Entry - #614201 - BLEEDING DISORDER, PLATELET-TYPE, 11; BDPLT11 - OMIM - (OMIM.ORG)

# 614201

BLEEDING DISORDER, PLATELET-TYPE, 11; BDPLT11


Alternative titles; symbols

GLYCOPROTEIN VI DEFICIENCY
GP VI DEFICIENCY


Phenotype-Gene Relationships

Location Phenotype Phenotype
MIM number
Inheritance Phenotype
mapping key
Gene/Locus Gene/Locus
MIM number
19q13.42 Bleeding disorder, platelet-type, 11 614201 AR 3 GP6 605546
Clinical Synopsis
 
Phenotypic Series
 

INHERITANCE
- Autosomal recessive
HEAD & NECK
Nose
- Epistaxis
SKIN, NAILS, & HAIR
Skin
- Ecchymoses
- Easy bruising
HEMATOLOGY
- Bleeding, mild
- Menorrhagia
- Postsurgical bleeding
- Normal platelet morphology
- Prolonged bleeding time
- Decreased platelet expression of GP6
- Defective platelet activation and aggregation in response to collagen
- Defective platelet binding to collagen
MISCELLANEOUS
- Onset in infancy
- Variable severity
MOLECULAR BASIS
- Caused by mutation in the platelet glycoprotein VI gene (GP6, 605546.0001)
Bleeding disorder, platelet-type - PS231200 - 28 Entries
Location Phenotype Inheritance Phenotype
mapping key
Phenotype
MIM number
Gene/Locus Gene/Locus
MIM number
1p36.12 ?Bleeding disorder, platelet-type, 22 AR 3 618462 EPHB2 600997
3p21.31 Gray platelet syndrome AR 3 139090 NBEAL2 614169
3q21.3 Bernard-Soulier syndrome, type C AR 3 231200 GP9 173515
3q25.1 Bleeding disorder, platelet-type, 8 AR 3 609821 P2RY12 600515
5q11.2 Bleeding disorder, platelet-type, 9 AD 2 614200 BDPLT9 614200
7q21.11 Platelet glycoprotein IV deficiency AR 3 608404 CD36 173510
7q34 Bleeding disorder, platelet-type, 14 AD 2 614158 BDPLT14 614158
9q21.11 ?Bleeding disorder, platelet-type, 19 AR 3 616176 PRKACG 176893
9q34.13 Bleeding disorder, platelet-type, 17 AD, AR 3 187900 GFI1B 604383
10q22.2 Quebec platelet disorder AD 3 601709 PLAU 191840
11q13.1 Bleeding disorder, platelet-type, 18 AR 3 615888 RASGRP2 605577
11q24.3 Bleeding disorder, platelet-type, 21 AD, AR 3 617443 FLI1 193067
12q12 Scott syndrome AR 3 262890 ANO6 608663
14q24.1 Bleeding disorder, platelet-type, 15 AD 3 615193 ACTN1 102575
17p13.2 von Willebrand disease, platelet-type AD 3 177820 GP1BA 606672
17p13.2 Bernard-Soulier syndrome, type A1 (recessive) AR 3 231200 GP1BA 606672
17q12 Bleeding disorder, platelet-type, 20 AD 3 616913 SLFN14 614958
17q21.31 Bleeding disorder, platelet-type, 16, autosomal dominant AD 3 187800 ITGA2B 607759
17q21.31 Glanzmann thrombasthenia 1 AR 3 273800 ITGA2B 607759
17q21.32 Bleeding disorder, platelet-type, 24, autosomal dominant AD 3 619271 ITGB3 173470
17q21.32 Glanzmann thrombasthenia 2 AR 3 619267 ITGB3 173470
19p13.3 {Bleeding disorder, platelet-type, 13, susceptibility to} AD 3 614009 TBXA2R 188070
19p13.12-p13.11 Bleeding disorder, platelet-type, 25 AD 3 620486 TPM4 600317
19q13.42 Bleeding disorder, platelet-type, 11 AR 3 614201 GP6 605546
22q11.21 Giant platelet disorder, isolated AR 3 231200 GP1BB 138720
22q11.21 Bernard-Soulier syndrome, type B AR 3 231200 GP1BB 138720
22q12.3 Macrothrombocytopenia and granulocyte inclusions with or without nephritis or sensorineural hearing loss AD 3 155100 MYH9 160775
Not Mapped Bleeding disorder, platelet-type, 12 AD 605735 BDPLT12 605735

TEXT

A number sign (#) is used with this entry because this form of platelet-type bleeding disorder (BDPLT11) can be caused by compound heterozygous mutation in the GP6 gene (605546) on chromosome 19q13.


Description

Platelet-type bleeding disorder-11 (BDPLT11) is an autosomal recessive mild to moderate bleeding disorder caused by defective platelet activation and aggregation in response to collagen (summary by Dumont et al., 2009).

For a discussion of genetic heterogeneity of BDPLT, see 231200.


Clinical Features

Dumont et al. (2009) reported a 10-year-old girl with a history of easy bruising since infancy. Laboratory studies showed a prolonged bleeding time and failure of platelet activation and aggregation in response to collagen. Platelet response to ADP, arachidonic acid, and ristocetin was normal. Flow cytometric analysis of platelets showed an incomplete deficiency of glycoprotein VI, and the capacity of the patient's platelets to form thrombi on collagen in flow conditions was strongly impaired, with a 43% decreased surface coverage compared to control. There was also a marked defect in collagen-activated platelet-catalyzed thrombin generation.

