Von Willebrand-Diana - a hereditary blood disease, characterized by the occurrence of episodic spontaneous bleeding, which are similar to bleeding in hemophilia. The cause of bleeding is a violation of blood clotting due to insufficient activity of von Willebrand factor, which is involved in the adhesion of platelets on collagen and protects factor VIII from proteolysis. With a deficiency of von Willebrand Factor VIII, the factor undergoes proteolysis, and its content in plasma decreases. In addition, in Willebrand disease, the serotonin content decreases and pathological dilatation of the vessels and an increase in their permeability develop. In von Willebrand disease, the longest bleedings are observed, since all three hemostasis links are disturbed in patients.
|ICD-10||D 68.0 68.0|
|ICD-10-KM||D69.8 and D68.0|
|eMedicine||ped / 2419|
The disease is inherited according to the principle of autosomal dominance. Possible inheritance and autosomal recessive type (2 and 3 type of disease). The prevalence of von Willebrand disease is 1 in 800-1000.
- Atrombopenic purpura,
- Atrombocytopenic purpura,
- Hemorrhagic capillaropathy,
- Constitutional thrombopathy, constitutional thrombopathy of von Willebrand-Jurgens,
- Hereditary pseudohemophilia, Jurgens syndrome,
- Vascular hemophilia, pseudohemophilia.
There are three types of von Willebrand disease.
- 1st type due to partial quantitative deficiency of von Willebrand factor. At the same time its multimeric structure is preserved. There is a decrease in procoagulant activity of factor VIII, platelet aggregation induced by ristocetin, ristocetin factoring activity, von Willebrand factor antigen. The frequency of this form is from 75% to 80% of all cases of von Willebrand disease. Autosomal dominant inheritance.
- Type 2 due to qualitative changes of von Willebrand factor associated with the violation of the formation of multimers and is divided into subtypes: 2A, 2B, 2M, 2N.
- Phenotype subtype 2A is the result of a violation of two different mechanisms: a defect in the synthesis of high molecular weight multimers and an increase in proteolysis of von Willebrand factor. With subtype 2B an increased affinity of von Willebrand factor to the receptor on the platelet membrane glycoprotein Ib is noted.
- Subtype 2M characterized by a violation of the connection of von Willebrand factor with the glycoprotein Ib receptor on the platelet membrane.
- Subtype 2N It is characterized by a normal level of von Willebrand factor and low procoagulant activity, which is due to the disruption of the relationship between factor VIII and von Willebrand factor.
The inheritance of Willebrand disease type 2 is autosomal dominant, with the exception of the 2N subtype, where it is recessive. The frequency of occurrence of these forms is from 5% to 15% of all cases of von Willebrand disease.
- 3rd type - The most severe form with a complete deficiency of von Willebrand factor. This form is characterized by the absence of von Willebrand factor in plasma, platelets and the vascular wall. Factor VIII is below 10%. Inheritance is autosomal recessive. The disease is manifested in homozygotes with the same defective alleles or double heterozygotes with two different defective alleles. In patients with type 3, there is a probability of occurrence of alloantibodies to von Willebrand factor. The frequency of occurrence of the disease of type 3 Willebrand disease is less than 5%.
In addition, there is platelet-type von Willebrand disease, which is caused by a mutation in the platelet glycoprotein Ib receptor gene, as a result of which the sensitivity of this receptor to high molecular weight multimers of von Willebrand factor increases. The phenotype is similar to subtype 2B.
- Acquired von Willebrand syndrome determined in patients with autoimmune, lymphoproliferative diseases, caused by the emergence of an inhibitor against von Willebrand factor, as well as qualitative anomalies of factor VIII due to the adsorption of high molecular weight multimers by pathological proteins.
The most characteristic and specific symptom in Willebrand disease is bleeding from the mucous membranes of the mouth, nose, internal organs. Symptoms of bleeding vary from moderately severe to extremely severe, occur mainly on the microcirculatory type. In patients with a severe deficiency of factor VIII, there are abundant and prolonged bleeding (nasal, gingival, uterine), as well as hemorrhages in the muscles and joints. In addition, there may be prolonged bleeding with injuries, extraction of teeth, operations.
