von Willebrand disease

637: 628:(during collecting storage and transportation of the specimen) especially when the testing is contracted to an outside facility and the specimen is frozen and transported long distances. Diagnostic errors are not uncommon, and the rate of testing proficiency varies amongst laboratories, with error rates ranging from 7 to 22% in some studies to as high as 60% in cases of misclassification of VWD subtype. To increase the probability of a proper diagnosis, testing should be done at a facility with immediate on-site processing in a specialized coagulation laboratory. 36: 794:. In VWD Type 2M, all multimers are identified but uniformly decreased in quantity, resembling the pattern seen in VWD Type 1. Conversely, in VWD Type 2A, high molecular weight multimers are either absent or present in very low quantities. VWD Type 2M can be further differentiated from VWD Type 1 based on the VWF Activity to antigen ratio. In Type 1, the ratio is >0.7. In Type 2M, the ratio is <0.7. In Type 2M, factor VIII activity can be normal or low while the 1225:. He ultimately assessed 66 members of her family and reported in a 1926 Swedish-language article that this was a previously undescribed bleeding disorder that differed from hemophilia. He published another article on the disorder in 1931, in the German language, which attracted international attention in the disease. The eponymous name was assigned to the disease between the late 1930s and the early 1940s, in recognition of von Willebrand's extensive research. 656: 1128:) three- to five-fold. Desmopressin is also available as a preparation for intranasal administration (Stimate) and as a preparation for intravenous administration. Desmopressin is contraindicated in VWD type 2b because of the risk of aggravated thrombocytopenia and thrombotic complications. Desmopressin is probably not effective in VWD type 2M and is rarely effective in VWD type 2N. It is totally ineffective in VWD type 3. 834:. The significantly reduced factor VIII levels in VWD Type 2N can sometimes lead to misdiagnosis as mild Hemophilia A. Like Hemophilia A, VWD Type 2N presents with joint and soft tissue bleeds. It is an autosomal recessive disorder, requiring either homozygosity or double heterozygosity for disease manifestation. Diagnostic tools include assessing the ratio of VWF binding to VWF antigen levels. A ratio <0.3 indicates 1156:

are commercially available for prophylaxis and treatment of VWD, and have varying levels of factor VIII. Products with higher VWF:RCo/FVIII ratios allow for more frequent dosing of VWF if needed, without the risk of accumulation to supranormal levels of FVIII. Recombinant factor VIII products contain insignificant quantity of VWF, so are not clinically useful as standalone therapy for VWD.

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platelet membrane which increases its affinity to bind to the VWF. Large platelet aggregates and high molecular weight VWF multimers are removed from the circulation resulting in thrombocytopenia and diminished or absent large VWF multimers. The ristocetin cofactor activity and loss of large VWF multimers are similar to VWD type 2B.

620:

and VWF propeptide to VWF propeptide antigen ratio. In cases of suspected acquired von Willebrand syndrome, a mixing study (analysis of patient plasma along with pooled normal plasma/PNP and a mixture of the two tested immediately, at one hour, and at two hours) should be performed. Detection of VWD is complicated by VWF being an

160:. It is known to affect several breeds of dogs as well as humans. The three forms of VWD are hereditary, acquired, and pseudo or platelet type. The three types of hereditary VWD are VWD type 1, VWD type 2, and VWD type 3. Type 2 contains various subtypes. Platelet type VWD is also an inherited condition. 1155:

For patients with VWD scheduled for surgery and cases of VWD disease complicated by clinically significant hemorrhage, human-derived medium purity factor VIII concentrates, which also contain von Willebrand factors, are available for prophylaxis and treatment. Humate P, Alphanate, Wilate and Koate HP

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The location of oral bleeds was as follows: labial frenum, 60%; tongue, 23%; buccal mucosa, 17% and gingiva and palate, 0.5%. Severe hemophilia will have most frequent bleeding occurrences, followed by moderate and then mild hemophilia. They mostly come from traumatic injuries. Bleeding will also be

1323:

In pigs, the causal mutation for VWD type 3 has also been identified. It is a large duplication within the VWF gene and causes serious damage to the gene function, so that virtually no VWF protein is produced. The clinical picture in pigs is most similar to that in humans with VWD type 3. Therefore,

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for the defective gene. It arises from failure to secrete VWF into the circulation or, in the case of Type 1C, from VWF being cleared more quickly than normal. If VWF levels are greater than 50%, VWD can be ruled out. If VWF activity is below 30%, VWD is present. Patients with VWF activity between

627:

The testing for VWD can be influenced by laboratory procedures. Numerous variables exist in the testing procedure that may affect the validity of the test results and may result in a missed or erroneous diagnosis. The chance of procedural errors are typically greatest during the preanalytical phase

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time. Type 2N may be considered if factor VIII levels are disproportionately low, but confirmation requires a "factor VIII binding" assay. Additional laboratory tests that help classify sub-types of VWD include von Willebrand multimer analysis, modified ristocetin induced platelet aggregation assay

364:

have a lower mean level than individuals with other blood groups. Unless ABO group-specific VWF:antigen reference ranges are used, normal group O individuals can be diagnosed as type I VWD, and some individuals of blood group AB with a genetic defect of VWF may have the diagnosis overlooked because

163:

In 2008 a new diagnostic category of "Low VWF" was proposed to include those individuals whose von Willebrand factor levels were in the 30–50 IU/dL range, below the normal reference range but not low enough to be von Willebrand disease. Patients with low VWF were sometimes noted to experience

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Platelet-type VWD (also known as pseudo-VWD) is an autosomal dominant genetic defect of the platelets. The VWF is qualitatively normal and genetic testing of the von Willebrand gene and VWF protein reveals no mutational alteration. The defect lies in the qualitatively altered GPIb receptor on the

421:

levels are also performed because factor VIII is bound to VWF which protects the factor VIII from rapid breakdown within the blood. Deficiency of VWF can then lead to a reduction in factor VIII levels, which explains the elevation in PTT. Normal levels do not exclude all forms of VWD, particularly

712:

Type 2 VWD (15-50% of cases) is a qualitative defect and the bleeding tendency can vary between individuals. Four subtypes exist: 2A, 2B, 2M, and 2N. These subtypes depend on the presence and behavior of the underlying multimers. Type 2 VWD (other than 2N) features an activity-to-antigen ratio of

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The protocols suggest the use of factor concentrate along with the use of local hemostatic techniques, such as suturing, and local measures, such as the use of oxidized cellulose, for example, Surgicel or fibrin glue in conjunction with post-operatively administered antifibrinolytic agents where

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that was approved for use in the United States in December 2015, and for use in the European Union in August 2018. If baseline factor VIII activity is >40%, rVWF may be administered as a standalone product when immediate response is needed, but if Factor VIII activity is <40% and immediate

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noted that patients with acquired VWD and aortic stenosis who underwent valve replacement experienced a correction of their hemostatic abnormalities, but that the hemostatic abnormalities can recur after 6 months when the prosthetic valve is a poor match with the patient. Similarly, acquired VWD

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The ristocetin cofactor activity is low when the patient's platelet-poor plasma is assayed against formalin-fixed, normal donor platelets. However, when the assay is performed with the patient's own platelets (platelet-rich plasma), a lower-than-normal amount of ristocetin causes aggregation to