Hermans et al. (2009) reported a 31-year-old woman with ecchymoses, epistaxis, several posttraumatic and postsurgery bleeding complications since childhood, and menorrhagia. Laboratory studies showed normal platelet numbers and morphology, but absent platelet activation and aggregation response to collagen. There was also increased adhesion of single platelets, likely due to other receptors. Flow cytometric analysis showed absent GP VI expression on platelets, whereas immunoblot analysis showed reduced but not absent GP VI expression.


Inheritance

The transmission pattern of BDPLT11 in the family reported by Dumont et al. (2009) was consistent with autosomal recessive inheritance.


Molecular Genetics

In a 10-year-old girl with mild platelet-type bleeding disorder-11, Dumont et al. (2009) identified compound heterozygosity for 2 mutations in the GP6 gene (605546.0001-605546.0002). Each parent was heterozygous for 1 of the mutations.

Hermans et al. (2009) identified compound heterozygous GP6 mutations (605546.0003-605546.0004) in a woman with a mild bleeding disorder since childhood.


REFERENCES

  1. Dumont, B., Lasne, D., Rothschild, C., Bouabdelli, M., Ollivier, V., Oudin, C., Ajzenberg, N., Grandchamp, B., Jandrot-Perrus, M. Absence of collagen-induced platelet activation caused by compound heterozygous GPVI mutations. Blood 114: 1900-1903, 2009. [PubMed: 19549989, related citations] [Full Text]

  2. Hermans, C., Wittevrongel, C., Thys, C., Smethurst, P. A., Van Geet, C., Freson, K. A compound heterozygous mutation in glycoprotein VI in a patient with a bleeding disorder. J. Thromb. Haemost. 7: 1356-1363, 2009. [PubMed: 19552682, related citations] [Full Text]


Creation Date:
Cassandra L. Kniffin : 8/31/2011
alopez : 04/06/2026
carol : 09/13/2011
ckniffin : 9/8/2011

# 614201

BLEEDING DISORDER, PLATELET-TYPE, 11; BDPLT11


Alternative titles; symbols

GLYCOPROTEIN VI DEFICIENCY
GP VI DEFICIENCY


SNOMEDCT: 765977002;   ORPHA: 73271, 98885;   DO: 0111057;   MONDO: 0013623;  


Phenotype-Gene Relationships

Location Phenotype Phenotype
MIM number
Inheritance Phenotype
mapping key
Gene/Locus Gene/Locus
MIM number
19q13.42 Bleeding disorder, platelet-type, 11 614201 Autosomal recessive 3 GP6 605546

TEXT

A number sign (#) is used with this entry because this form of platelet-type bleeding disorder (BDPLT11) can be caused by compound heterozygous mutation in the GP6 gene (605546) on chromosome 19q13.


Description

Platelet-type bleeding disorder-11 (BDPLT11) is an autosomal recessive mild to moderate bleeding disorder caused by defective platelet activation and aggregation in response to collagen (summary by Dumont et al., 2009).

For a discussion of genetic heterogeneity of BDPLT, see 231200.


Clinical Features

Dumont et al. (2009) reported a 10-year-old girl with a history of easy bruising since infancy. Laboratory studies showed a prolonged bleeding time and failure of platelet activation and aggregation in response to collagen. Platelet response to ADP, arachidonic acid, and ristocetin was normal. Flow cytometric analysis of platelets showed an incomplete deficiency of glycoprotein VI, and the capacity of the patient's platelets to form thrombi on collagen in flow conditions was strongly impaired, with a 43% decreased surface coverage compared to control. There was also a marked defect in collagen-activated platelet-catalyzed thrombin generation.

Hermans et al. (2009) reported a 31-year-old woman with ecchymoses, epistaxis, several posttraumatic and postsurgery bleeding complications since childhood, and menorrhagia. Laboratory studies showed normal platelet numbers and morphology, but absent platelet activation and aggregation response to collagen. There was also increased adhesion of single platelets, likely due to other receptors. Flow cytometric analysis showed absent GP VI expression on platelets, whereas immunoblot analysis showed reduced but not absent GP VI expression.


Inheritance

The transmission pattern of BDPLT11 in the family reported by Dumont et al. (2009) was consistent with autosomal recessive inheritance.


Molecular Genetics

In a 10-year-old girl with mild platelet-type bleeding disorder-11, Dumont et al. (2009) identified compound heterozygosity for 2 mutations in the GP6 gene (605546.0001-605546.0002). Each parent was heterozygous for 1 of the mutations.

Hermans et al. (2009) identified compound heterozygous GP6 mutations (605546.0003-605546.0004) in a woman with a mild bleeding disorder since childhood.


REFERENCES

  1. Dumont, B., Lasne, D., Rothschild, C., Bouabdelli, M., Ollivier, V., Oudin, C., Ajzenberg, N., Grandchamp, B., Jandrot-Perrus, M. Absence of collagen-induced platelet activation caused by compound heterozygous GPVI mutations. Blood 114: 1900-1903, 2009. [PubMed: 19549989] [Full Text: https://doi.org/10.1182/blood-2009-03-213504]

  2. Hermans, C., Wittevrongel, C., Thys, C., Smethurst, P. A., Van Geet, C., Freson, K. A compound heterozygous mutation in glycoprotein VI in a patient with a bleeding disorder. J. Thromb. Haemost. 7: 1356-1363, 2009. [PubMed: 19552682] [Full Text: https://doi.org/10.1111/j.1538-7836.2009.03520.x]


Creation Date:
Cassandra L. Kniffin : 8/31/2011

Edit History:
alopez : 04/06/2026
carol : 09/13/2011
ckniffin : 9/8/2011