In childhood, there are often bleeding from the mucous membranes of the mouth, nosebleeds, bruises on the skin. A more severe hemorrhagic diathesis is observed during or shortly after an infectious disease. The most likely trigger for bleeding in the face of infection is a violation of vascular permeability. As a result, spontaneous hemorrhages of the diapedetic type appear.
Hematomas - hemorrhages in the subcutaneous tissue and muscle tissue are observed mainly after injuries in patients with severe forms of the disease.
In Willebrand disease, hemorrhagic syndrome does not always manifest itself, periods of exacerbation alternate with periods of complete or almost complete absence of hemorrhages. In some patients, von Willebrand disease can be combined with signs of mesenchymal dysplasia: increased skin elasticity, weak ligaments with increased mobility of the joints, prolapse of the valvals of the heart.
Autosomal inheritance causes the same incidence of von Willebrand disease in patients of both sexes. In women, due to the characteristics of the physiological structure of the body associated with reproductive function, there is a more frequent manifestation of hemorrhagic symptoms. About 65% of women with von Willebrand disease suffer menorrhagias. Recurrent uterine bleeding, lasting more than 10 days, accompanied by post-hemorrhagic anemia.
Gastrointestinal bleeding in patients with von Willebrand disease, they are not the predominant form of bleeding. They can be caused by taking medications that affect platelet aggregation (acetylsalicylic acid and other nonsteroidal anti-inflammatory drugs). In addition, the sources of bleeding are latent ulcers of the stomach and duodenum, also erosive gastritis, hemorrhoids.
Patients with von Willebrand disease may have prolonged bleeding during operations, women - during childbirth. Childbirth in women with von Willebrand disease is associated with the risk of significant blood loss. In most patients with moderate and mild forms of the disease during pregnancy, the level of factor VIII increases by 2-3 times and reaches normal values, however, in the postpartum period, it returns to the initial level.
Hemarthrosis - the most rare manifestation of von Willebrand disease, characteristic of the disease of the 3rd type. Acute hemarthrosis is accompanied by pain due to increased intra-articular pressure. The joint is enlarged in volume, the skin over it is hyperemic and hot to the touch. If hemarthrosis occurs after injury, additional damage should be excluded (intraarticular fracture, tearing of the condyle, tissue incarceration). Recurrent hemarthrosis causes chronic synovitis. At the stage of synovitis, the synovial membrane hypertrophies and becomes the main source of hemorrhage into the joint. In acute synovitis, hemarthrosis can recur, despite transfusions of coagulation factor VIII, which is caused by the inflammatory process in the synovial membrane. In chronic synovitis, the pain syndrome may be absent because the joint capsule is destroyed.
In contrast to hemophilia in von Willebrand disease, the further progression of the pathological process and the development of deforming osteoarthrosis, as a rule, are not observed.
Hemorrhages in the brain and spinal cord and their membranes in Willebrand disease occur due to injury. In some cases, the cause of such hemorrhages may be a hypertensive crisis or taking medications that significantly disturb the hemostatic function of platelets (acetylsalicylic acid, butadion, etc.).
Given the autosomal dominant mode of inheritance, the genetic risk for offspring is 50% regardless of the sex of the fetus.
Treatment depends on the type of disease. There are two main ways. At first, plasma preparations with a high content of Willebrand factor or factor VIII preparations are used. In mild cases, a single administration may be sufficient, for severe injuries and operations, the drugs are administered twice a day for 2-3 days. The second approach to treatment is applicable for milder forms. Patients assigned desmopressin. There is a danger of addiction when using desmopressin for more than 2 days.
Causes and risk factors
The disease is inherited in an autosomal recessive or autosomal dominant manner. The probability of transmission of the disease from mother to child is 50%, but only in 1/3 of the cases there are clinically significant manifestations of the disease.
The main cause of the pathology is a violation of the gene encoding von Willebrand factor, which is located on the short arm of the 12th chromosome.