1374:

The use of any non-steroidal anti-inflammatory drug (NSAID) must be discussed beforehand with the patient's hematologist because of their effect on platelet aggregation. There are no restrictions regarding the type of local anaesthetic agent used although those with vasoconstrictors may provide

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Variant forms of VWF were recognized in the 1970s, and these variations are now recognized as the result of synthesis of an abnormal protein. During the 1980s, molecular and cellular studies distinguished hemophilia A and VWD more precisely. Persons who had VWD had a normal FVIII gene on the X

890:

inheritance pattern. Additional diagnostic tools for VWD type 3 include assessing VWF activity using the Ristocetin cofactor assay and Collagen binding assay. In VWD type 3, VWF activity is either absent or approaching undetectable. VWF multimer analysis reveals no bands or very faint bands on

737:

inheritance pattern with only occasional cases following autosomal recessive pattern. It accounts for 10-15% of all VWD cases. It manifests with moderate to moderately severe bleeding. Diagnostic features of VWD Type 2A include greater reduction in VWF activity (measured by a functional assay)

766:(GPIb) receptor on the platelet membrane is abnormally enhanced, leading to its spontaneous binding to platelets and subsequent rapid clearance of the bound platelets and of the large VWF multimers. Thrombocytopenia may occur. Large VWF multimers are reduced or absent from the circulation. 401:

assays may be performed depending on the results of a coagulation screen. Patients with von Willebrand disease typically display a normal prothrombin time and a variable prolongation of APTT, depending on whether sufficient VWF is available to perform its carrier function for factor VIII.

1320:. In dogs affected by type 1 VWD, the causal mutation was the same across all breeds and the same mutation was also detected in some human VWD type 1 patients. In contrast, the mutations causing VWD type 3 in dogs are specific to each breed. Genetic screening is offered for known breeds. 1241:

chromosome, and some had an abnormal VWF gene on chromosome 12. Gene sequencing identified many of these persons as having a VWF gene mutation. The genetic causes of milder forms of low VWF are still under investigation, and these forms may not always be caused by an abnormal VWF gene.

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Literature review current through: Jan 2021. This topic last updated: Feb 05, 2021. In turn adapted from The National Heart, Lung and Blood Institute. The Diagnosis, Evaluation, and management of Von Willebrand Disease. National Institutes of Health Publication 08-5832, December

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to other medical procedures requiring a blood work-up. Most cases of low VWF are never diagnosed due to its asymptomatic or mild presentation, and most people with type I VWD end up leading a normal life free of complications, with many being unaware that they have the disorder.

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of VWD is about one in 100 individuals. However, the majority of these people do not have symptoms. The prevalence of clinically significant cases is one per 10,000. Because most forms are rather mild, they are detected more often in women, whose bleeding tendency shows during

2043:

Boender J, Eikenboom J, van der Bom JG, Meijer K, de Meris J, Fijnvandraat K, Cnossen MH, Laros-van Gorkom BA, van Heerde WL, Mauser-Bunschoten EP, de Maat MP, Leebeek FW (December 2018). "Clinically relevant differences between assays for von Willebrand factor activity".

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Risks of thrombosis, development of alloantibodies, and allergic reactions including anaphylaxis must be considered when administering these preparations. Such risks have emerged as the main concerns in factor replacement therapies as infectious risks have diminished.

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occur. This is due to the large VWF multimers remaining bound to the patient's platelets. Patients with this subtype are unable to use desmopressin as a treatment for bleeding, because it can lead to unwanted platelet aggregation and aggravation of thrombocytopenia.

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For women with heavy menstrual bleeding, estrogen-containing oral contraceptive medications are effective in reducing the frequency and duration of the menstrual periods. Estrogen and progesterone compounds available for use in the correction of menorrhagia include

2211:

Favaloro EJ, Bonar R, Kershaw G, Sioufi J, Baker R, Hertzberg M, Street A, Marsden K (July 2006). "Reducing errors in identification of von Willebrand disease: the experience of the royal college of pathologists of australasia quality assurance program".

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induced by iatrogenic factors and poor oral hygiene practices. The frequency of oral hemorrhage by location in people with deficiency of F VIII and F IX is: gingiva, 64%; dental pulp, 13%; tongue, 7.5%; lip, 7%; palate, 2% and buccal mucosa, 1%.

430:(RIPA), collagen binding, and/or VWF multimer assays may be performed to follow up abnormal screening tests. A platelet aggregation assay will show an abnormal response to ristocetin with normal responses to the other agonists used: 266:. However, some individuals heterozygous for type 3 may be diagnosed with VWD type 1, indicating an intermediate inheritance in those cases. VWD occurs in approximately 1% of the population and affects men and women equally. 164:

bleeding, despite mild reductions in VWF levels. The 2021 ASH/ISTH guidelines re-classified patients with levels in the 30–50 IU/dl range as "Low VWF" if they have no bleeding, but as having VWD if they have bleeding.

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could correct both the plasma deficiency of FVIII and the prolonged bleeding time. Since this time, the factor causing the long bleeding time was called the "von Willebrand factor" in honor of Erik Adolf von Willebrand.

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and cyproterone. Administration of ethinylestradiol diminishes the secretion of luteinizing hormone and follicle-stimulating hormone from the pituitary, leading to stabilization of the endometrial surface of the uterus.

1353:

Platelet or coagulation disorders with severely altered hemostasis can cause spontaneous gingival bleeding, as seen in conjunction with hyperplastic hyperemic gingival enlargements in leukemic patients. Deposition of

1549:

Lavin M, Aguila S, Schneppenheim S, Dalton N, Jones KL, O'Sullivan JM, O'Connell NM, Ryan K, White B, Byrne M, Rafferty M, Doyle MM, Nolan M, Preston RJ, Budde U, James P, Di Paola J, O'Donnell JS (November 2017).

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Blood transfusions are given as needed to correct anemia and hypotension secondary to hypovolemia. Infusion of platelet concentrates is recommended for correction of hemorrhage associated with platelet-type VWD.

790:(similar to VWD Type 2A) or with collagen. Like other Type 2 VWD subtypes, there is a decreased ratio of VWF Activity to antigen. Differentiating VWD Type 2M from Type 2A involves analyzing VWF multimers through 4124: 4109: 1080:, either interfering with platelet or collagen binding; increasing VWF clearance from the plasma; adsorption to myeloma cells or platelets; or proteolytic cleavage of VWF after shear stress-induced unfolding. 3344:

Laffan M, Brown SA, Collins PW, Cumming AM, Hill FG, Keeling D, Peake IR, Pasi KJ (May 2004). "The diagnosis of von Willebrand disease: a guideline from the UK Haemophilia Centre Doctors' Organization".

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Wang L, Chen R, Tian F, Wang W, Wang L, Yu B, Huang X, Zhang Y, Su S, Ma G, Wang K (August 2016). "Life threatening biphasic adverse reactions to desmopressin: case report and review of the literature".

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is typically not part of the initial workup for von Willebrand disease, and is not needed for people diagnosed with type 1 VWD based on clinical history and laboratory tests. It is mainly useful for:

1346:. Symptoms of VWD include postoperative bleeding, bleeding after dental extraction, gingival bleeding, epistaxis and easy bruising. The intake of oral contraceptives as the first-line treatment for 704:

Type 1C VWD indicates patients with quantitative deficiency due to an enhanced VWF clearance, accounting for ∼15% to 20% of cases. Such patients may require VWF concentrate to treat/prevent bleeds.

