - Patient 2 was diagnosed with CDKL5 disorder.

      Patient 2 had severe delayed gross motor development, severe delayed fine motor development, severe delayed language development and delayed social development. Patient 2 had hyperoral and hand flapping stereotypies. She also had microcephaly (< 2 SD) and axial hypotonia.

      Patient 2 was given a brain EEG which detected Delta slowing of the background followed by generalized attenuation during seizures and multifocal interictal epileptiform abnormalities.

      @ 2.5 years - Patient 2 experienced seizures in clusters.

      Treatments

      Antiepleptic treatments included:Phenobarbital, Topirimate, Clobazam, Valproate, Keppra, Vitamin B6, Phenytoin, Lamotrigine, Nitrazepam, Oxcarbazepine, Mirtazipine, KCI, Levetiracetam, ant ketogenic diet.

      Patient 2 was also treated with Carnitine. Patient 2's seizures seem to have changed in type over time but continued.

      Other testing

      Tests were conducted on Patient 2 to obtain data in the following areas: NBS, lactate, lipoprotein profile, plasma and urine amino acids, urine organic acids, acylcarnitine profile, total and free serum carnitine levels, plasma ammonia, total plasma homocysteine, serum CK, liver enzymes, urine alpha-AASA, creatine, biotinidase, VLCFA, Batten disease screen, CSF analysis (amino acids, lactate, glucose, protein, cell count, neurotransmitters), MRI-brain with spectroscopy, and karyotype.

      CaseNotHPOs:Not provided

      CaseNotHPOFreeText:Not provided

      CasePreviousTesting:Patient 2 was given a gene sequence test for the genes SCNIA and MECP2. No gene mutation was found for these two genes.

      PreviouslyPublished:Not previously published

      GenotypingMethod:Patient 2 was given a CDKL5 gene sequence test. The test detected a mutation in the CDKL5 gene.

      Gene:CDKL5

      Variant:c. 2480_2486dupCAGATCT. frameshift

      The authors state that CDKL5 gene sequencing detected a de novo duplication in exon 17, c. 2480_2486dupCAGATCT, resulting in a frameshift (Boston University School of Medicine, Center for Human Genetics, Boston, MA). This is a novel change that has not been reported before in ExAC. Only pathogenic point mutations in exon 17 have previously been reported. In a patient with a previously reported frameshift mutation in exon 18, a truncated CDKL5 transcript was detected. A truncated protein would lack the C-terminus and would not localize correctly in the cell, as demonstrated in vitro. Accordingly, any reading frame altering mutations proximal to exon 18 are null-variants. Therefore, this mutation is classified as pathogenic according to ACMG criteria.

      HGVS:Not provided

      ClinVarID:547188

      NM_001323289.2 (CDKL5): c. 2480_2486dup (p. Gln830fs)

      Allele ID: 538303

      CAID:Not found

      gnomAD:Not found

      MultipleGeneVariants:Not provided