As a result of mutation, a number of changes occur:
- lack of large von Willebrand multimers,
- increased affinity (bond strength, affinity) factor for the platelet receptor GB-Ib in combination with the absence of large multimers,
- decrease in the affinity of von Willebrand factor to the platelet receptor GP-Ib without disturbing the multimeric structure,
- decrease in the affinity of von Willebrand factor to factor VIII, etc.
Based on the variants of functional defects, the corresponding types of disease are distinguished.
Forms of the disease
According to the recommendations of the Scientific and Standardization Committee (SSC) of the International Society for Thrombosis and Hemostasis, von Willebrand disease is classified as follows:
- Type I - reduced synthesis of von Willebrand factor and its associated antigen. In type I plasma, all multimers of the factor are present. Occurs in 55–75% of cases
- Type II - a sharp decrease in the formation and blood levels of the most active large multimers of von Willebrand factor, the predominance of small multimers with low hemostatic activity,
- Type III - the almost complete absence of von Willebrand factor, is extremely rare (1-3% of cases).
Willebrand disease is the most common hemorrhagic diathesis: it is found in about 1% of the population.
Depending on the phenotype, type II disease is divided into several subtypes:
- IIA - qualitative defects of the factor with a decrease in vWF-dependent platelet adhesion and an isolated deficiency of high molecular weight multimers,
- IIB - qualitative defects of von Willebrand factor with increased affinity for the platelet receptor GP-Ib,
- IIN - impaired ability of von Willebrand factor to bind to coagulation factor VIII,
- IIM - the presence of vWF-defects in the absence of a shortage of multimers.
The level of von Willebrand factor in blood is affected by a number of factors:
- age (level increases as you get older)
- ethnos (the level is higher among Africans and African Americans),
- blood group (the half-life of the factor in persons with blood group I is approximately 1/4 less than that of carriers of other groups),
- hormonal background (decreased with hypothyroidism, increased during pregnancy).
The symptomatology of the disease is extremely diverse: from minor episodic bleeding to massive, debilitating, leading to severe blood loss.
More often, increased bleeding is observed in children, decreasing as they mature, and thereafter there is an alternation of exacerbations and remissions.
Signs characteristic of von Willebrand disease:
- bleeding more than 15 minutes after minor injuries or spontaneously recurring bleeding after 7 days or more after injury,
- severe, prolonged or spontaneously recurring bleeding after minor surgical interventions, extraction of teeth,
- subcutaneous hematomas that appear after minor traumatic or spontaneous effects,
- hemorrhagic skin rash,
- spontaneous nasal bleeding lasting more than 10 minutes or requiring, due to the intensity of medical intervention,
- blood in the feces in the absence of gastrointestinal tract pathology, which can provoke the development of gastrointestinal bleeding,
- severe anemia
- intense, prolonged menstruation.
About 2/3 of the patients have mild Willebrand disease, most of them have no symptoms. Approximately 30% suffer from severe and moderate forms.
Features of the course of the disease during pregnancy
Pregnancy has an ambiguous effect on the course of von Willebrand's disease. Often, when pregnancy occurs under the influence of estrogen, the level of von Willebrand factor in the blood plasma increases, the same tendency can be observed before childbirth. However, these changes do not occur in all women.
According to the results of research, there is a high frequency of spontaneous abortion in the early stages - 22–25% in women suffering from this pathology. Approximately 1/3 of women report bleeding in the first trimester of pregnancy.
Most women with von Willebrand disease of type I reach the normal (for non-pregnant) level of factor in the last trimester of pregnancy. In type II disease, levels of factor VIII and von Willebrand factor often increase during pregnancy, but most studies show minimal or no change in the level of activity of coagulation factors and the preservation of the pathological structure of multimers. In women with type III von Willebrand disease, levels of factor VIII and von Willebrand factor practically do not increase during pregnancy.
Women with von Willebrand disease are at increased risk of primary (more than 500 ml on the first day after birth) and secondary postpartum hemorrhage (from 24 hours to 6 weeks) due to the rapid decrease in the activity of coagulation factors after birth.