1116:

is available as different preparations, recommended for use in cases of minor trauma, or in preparation for dental or minor surgical procedures. Desmopressin stimulates the release of VWF from the

409:

of a patient must be investigated for quantitative and qualitative deficiencies of VWF. This is achieved by measuring the amount of VWF in a VWF antigen assay and the functionality of VWF with a

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Peyvandi F, Kouides P, Turecek PL, Dow E, Berntorp E (November 2019). "Evolution of replacement therapy for von Willebrand disease: From plasma fraction to recombinant von Willebrand factor".

2724:

Othman M, Gresele P (August 2020). "Guidance on the diagnosis and management of platelet-type von Willebrand disease: A communication from the Platelet Physiology Subcommittee of the ISTH".

2579:"Acquired von Willebrand syndrome after continuous-flow mechanical device support contributes to a high prevalence of bleeding during long-term support and at the time of transplantation" 1800:

De Wee EM, Knol HM, Mauser-Bunschoten EP, van der Bom JG, Eikenboom JC, Fijnvandraat K, De Goede-Bolder A, Laros-van Gorkom B, Ypma PF, Zweegman S, Meijer K, Leebeek FW (November 2011).

1961:

James PD, Notley C, Hegadorn C, Leggo J, Tuttle A, Tinlin S, Brown C, Andrews C, Labelle A, Chirinian Y, O'Brien L, Othman M, Rivard G, Rapson D, Hough C, Lillicrap D (January 2007).

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Borhany, Munira; Pahore, Zaen; ul Qadr, Zeeshan; Rehan, Muhammad; Naz, Arshi; Khan, Asif; Ansari, Saqib; Farzana, Tasneem; Nadeem, Muhammad; Raza, Syed Amir; Shamsi, Tahir (2010).

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The four hereditary types of VWD described are type 1, type 2, type 3, and pseudo- or platelet-type. Most cases are hereditary, but acquired forms of VWD have been described. The

677:

0.30-0.50 IU/mL are classified based on their bleeding phenotype. If they have bleeding symptoms, they have VWD. If they have no bleeding, they are considered to have "Low VWF".

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levels are typically low (usually 5-15%) due to impaired VWF binding. This vulnerability to proteolysis in the circulation leads to clinical manifestations resembling those of

422:

type 2, which may only be revealed by investigating platelet interaction with subendothelium under flow, a highly specialized coagulation study not routinely performed in most

738:

compared to VWF antigen (quantity). This results in a decreased VWF Activity to Antigen ratio. Additionally, high molecular weight multimers are either absent or very low on

1327:

Mice affected by VWD type 3 were produced by genetic engineering to obtain a small sized model for the human disease. In these strains, the VWF gene has been knocked out.

3486: 1510:"von Willebrand disease (VWD): evidence-based diagnosis and management guidelines, the National Heart, Lung, and Blood Institute (NHLBI) Expert Panel report (USA)" 2301:

Meiring, Muriel; Coetzee, Marius; Kelderman, Mareli; Badenhorst, Philip (2011). "Laboratory Diagnosis and Management of von Willebrand Disease in South Africa".

3005: 2689:

Chandran R, Tohit ER, Stanslas J, Salim N, Mahmood TM, Rajagopal M (July 2024). "Shifting Paradigms and Arising Concerns in Severe Hemophilia A Treatment".

649: 1703: 1617: 874:

degradation, the total absence of VWF leads to extremely low factor VIII levels (typically 1-10%). These low levels are equivalent to those seen in

692:

Trouble may, however, arise in some patients in the form of bleeding following surgery (including dental procedures), noticeable easy bruising, or

2352:

Seidizadeh O, Baronciani L, Lillicrap D, Peyvandi F (August 2024). "Application of genetic testing for the diagnosis of von Willebrand disease".

842:

VWD Type 2N. Conversely, a VWF antigen-to-binding ratio >3 confirms the diagnosis of VWD Type 2N. Ristocetin-Induced Platelet Agglutination (

357: 17: 3479: 1751:

Lavin M, Aguila S, Dalton N, Nolan M, Byrne M, Ryan K, White B, O'Connell NM, O'Sullivan JM, Di Paola J, James PD, O'Donnell JS (July 2018).

2441:

Casonato A, Galletta E, Sarolo L, Daidone V (January 2018). "Type 2N von Willebrand disease: Characterization and diagnostic difficulties".

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in humans. An acquired form can sometimes result from other medical conditions. It arises from a deficiency in the quality or quantity of

1358:

and other blood degradation products on the tooth surfaces turning them brown can occur with continuous oral bleeding over long periods.

3447: 439: 427: 3472: 1858: 1673: 1508:

Nichols WL, Hultin MB, James AH, Manco-Johnson MJ, Montgomery RR, Ortel TL, Rick ME, Sadler JE, Weinstein M, Yawn BP (March 2008).

2481: 2536:

Vincentelli A, Susen S, Le Tourneau T, Six I, Fabre O, Juthier F, Bauters A, Decoene C, Goudemand J, Prat A, Jude B (July 2003).

923: 892: 843: 795: 747: 2852: 2759: 3603: 2257:"Von Willebrand factor assay proficiency testing. The North American Specialized Coagulation Laboratory Association experience" 886:, meaning that both parents must carry the defective gene for their child to be affected. In contrast, hemophilia A follows an 4234: 3391: 3218: 2988: 2902: 1208: 2390:

Beltran A, Jaramillo AP, Vallejo MP, Acosta L, Barberan Parraga GC, Guanín Cabrera CL, Gaibor VG, Cueva MG (August 2023).

4139: 3778: 3761: 2577:

Uriel N, Pak SW, Jorde UP, Jude B, Susen S, Vincentelli A, Ennezat PV, Cappleman S, Naka Y, Mancini D (October 2010).

1249:

VWD can also affect dogs, pigs, and mice. Furthermore, cases have been reported in cats, horses, cattle, and rabbits.

2195: 185:

who first described the condition in 1926. Guidelines for the diagnosis and management of VWD were updated in 2021.

3840: 3792: 636: 2501:

Tiede A, Rand JH, Budde U, Ganser A, Federici AB (June 2011). "How I treat the acquired von Willebrand syndrome".

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is typically low. It is uncommon and manifests with moderate to severe bleeding. The disease may follow either an

3044: 866:

production. In VWD type 3, VWF is undetectable in the VWF antigen assay. Since VWF normally protects coagulation

2618:

Selmi C, La Marca A (December 2023). "Oral hormonal therapy as treatment option for abnormal uterine bleeding".

3559: 3255: 1702:

Connell NT, Flood VH, Brignardello-Petersen R, Abdul-Kadir R, Arapshian A, Couper S, et al. (2021-01-12).

1393: 887: 1438:

Kaur V, Elghawy O, Deshpande S, Riley D (February 2024). "von Willebrand disease: A guide for the internist".

3846: 3832: 3097:

Lehner S, Ekhlasi-Hundrieser M, Detering C, Allerkamp H, Pfarrer C, von Depka Prondzinski M (February 2018).