The diagnosis is made on the basis of indicators of the hemostatic system:
- prolonged bleeding time (with type I in some patients, the rate is within the normal range),
- activated partial thromboplastin time (APTT) (normal or extended),
- significant change in ristocetin-induced platelet aggregation,
- changing the level of von Willebrand factor in the blood plasma and the balance of its multimers depending on the type of disease,
- change in the level of von Willebrand factor antigen in the blood,
- normal blood clotting time (with the exception of type III disease).
General and biochemical blood tests do not show characteristic changes, in rare cases there is a reduced iron content, up to anemia.
In addition to the study of hemostasis, shown instrumental methods of examination of patients (FGDS, abdominal ultrasound, MRI) to exclude hidden bleeding.
The goal of treatment is to increase the concentration or replace the missing coagulation factors. Treatment may be prophylactic or on demand - for acute bleeding.
Therapy of von Willebrand disease is carried out in three ways (depending on the severity of the condition):
- The use of drugs that increase the level of von Willebrand factor.
- Replacement therapy with blood products containing von Willebrand factor.
- Local therapy of injuries of the mucous membranes and skin.
The main groups of drugs used in the treatment of:
- hormonal drugs
- antifibrinolytic drugs
- local hemostatics,
- plasma concentrates.
Since the disease is genetic, it is not possible to prevent its development, but there are a number of measures that can significantly reduce the risk of bleeding:
- refusal to take non-steroidal anti-inflammatory drugs,
- elimination of antiaggregants (acetylsalicylic acid, clopidogrel),
- regular check-ups,
- prevention of traumatic effects.
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Education: higher, 2004 (GOU VPO “Kursk State Medical University”), specialty “General Medicine”, qualification “Doctor”. 2008-2012 - Post-graduate student of the Department of Clinical Pharmacology of the SBEI HPE "KSMU", Candidate of Medical Sciences (2013, specialty "Pharmacology, Clinical Pharmacology"). 2014-2015 - professional retraining, specialty "Management in education", FSBEI HPE "KSU".
The information is generalized and is provided for informational purposes only. At the first signs of illness, consult a doctor. Self-treatment is dangerous for health!
Classification of von Willebrand disease
Depending on the nature of the course of the disease, its following types are distinguished:
The first type of disease, which is the most common. In this case, there is a decrease in the level of von Willebrand factor, but in insignificant quantities. Therefore, the work of the blood coagulation system is disturbed, but not too much. A person with this type of illness feels satisfactory. Development of bleeding is possible, which is difficult to stop, but it manifests during surgery or during dental procedures, and not by itself. In such people, bruises appear even from slight pressure on the skin.
The second type of disease, in which the level of von Willebrand factor in the blood does not decrease, but the structure of the substance itself is disturbed. When exposed to the body of factors provocateurs may develop sudden bleeding, which can be very intense.
The third type of von Willebrand disease is the most severe pathology. In the patient's blood, the VIII clotting factor is completely absent, which leads to microcirculatory bleeding and accumulation of blood in the cavities of the joints.
Platelet-type von Willebrand disease is a pathology that should be considered separately. At the same time, a gene mutation occurs in the human body, which is responsible for the platelet von Willebrand factor receptor. It is released from active platelets and prevents them from sticking together and attached to the vascular wall.
Very rarely, people are diagnosed with an acquired form of the disease, which develops not from birth, but against the background of the appearance in the blood of autoantibodies to its own tissues. Becoming a triggering factor may be transferred infections and stress, injuries. This type of von Willebrand disease most often develops in people with autoimmune pathologies, cancers, and thyroid diseases.
Causes of von Willebrand disease
Willebrand disease is characterized by a clotting disorder, which is an essential part of the hemostatic system. At the same time, the blood clotting factor, which is called Willebrand factor, is not enough in the body, or it has a number of structural disorders. This leads to insolvency of the blood coagulation system, since platelets lose the ability to normal aggregation and adhesion.
Willebrand disease is a gene pathology. Although it can affect both men and women, representatives of the weaker half of humanity suffer from this disorder more often.
Sometimes von Willebrand disease is so mild that a person does not even suspect its presence. Bleeding (if it occurs) will be localized in the area of the uterus, skin or the gastrointestinal tract, that is, in those organs that have developed capillary network.
If a person has the first blood group, then the pathology can have a severe course. Ingoda, even the usual nosebleeds can end very badly
Symptoms of von Willebrand disease
If bleeding develops in a healthy person, then platelets are sent to the site of damage to the vessel, which, sticking together with one another, clog up the existing wound. In people with von Willebrand disease, this process occurs with impairment.
Bleeding is the main symptom of the disease. They can be provoked by surgery, tooth removal, trauma. During bleeding, a person’s condition worsens, the skin turns pale, the head begins to spin, and blood pressure may decrease. Symptomatology will worsen quickly if the bleeding is extensive and intense.
Children with von Willebrand disease suffer from hemorrhagic diathesis, which is especially acute after acute respiratory viral infections. The body, which is subjected to intoxication, responds to this by increasing the permeability of the vascular walls, which threatens the development of spontaneous bleeding.
It is impossible to completely cure von Willebrand disease. Pathology has an undulating course, with periods of calm and aggravation.
The symptoms of von Willebrand disease are the following:
While receiving nonsteroidal anti-inflammatory drugs, gastrointestinal bleeding is often observed. Also its development contributes to the treatment of antipagi. Hemorrhagic nodes and ulcerative lesions of the mucous membrane of the stomach and intestines bleed. The dark feces indicate the bleeding of the digestive organs, which assumes a tarry consistency. At the same time its color becomes almost black. Also, the patient may experience vomiting with blood.
Hemarthrosis is a hemorrhage in the joint cavity. The person experiences painful sensations in the relevant area, the functions of the joint are limited, and the skin around it swells. If the bleeding is not stopped, the swelling will increase, the soft tissues will get a bluish tinge, become strained and taut. The skin at the site of the lesion will be hot to the touch.
In addition to hemorrhagic syndrome, people with von Willebrand disease may experience signs of mesenchymal dysplasia. In this case, the bleeding will have a certain localization, they will start to happen in these places regularly.
Over time, the symptoms of the disease may change. Periodically, a person feels completely healthy, since there are no signs of pathology at all. Many people diagnosed with von Willebrand disease do not experience any discomfort from this pathology at all. At the same time, other patients are constantly suffering from regular bleeding, which is a mortal threat. The quality of life of such patients will suffer from birth. Bleeding can be so intense that to stop them requires treatment in the hospital.
Symptoms of mild Willebrand disease:
Nosebleeds that recur frequently.
Menstrual bleeding in women is characterized by abundant secretions.
Bruises appear on the skin, even with minor injuries.
Petechiae are often formed on the skin.
In the place of the injuries formed extensive hematomas.
If the disease has a severe course, then it will be accompanied by the following symptoms:
The presence of blood in the urine. In this case, the person will experience pain in the lumbar region, suffer from dysuric disorders.
After a minor injury, large bruises will appear on a person’s skin. Hemorrhages strongly swell, exert pressure on the nerve endings that respond with pain.
Frequent hemorrhages in the joint cavity.
Long and incessant bleeding from the gums.
Bleeding from the nose and nasopharynx, which can lead to bronchial obstruction.
Hemorrhage in the brain. This situation is fatal.
In severe cases of von Willebrand disease, its symptoms are similar to hemophilia.
Willebrand disease treatment
Hematologist is involved in the treatment of von Willebrand disease. It is necessary to pre-tune in to the fact that a complete recovery cannot be achieved, since gene abnormalities cause pathology. However, to improve the quality of life of patients is quite realistic.
Treatment is based on substitution transfusion therapy, it allows to normalize the work of all levels of hemostasis. Patients are prescribed hemopreparations which contain von Willebrand factor. This may be cryoprecipitate or antihemophilic plasma. Such treatment makes it possible to increase the production of factor VIII in the patient's body.
If a person develops minor bleeding, then you can try to stop it with a tourniquet and a hemostatic sponge. Treatment of the wound with thrombin also prevents blood loss.