576: 3820: 3783: 3653: 1384: 551: 315: 3973: 3549: 696:(heavy menstrual periods). The minority of cases of type 1 may present with severe hemorrhagic symptoms. 3928: 3773: 3061: 1301: 1221:, Finland, was brought to the Deaconess Hospital in Helsinki, where she was seen by Finnish physician 4044: 3615: 3596: 2790: 1297: 1222: 1101: 1088: 779: 182: 4150: 4014: 3757: 3586: 1473:

Swystun LL, James PD (January 2017). "Genetic diagnosis in hemophilia and von Willebrand disease".

1347: 1152:. Its overuse can lead to water retention and dilutional hyponatremia with consequent convulsion. 1095:). This form of acquired VWD may be more prevalent than is presently thought. In 2003, Vincentelli 460: 341:

In more severe cases of type 1 VWD, genetic changes are common within the VWF gene and are highly

4244: 4239: 4004: 3797: 1963:"The mutational spectrum of type 1 von Willebrand disease: Results from a Canadian cohort study" 1330:

In animals of other species affected by VWD, the causal mutations have not yet been identified.

3918: 3851: 1117: 350: 4190: 1178:

response is needed, rVWF must be administered in conjunction with FVIII replacement therapy.

218: 3913: 3903: 3721: 2785: 2003: 1174: 1084: 863: 819: 783: 726: 616: 455: 397:

level. Patients with abnormal tests typically undergo further testing for hemophilias. Other

299: 293: 247: 178:

VWD type 2 is the second most common type of the disorder and has mild to moderate symptoms.

146: 2886: 1616:

James PD, Connell NT, Ameer B, Di Paola J, Eikenboom J, Giraud N, et al. (2021-01-12).

3669: 3564: 3554: 1273: 1261: 1233: 621: 374: 331: 2392:"Desmopressin as a Treatment in Patients With Von Willebrand Disease: A Systematic Review" 1552:"Novel insights into the clinical phenotype and pathophysiology underlying low VWF levels" 438: 279:

Differentiating between type 2B and platelet-type VWD, as well as between type 2N VWD and

8: 4128: 3908: 3898: 3694: 3574: 1893: 1285: 1171: 1092: 883: 791: 685: 660: 499: 263: 206: 2418: 2391: 167:

VWD type 1 is the most common type of the disorder, with mild bleeding symptoms such as

4034: 3716: 3674: 3648: 3521: 3370: 3172: 3163: 3147: 3123: 3098: 3036: 2951: 2334: 2237: 1938: 1913: 1832: 1777: 1752: 1576: 1551: 1269: 1265: 854:

VWD type 3 is a rare but the most severe form of VWD. It occurs in individuals who are

799: 734: 713:

less than 0.7. This ratio is obtained by dividing the VWF activity by the VWF antigen.

680:

Many patients are asymptomatic or may have mild symptoms and not have clearly impaired

423: 398: 259: 44: 4133: 3246: 1801: 1728: 1650: 652:'s classification depends on the definition of qualitative and quantitative defects. 4161: 3923: 3699: 3608: 3464: 3434: 3397: 3387: 3362: 3358: 3332: 3303: 3298: 3281: 3224: 3214: 3177: 3128: 3028: 2984: 2955: 2943: 2939: 2908: 2898: 2872: 2864: 2831: 2741: 2706: 2671: 2635: 2600: 2559: 2518: 2458: 2423: 2369: 2338: 2326: 2318: 2278: 2241: 2229: 2191: 2160: 2119: 2111: 2061: 2025: 1984: 1943: 1824: 1802:"Gynaecological and obstetric bleeding in moderate and severe von Willebrand disease" 1782: 1768: 1733: 1719: 1655: 1637: 1633: 1581: 1531: 1526: 1509: 1490: 1455: 1317: 1253: 521: 445: 434: 224: 194: 118: 3040: 4201: 3749: 3689: 3684: 3544: 3354: 3324: 3293: 3167: 3159: 3118: 3110: 3024: 3020: 2976: 2935: 2823: 2733: 2698: 2663: 2627: 2590: 2549: 2510: 2450: 2413: 2403: 2361: 2310: 2268: 2221: 2183: 2150: 2101: 2053: 2015: 1974: 1933: 1925: 1836: 1816: 1772: 1764: 1753:"Significant gynecological bleeding in women with low von Willebrand factor levels" 1723: 1715: 1645: 1629: 1571: 1563: 1521: 1482: 1447: 1313: 1133: 815: 386: 240: 60: 3374: 2631: 2139:"von Willebrand Disease: A Concise Review and Update for the Practicing Physician" 2020: 1929: 1423: 684:, which might suggest a bleeding disorder. Often, the discovery of low VWF occurs 4155: 4029: 3863: 3704: 3569: 3195:"Hemophilia A" (PDF). College of Dental Hygienists of Ontario. September 2, 2015. 2970: 2514: 1979: 1962: 1567: 1388: 1305: 1281: 1257: 763: 739: 269: 150: 2980: 4166: 4054: 3766: 3709: 3591: 2827: 2595: 2578: 2365: 1486: 1289: 1137: 1104:(a pump that pumps blood from the left ventricle of the heart into the aorta). 327: 323: 262:

traits. Occasionally, type 2 also inherits recessively. Type 3 is inherited as

4212: 4118: 3428: 2912: 1891: 1704:"ASH ISTH NHF WFH 2021 guidelines on the management of von Willebrand disease" 1338:

In the case of severe deficiency, there may be spontaneous gingival bleeding,

4228: 4064: 3886: 3881: 3876: 3633: 3401: 3248:

Guidelines for dental treatment of patients with inherited bleeding disorders

3228: 2322: 2273: 2256: 2155: 2138: 2115: 1641: 1618:"ASH ISTH NHF WFH 2021 guidelines on the diagnosis of von Willebrand disease" 1309: 875: 831: 3807: 1701: 157: 4074: 3516: 3438: 3366: 3336: 3181: 3132: 3032: 2947: 2868: 2835: 2745: 2710: 2702: 2675: 2639: 2604: 2563: 2522: 2462: 2427: 2373: 2330: 2314: 2282: 2233: 2164: 2123: 2106: 2089: 2065: 1988: 1947: 1828: 1786: 1737: 1659: 1585: 1535: 1494: 1459: 1451: 1192: 1167: 1141: 1113: 1077: 839: 822:(VWF) to factor VIII. Although VWF antigen (quantity) and activity levels ( 673: 641: 477: 410: 406: 303: 280: 228: 142: 3307: 3114: 2225: 2187: 2029: 2004:"The effect of ABO blood group on the diagnosis of von Willebrand disease" 1324:

those pigs are valuable models for clinical and pharmacological research.

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electrophoresis. Additionally, Ristocetin-Induced Platelet Agglutination (

746:(a protease that cleaves VWF). Factor VIII activity can be normal or low. 35: 4207: 4185: 3871: 3679: 3511: 3500: 3445: 3328: 3096: 3079: 2853:"Molecular basis of von Willebrand disease and its clinical implications" 2554: 2537: 2408: 2002:

Gill JC, Endres-Brooks J, Bauer PJ, Marks WJ, Montgomery RR (June 1987).

1820: 1418: 1355: 1229: 1149: 1125: 1121: 1100:

contributes to the bleeding tendency in people with an implant of a left

1022: 878:, with clinical manifestations of life-threatening external and internal 871: 867: 827: 693: 681: 612: 418: 306:. Deficiency of VWF, therefore, shows primarily in organs with extensive 210: 1252:

The causal mutation for VWD type 1 was identified in dogs of the breeds

360:

can influence presentation and pathology of VWD. Those individuals with

4059: 4024: 3999: 3643: 3625: 2090:"Bleeding disorders in the tribe: result of consanguineous in breeding" 1339: 1214: 1196: 1187: 1148:

Desmopressin is a synthetic analog of the natural antidiuretic hormone

862:, resulting in a severe quantitative deficiency or complete absence of 855: 835: 823: 672:

Type 1 VWD (40-80% of all VWD cases) is a quantitative defect which is

470: 414: 394: 361: 342: 311: 214: 172: 123: 4101: 2737: 2454: 2057: 1799: 659:

von Willebrand disease type III (and sometimes II) is inherited in an

4196: 4049: 3994: 3581: 2667: 2351: 1343: 1293: 803: 346: 335: 307: 202: 168: 3315:

Mannucci PM (August 2004). "Treatment of von Willebrand's Disease".

1296:. Causal mutations for type 2 were identified in dogs of the breeds 762:" defect. The ability of the qualitatively defective VWF to bind to 640:

Pie chart of relative incidences of von Willebrand disease types in

3963: 3958: 3948: 3638: 3496: 914: 879: 838:

or double heterozygous VWD Type 2N, while a ratio <0.5 suggests

759: 743: 722: 465: 390: 378: 255: 154: 139: 18:

Microsoft Visual Studio Express § Visual Web Developer Express

3448:

The Diagnosis, Evaluation and Management of von Willebrand Disease

1218: 373:

Basic tests performed in any patient with bleeding problems are a

4009: 3968: 2300: 2254: 2042: 1398: 742:

due to impaired multimer assembly or increased susceptibility to

608: 345:. In milder cases of type 1 VWD, a complex spectrum of molecular 276:

Evaluating family members of individuals who have known variants.

4144: 2255:

Chandler WL, Peerschke EI, Castellone DD, Meijer P (June 2011).

655: 4113: 3953: 2482:"Clinical presentation and diagnosis of von Willebrand disease" 1507: 1277: 319: 198: 2926:

Von Willebrand EA (May 1999). "Hereditary pseudohaemophilia".

2535: 2178:

Lee, Christine A.; Kadir, Rezan A.; Kouides, Peter A. (2009).

1856: 1548: 2440: 2389: 1124:, thereby increasing the levels of VWF (as well as coagulant 787: 730: 251: 175:

can affect the presentation and severity of symptoms of VWD.

96: 3148:"Animal models of hemophilia and related bleeding disorders" 3099:"VWF Gene in Pigs Affected by Von Willebrand Disease Type 3" 2969:

Beighton P, Beighton G (2012). "Portraits and Biographies".

2897:(6th ed.). St Louism Missouri: Elsevier. p. 662. 2893:

Keohane, Elaine; Otto, Catherine; Walenga, Jeanine (2020).

2001: 859: 382: 3446:

NHLBI von Willebrand Disease Expert Panel (January 2008).

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are uncommon in all but the most severe type, VWD type 3.

43:

von Willebrand disease types I and II are inherited in an

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The various types of VWD present with varying degrees of

87: 81: 69: 2895:

Rodak's Hematology: Clinical Principles and Applications

1960: 1892:

Karen A. Moser; George M. Rodgers III; Kristi J. Smock.

1350:

may lead to gingival enlargement and bleeding in women.

624:

with levels rising in infection, pregnancy, and stress.

1914:"Special considerations in GI bleeding in VWD patients" 1209:

Erik Adolf von Willebrand § Von Willebrand disease

338:, and the risk of bleeding is increased concomitantly. 292:

For the normal function of the coagulation factor, see

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In the 1950s, it became clear that a "plasma factor",

302:

is mainly active in conditions of high blood flow and

171:, though occasionally more severe symptoms can occur. 2538:"Acquired von Willebrand syndrome in aortic stenosis" 786:. This mutation leads to reduced binding of VWF with 99: 72: 66: 63: 4091: 3433:. GeneReviews® . University of Washington, Seattle. 3282:"Biochemistry and genetics of von Willebrand factor" 2500: 2083: 2081: 2079: 2077: 2075: 102: 93: 90: 84: 78: 16:"VWD" redirects here. For Visual Web Developer, see 2478:Unless otherwise specified in boxes, reference is: 1911: 1195:. It may be more severe or apparent in people with 846:) and VWF multimer analysis are typically normal. 650:

International Society on Thrombosis and Haemostasis

615:

closure time, and in most cases, a normal collagen/

75: 2892: 2760:"Vonvendi (von willebrand factor- recombinant kit" 2752: 1076:Acquired Von Willebrand syndrome can occur due to 729:, leading to reduced binding of VWF with Platelet 3410:Ch. 112 Hereditary qualitative platelet disorders 3245:Brewer, Andrew; Correa, Maria Elvira (May 2006). 3213:. People's Medical. pp. 473, 475, 481, 482. 3062:"Canine von Willebrand Disease - Breed Summaries" 2576: 2072: 1912:Chornenki NL, Ocran E, James PD (December 2022). 1902:Last Update: July 2020. Content Review: June 2020 968:Often decreased at high ristocetin concentrations 4226: 3381: 2968: 2847: 2845: 2652: 181:The factor is named after the Finnish physician 3003: 2385: 2383: 2177: 1466: 1083:A form of acquired VWD occurs in patients with 413:(GP)Ib binding assay, VWF antibody assay, or a 2925: 2296: 2294: 2292: 1387:, caused by a deficiency in the VWF receptor, 1112:For patients with VWD type 1 and VWD type 2A, 796:ristocetin-induced platelet aggregation (RIPA) 748:Ristocetin-induced platelet aggregation (RIPA) 334:, shear stress is much higher than in average 3480: 3145: 2842: 2778: 2723: 2617: 2583:Journal of the American College of Cardiology 1857:National Hemophilia Federation (2014-03-05). 3426: 3244: 2919: 2529: 2380: 1472: 365:VWF levels are elevated due to blood group. 2479: 2289: 1697: 1695: 1010:Decreased at high ristocetin concentrations 882:. The inheritance pattern of VWD type 3 is 389:with International Normalized Ratio-PTINR, 3487: 3473: 3204: 3202: 2143:Clinical and Applied Thrombosis/Hemostasis 1232:, was decreased in these persons and that 34: 3452:National Heart, Lung, and Blood Institute 3297: 3171: 3122: 2594: 2553: 2417: 2407: 2272: 2154: 2136: 2105: 2019: 1978: 1937: 1776: 1727: 1649: 1611: 1609: 1607: 1605: 1603: 1601: 1599: 1597: 1595: 1575: 1525: 428:Ristocetin-induced platelet agglutination 3314: 3274:Harrison's textbook of Internal Medicine 1692: 1433: 1431: 1365: 654: 635: 3741: 3199: 2975:. Springer. pp. 1–201 See p. 187. 2474: 2472: 1887: 1885: 1883: 1881: 1879: 1852: 1850: 1848: 1846: 1308:; and for type 3 in dogs of the breeds 895:) is typically absent or severely low. 4227: 3279: 2261:American Journal of Clinical Pathology 1918:Hematology Am Soc Hematol Educ Program 1592: 1333: 1013:Similar decrease among multimer types 948:Similar decrease among multimer types 644:. Platelet-type was <0.5% of cases. 437:by main disorders and agonists 3468: 3240: 3238: 3208: 2303:Seminars in Thrombosis and Hemostasis 2214:Seminars in Thrombosis and Hemostasis 2180:Inherited Bleeding Disorders in Women 1428: 809: 383:activated partial thromboplastin time 188: 3146:Lozier JN, Nichols TC (April 2013). 2469: 1876: 1843: 733:receptors. This disorder follows an 3427:Goodeve A, James P (October 2017). 3317:The New England Journal of Medicine 2620:Eur J Contracept Reprod Health Care 2542:The New England Journal of Medicine 13: 3266: 3235: 3164:10.1053/j.seminhematol.2013.03.023 1001:Decreased binding to GPIb receptor 287: 14: 4256: 3460: 3382:Lichtman MA, Williams WJ (2006). 2137:Swami A, Kaur V (November 2017). 2094:Orphanet Journal of Rare Diseases 979:Enhanced binding to GPIb receptor 959:Inability to form large multimers 446:Platelet § Tests of function 417:cofactor activity (RiCof) assay. 258:. Types 1 and 2 are inherited as 3841:platelet storage pool deficiency 3793:Heparin-induced thrombocytopenia 3359:10.1111/j.1365-2516.2004.00894.x 3299:10.1146/annurev.biochem.67.1.395 2940:10.1046/j.1365-2516.1999.00302.x 1769:10.1182/bloodadvances.2018017418 1720:10.1182/bloodadvances.2020003264 1634:10.1182/bloodadvances.2020003265 1527:10.1111/j.1365-2516.2007.01643.x 1244: 1213:In 1924, a 5-year-old girl from 1062: 59: 3188: 3139: 3090: 3080:"Canine von Willebrand Disease" 3072: 3054: 2997: 2962: 2807: 2717: 2682: 2646: 2611: 2570: 2494: 2434: 2345: 2248: 2204: 2171: 2130: 2036: 1995: 1954: 1905: 1793: 1181: 826:cofactor assay) remain normal, 432: 239:The VWF gene is located on the 3560:Activated protein C resistance 3418:Ch. 118 von Willebrand disease 3256:World Federation of Hemophilia 3025:10.1016/J.THROMRES.2007.03.010 3004:Lassila R, Lindberg O (2013). 1894:"Von Willebrand Disease - VWD" 1863:National Hemophilia Federation 1744: 1666: 1542: 1501: 1411: 1394:List of hematologic conditions 611:may give an abnormal collagen/ 197:, usually in the form of easy 1: 3386:(7th ed.). McGraw-Hill. 3286:Annual Review of Biochemistry 2934:(3): 223–31, discussion 222. 2632:10.1080/13625187.2023.2270098 2021:10.1182/blood.V69.6.1691.1691 1930:10.1182/hematology.2022000390 1404: 1375:additional local hemostasis. 904:Von Willebrand disease types 898: 435:Platelet aggregation function 153:protein that is required for 4235:Autosomal dominant disorders 3654:Trousseau sign of malignancy 2515:10.1182/blood-2010-11-297580 1980:10.1182/blood-2006-05-021105 1568:10.1182/blood-2017-05-786699 1107: 1053:Absent or markedly decreased 1050:Absent or markedly decreased 818:that reduces the binding of 368: 7: 3974:Nonthrombocytopenic purpura 3550:Antithrombin III deficiency 2981:10.1007/978-1-4471-1415-4_1 2972:The Man Behind the Syndrome 2863:(9): 1036. September 2004. 1378: 1071: 864:von Willebrand factor (VWF) 814:Type 2N VWD results from a 784:von Willebrand factor (VWF) 778:VWD Type 2M results from a 727:von Willebrand factor (VWF) 721:VWD Type 2A results from a 234: 10: 4261: 3929:Congenital afibrinogenemia 3833:Glanzmann's thrombasthenia 2828:10.1016/j.blre.2019.04.001 2596:10.1016/j.jacc.2010.05.016 2366:10.1016/j.jtha.2024.05.006 1809:Thrombosis and Haemostasis 1487:10.1016/j.blre.2016.08.003 1302:German Shorthaired Pointer 1206: 1202: 993:Decreased large multimers 971:Decreased large multimers 773: 753: 716: 699: 577:Glanzmann's thrombasthenia 443: 291: 15: 4176: 4095: 4045:Gastrointestinal bleeding 3984: 3941: 3862: 3847:Hermansky–Pudlak syndrome 3806: 3748: 3734: 3662: 3624: 3616:Antiphospholipid syndrome 3597:Essential thrombocythemia 3537: 3530: 3507: 2791:European Medicines Agency 2656:Int J Clin Pharmacol Ther 1298:German Wirehaired Pointer 1223:Erik Adolf von Willebrand 1102:ventricular assist device 1089:gastrointestinal bleeding 1040: 952: 932: 908: 849: 816:loss-of-function mutation 780:loss-of-function mutation 723:loss-of-function mutation 707: 667: 349:may exist in addition to 183:Erik Adolf von Willebrand 117: 51: 42: 33: 28: 4015:Subconjunctival bleeding 3821:Bernard–Soulier syndrome 3784:Upshaw–Schulman syndrome 3758:Thrombocytopenic purpura 3587:Sticky platelet syndrome 2274:10.1309/AJCPH5JK4ONENPAE 2156:10.1177/1076029616675969 1859:"Von Willebrand Disease" 1674:"Von Willebrand Disease" 1419:MedlinePlus Encyclopedia 1385:Bernard–Soulier syndrome 806:pattern of inheritance. 631: 552:Bernard–Soulier syndrome 4005:Intracranial hemorrhage 3209:Glick, Michael (2015). 936:Decreased VWF quantity 609:platelet function assay 405:When VWD is suspected, 353:of the VWF gene alone. 211:heavy menstrual periods 209:. Women may experience 143:blood-clotting disorder 4213:von Willebrand Disease 3919:Factor XIII deficiency 3899:Hypoprothrombinemia/II 3894:von Willebrand disease 3852:Gray platelet syndrome 3430:von Willebrand Disease 3211:Burket's Oral Medicine 3152:Seminars in Hematology 2703:10.1055/s-0043-1778103 2315:10.1055/s-0031-1281045 2107:10.1186/1750-1172-5-23 1452:10.3949/ccjm.91a.22033 1424:Von Willebrand disease 1021:Decreased binding to 664: 645: 546:Von Willebrand disease 316:gastrointestinal tract 132:Von Willebrand disease 29:von Willebrand disease 3914:Factor XII deficiency 3904:Factor VII deficiency 3722:Renal vein thrombosis 3115:10.1534/g3.117.300432 3006:"Erik von Willebrand" 2226:10.1055/s-2006-947865 2188:10.1002/9781444303490 1366:Dental considerations 1175:von Willebrand factor 1085:aortic valve stenosis 1056:Usually undetectable 1004:Dominant or recessive 962:Dominant or recessive 820:von Willebrand factor 658: 639: 444:Further information: 300:Von Willebrand factor 294:von Willebrand factor 250:(12p13.2). It has 52 147:von Willebrand factor 138:) is the most common 3670:Deep vein thrombosis 3565:Protein S deficiency 3555:Protein C deficiency 3329:10.1056/NEJMra040403 3066:ahdc.vet.cornell.edu 2555:10.1056/NEJMoa022831 2409:10.7759/cureus.44310 1821:10.1160/TH11-03-0180 1274:Cardigan Welsh Corgi 1262:Bernese Mountain Dog 1118:Weibel–Palade bodies 945:Normal or decreased 622:acute-phase reactant 480:inhibitor or defect 424:medical laboratories 375:complete blood count 229:bleeding into joints 3909:Factor X deficiency 3798:May–Hegglin anomaly 3575:Prothrombin G20210A 3384:Williams Hematology 2795:. 20 September 2018 2691:Semin Thromb Hemost 1334:Oral manifestations 1286:Drentse Patrijshond 905: 884:autosomal recessive 876:severe hemophilia A 661:autosomal recessive 568:Decreased or absent 534:Decreased or absent 500:Adrenergic receptor 449: 264:autosomal recessive 4177:External resources 4035:Pulmonary hematoma 3942:Signs and symptoms 3717:Pulmonary embolism 3522:Bleeding diathesis 3280:Sadler JE (1998). 2766:. 13 February 2019 1270:Kerry Blue Terrier 1266:Manchester Terrier 928:Multimer quantity 903: 888:X-linked recessive 858:for the defective 810:Type 2N (Normandy) 800:autosomal dominant 750:is typically low. 735:autosomal dominant 665: 646: 433: 399:coagulation factor 260:autosomal dominant 189:Signs and symptoms 45:autosomal dominant 4222: 4221: 4089: 4088: 4085: 4084: 3937: 3936: 3924:Dysfibrinogenemia 3808:Platelet function 3730: 3729: 3609:Purpura fulminans 3420:. pp. 1937–. 3412:. pp. 1806–. 3393:978-0-07-143591-8 3220:978-1-60795-188-9 2990:978-1-4471-1415-4 2904:978-0-323-53045-3 2738:10.1111/jth.14827 2480:Margaret E Rick. 2455:10.1111/hae.13366 2058:10.1111/jth.14319 1898:ARUP laboratories 1318:Shetland Sheepdog 1254:Doberman Pinscher 1234:Cohn fraction I-0 1122:endothelial cells 1060: 1059: 605: 604: 522:Collagen receptor 377:-CBC (especially 356:The individual's 225:internal bleeding 195:bleeding tendency 129: 128: 23:Medical condition 4252: 4093: 4092: 3750:Thrombocytopenia 3746: 3745: 3739: 3738: 3695:Lowenberg's sign 3545:Clotting factors 3535: 3534: 3489: 3482: 3475: 3466: 3465: 3455: 3442: 3421: 3413: 3405: 3378: 3340: 3311: 3301: 3260: 3259: 3253: 3242: 3233: 3232: 3206: 3197: 3192: 3186: 3185: 3175: 3143: 3137: 3136: 3126: 3094: 3088: 3087: 3076: 3070: 3069: 3058: 3052: 3051: 3049: 3043:. Archived from 3010: 3001: 2995: 2994: 2966: 2960: 2959: 2923: 2917: 2916: 2890: 2884: 2883: 2881: 2880: 2871:. Archived from 2849: 2840: 2839: 2811: 2805: 2804: 2802: 2800: 2782: 2776: 2775: 2773: 2771: 2756: 2750: 2749: 2726:J Thromb Haemost 2721: 2715: 2714: 2686: 2680: 2679: 2668:10.5414/CP202461 2650: 2644: 2643: 2615: 2609: 2608: 2598: 2574: 2568: 2567: 2557: 2533: 2527: 2526: 2498: 2492: 2489: 2476: 2467: 2466: 2438: 2432: 2431: 2421: 2411: 2387: 2378: 2377: 2354:J Thromb Haemost 2349: 2343: 2342: 2298: 2287: 2286: 2276: 2252: 2246: 2245: 2208: 2202: 2201: 2175: 2169: 2168: 2158: 2134: 2128: 2127: 2109: 2085: 2070: 2069: 2046:J Thromb Haemost 2040: 2034: 2033: 2023: 1999: 1993: 1992: 1982: 1958: 1952: 1951: 1941: 1909: 1903: 1901: 1889: 1874: 1873: 1871: 1869: 1854: 1841: 1840: 1806: 1797: 1791: 1790: 1780: 1748: 1742: 1741: 1731: 1699: 1690: 1689: 1687: 1685: 1670: 1664: 1663: 1653: 1613: 1590: 1589: 1579: 1546: 1540: 1539: 1529: 1505: 1499: 1498: 1470: 1464: 1463: 1440:Cleve Clin J Med 1435: 1426: 1415: 1314:Scottish Terrier 1134:ethinylestradiol 1093:Heyde's syndrome 906: 902: 760:gain of function 548:(except Type 2B) 450: 442: 387:prothrombin time 109: 108: 105: 104: 101: 98: 95: 92: 89: 86: 83: 80: 77: 74: 71: 68: 65: 38: 26: 25: 4260: 4259: 4255: 4254: 4253: 4251: 4250: 4249: 4225: 4224: 4223: 4218: 4217: 4172: 4171: 4104: 4090: 4081: 4030:Hemopericardium 3980: 3933: 3864:Clotting factor 3858: 3802: 3726: 3675:Bancroft's sign 3658: 3649:Virchow's triad 3620: 3570:Factor V Leiden 3526: 3503: 3493: 3463: 3458: 3416: 3408: 3394: 3269: 3267:Further reading 3264: 3263: 3251: 3243: 3236: 3221: 3207: 3200: 3193: 3189: 3144: 3140: 3095: 3091: 3078: 3077: 3073: 3060: 3059: 3055: 3047: 3008: 3002: 2998: 2991: 2967: 2963: 2924: 2920: 2905: 2891: 2887: 2878: 2876: 2851: 2850: 2843: 2812: 2808: 2798: 2796: 2786:"Veyvondi EPAR" 2784: 2783: 2779: 2769: 2767: 2758: 2757: 2753: 2722: 2718: 2687: 2683: 2651: 2647: 2616: 2612: 2589:(15): 1207–13. 2575: 2571: 2534: 2530: 2509:(25): 6777–85. 2499: 2495: 2477: 2470: 2439: 2435: 2388: 2381: 2350: 2346: 2299: 2290: 2253: 2249: 2209: 2205: 2198: 2176: 2172: 2135: 2131: 2086: 2073: 2052:(12): 2413–24. 2041: 2037: 2000: 1996: 1959: 1955: 1910: 1906: 1890: 1877: 1867: 1865: 1855: 1844: 1804: 1798: 1794: 1763:(14): 1784–91. 1749: 1745: 1700: 1693: 1683: 1681: 1672: 1671: 1667: 1614: 1593: 1562:(21): 2344–53. 1547: 1543: 1506: 1502: 1471: 1467: 1436: 1429: 1416: 1412: 1407: 1381: 1368: 1336: 1306:Chinese Crested 1282:Coton de Tulear 1258:German Pinscher 1247: 1211: 1205: 1184: 1110: 1074: 1065: 901: 852: 812: 792:electrophoresis 776: 764:glycoprotein Ib 756: 740:electrophoresis 719: 710: 702: 670: 634: 448: 371: 358:ABO blood group 297: 290: 288:Pathophysiology 270:Genetic testing 237: 191: 113: 62: 58: 24: 21: 12: 11: 5: 4258: 4248: 4247: 4245:Rare syndromes 4242: 4240:Coagulopathies 4237: 4220: 4219: 4216: 4215: 4204: 4193: 4181: 4180: 4178: 4174: 4173: 4170: 4169: 4158: 4147: 4136: 4121: 4105: 4100: 4099: 4097: 4096:Classification 4087: 4086: 4083: 4082: 4080: 4079: 4078: 4077: 4069: 4068: 4067: 4062: 4057: 4055:Hemoperitoneum 4052: 4047: 4039: 4038: 4037: 4032: 4027: 4019: 4018: 4017: 4012: 4007: 4002: 3997: 3988: 3986: 3982: 3981: 3979: 3978: 3977: 3976: 3966: 3961: 3956: 3951: 3945: 3943: 3939: 3938: 3935: 3934: 3932: 3931: 3926: 3921: 3916: 3911: 3906: 3901: 3896: 3891: 3890: 3889: 3884: 3879: 3868: 3866: 3860: 3859: 3857: 3856: 3855: 3854: 3849: 3837: 3836: 3835: 3825: 3824: 3823: 3812: 3810: 3804: 3803: 3801: 3800: 3795: 3789: 3788: 3787: 3786: 3781: 3771: 3770: 3769: 3767:Evans syndrome 3754: 3752: 3743: 3736: 3732: 3731: 3728: 3727: 3725: 3724: 3719: 3714: 3713: 3712: 3707: 3702: 3700:Peabody's sign 3697: 3692: 3687: 3682: 3677: 3666: 3664: 3660: 3659: 3657: 3656: 3651: 3646: 3641: 3636: 3630: 3628: 3622: 3621: 3619: 3618: 3613: 3612: 3611: 3601: 3600: 3599: 3594: 3592:Thrombocytosis 3589: 3579: 3578: 3577: 3572: 3567: 3562: 3557: 3552: 3541: 3539: 3532: 3528: 3527: 3525: 3524: 3519: 3514: 3508: 3505: 3504: 3492: 3491: 3484: 3477: 3469: 3462: 3461:External links 3459: 3457: 3456: 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NBK7014. 3084:vetgen.com 2913:1229771843 2879:2009-01-30 2822:: 100572. 1868:3 December 1405:References 1340:ecchymosis 1207:See also: 1197:blood type 1188:prevalence 899:Comparison 856:homozygous 836:homozygous 824:Ristocetin 598:Normal or 471:Ristocetin 415:ristocetin 395:fibrinogen 310:, such as 241:short arm 215:blood loss 203:nosebleeds 173:Blood type 169:nosebleeds 151:multimeric 140:hereditary 124:Hematology 4197:eMedicine 4050:Hemobilia 3995:Epistaxis 3582:Platelets 3454:(Report). 3402:780625008 3229:903962852 2956:221750622 2816:Blood Rev 2339:260318180 2323:0094-6176 2242:260321152 2116:1750-1172 1642:2473-9529 1344:epistaxis 1294:Stabyhoun 1108:Treatment 1047:Recessive 1027:Recessive 1007:Decreased 989:Increased 985:Decreased 965:Decreased 942:Decreased 915:Autosomal 911:Mechanism 804:recessive 600:decreased 594:Decreased 589:Decreased 584:Decreased 509:Decreased 484:Decreased 381:counts), 369:Diagnosis 347:pathology 343:penetrant 149:(VWF), a 119:Specialty 4202:ped/2419 4041:abdomen 3964:Petechia 3959:Hematoma 3949:Bleeding 3816:adhesion 3742:By cause 3735:Bleeding 3639:Thrombus 3538:By cause 3531:Clotting 3501:clotting 3497:bleeding 3439:20301765 3367:15086318 3337:15306670 3182:23956467 3133:29208651 3041:11256355 3033:23980590 2948:10444294 2869:15377463 2836:31229334 2799:27 March 2770:27 March 2764:DailyMed 2746:32279414 2711:38224699 2676:27142268 2640:37955241 2605:20598466 2564:12878741 2523:21540459 2486:UpToDate 2463:29115006 2428:37649925 2419:10464544 2374:38762018 2331:22102202 2283:21571959 2234:16862524 2165:27920237 2124:20822539 2066:30358069 1989:17190853 1948:36485078 1829:21947221 1787:30042144 1738:33570647 1660:33570651 1586:28916584 1536:18315614 1495:27596108 1460:38307601 1379:See also 1290:Papillon 1072:Acquired 982:Dominant 939:Dominant 744:ADAMTS13 682:clotting 663:pattern. 466:Collagen 391:thrombin 379:platelet 235:Genetics 199:bruising 158:adhesion 155:platelet 47:pattern. 4156:D014842 4010:Hyphema 3985:By site 3969:Purpura 3663:By site 3308:9759493 3173:3742033 3124:5919753 2030:3495304 1939:9820382 1837:8677623 1778:6058240 1684:4 April 1577:5881608 1399:Purpura 1203:History 1041:Type 3 1036:Normal 953:Type 2 933:Type 1 774:Type 2M 754:Type 2B 717:Type 2A 700:Type 1C 538:Normal 524:defect 516:Normal 502:defect 494:Normal 385:-APTT, 330:of the 223:Severe 217:during 4191:000544 4145:193400 4071:joint 4021:torso 3954:Bruise 3877:A/VIII 3437: 3400: 3390: 3375:731315 3373: 3365: 3335: 3306: 3227: 3217: 3180: 3170: 3131: 3121: 3039: 3031: 2987: 2954: 2946: 2911: 2901: 2867: 2834: 2744: 2709: 2674: 2638: 2603: 2562: 2521: 2461: 2426: 2416: 2396:Cureus 2372: 2337: 2329: 2321: 2281: 2240: 2232: 2194: 2163: 2122: 2114: 2064: 2028: 1987: 1946: 1936: 1835: 1827: 1785: 1775: 1736: 1729:805326 1726: 1658: 1651:805340 1648: 1640: 1584: 1574: 1534: 1493: 1458: 1342:, and 1304:, and 1292:, and 1278:Poodle 1097:et al. 1033:Normal 1030:Normal 850:Type 3 708:Type 2 668:Type 1 564:Normal 561:Normal 558:Normal 530:Normal 527:Normal 513:Normal 505:Normal 491:Normal 488:Normal 320:uterus 318:, and 205:, and 110: 4167:14007 4134:286.4 4119:D68.0 3991:head 3626:Clots 3371:S2CID 3258:. 40. 3252:(PDF) 3048:(PDF) 3037:S2CID 3009:(PDF) 2952:S2CID 2793:(EMA) 2503:Blood 2335:S2CID 2238:S2CID 2100:(1). 2008:Blood 1967:Blood 1833:S2CID 1805:(PDF) 1556:Blood 1219:Åland 1215:Föglö 1170:is a 870:from 632:Types 332:colon 322:. 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