To stop the bleeding, the patient may be prescribed such drugs as: antifibrinolytics, hormonal oral contraceptives, Desmopressin.
A fibrin gel may be applied to the wound surface that is bleeding.
Gypsum Longuet superimposed on the limb with the affected joint (with the development of hemarthrosis). Be sure to give the joint an exalted position. When the hemorrhage is stopped, the patient is prescribed UHF. Sore joints need to be limited in loads. If the patient's condition is severe, then he is prescribed a puncture with pumping blood.
Desmopressin is a drug that is prescribed for the treatment of Willebrand disease type 1 and 2. Taking this drug stimulates the body to produce factor VIII. The drug can be used in the form of a nasal spray, and in the form of injections. If the therapy does not bring the desired success, then the patient is prescribed a plasma factor transfusion of the missing factor.
Tranexamic acid and aminocaproic acid are anti-fibrinolytic drugs. They are administered intravenously or taken orally. These drugs are prescribed for repeated uterine bleeding, nasal and gastrointestinal bleeding.
If the disease has an uncomplicated course, then use of the drug Tranexam is possible. In severe cases, Tranexam is combined with etamzilat or Ditsinon.
It is impossible to prevent the development of von Willebrand disease, since it is inherited. However, you can try to minimize the risk of bleeding at different locations.
To do this, observe the following preventive measures:
Inform couples who are at risk for this disease.
Children with an established diagnosis are subject to follow-up.
Patients should be monitored regularly by the attending doctor.
Care should be taken to avoid injury.
You can not take aspirin and other drugs that help reduce the functionality of platelets.
Surgery for such patients is carried out only if there are vital indications.
Be sure to lead a healthy lifestyle and eat right.
These recommendations will make it possible to avoid intra-articular and intramuscular bleeding, as well as related complications. The faster the diagnosis is made and the treatment is started, the better the prognosis. It is unfavorable only in the case when the disease is severe.
Video: Willebrand disease lecture for the doctor:
Video: von Willebrand disease in the program "To live healthy":
Education: In 2013, the Kursk State Medical University was completed and the diploma in “General Medicine” was obtained. After 2 years, the residency in the specialty "Oncology" was completed. In 2016, completed postgraduate studies at the National Medical-Surgical Center named after NI Pirogov.
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Willebrand disease (angiohemophilia) is a type of hereditary hemorrhagic diathesis due to a deficiency or decreased activity of the plasma component of the VIIIth blood coagulation factor, von Willebrand factor (VWF). Willebrand disease is a common pathology of blood clotting, occurring with a frequency of 1-2 cases per 10,000 people, and among hereditary hemorrhagic diathesis is on the 3rd place after thrombocytopathy and hemophilia A. Willebrand disease is equally diagnosed in people of both sexes, but due to more severe course more often detected in women. The disease can be combined with connective tissue dysplasia, weak ligaments and hypermobility of the joints, increased skin elasticity, prolapse of heart valves (Ehlers-Danlos syndrome).
Causes of von Willebrand disease
The basis of von Willebrand disease is quantitative (type I and III) and qualitative (type II) violation of von Willebrand factor synthesis - a complex blood plasma glycoprotein, which is a complex of oligomers (from dimers to multimers). The von Willebrand factor is secreted by vascular endothelial cells and megakaryocytes as proprotein, enters the blood and subendothelial matrix, where it is deposited in platelet a-granules and Wable-Pallas calves.
The von Willebrand factor is involved in vascular platelet (primary) and in coagulation (secondary) hemostasis.VWF is a subunit of antihemophilic globulin (VIII coagulation factor), ensuring its stability and protection against premature inactivation. Due to the presence of specific receptors, von Willebrand factor mediates strong adhesion of platelets (platelets) to subendothelial structures and aggregation between themselves in places of damage to blood vessels.
The plasma level of VWF in normal amounts to 10 mg / l, temporarily increases during physical activity, pregnancy, stress, inflammatory and infectious processes, estrogen, is constitutionally reduced in persons with blood type I. The activity of von Willebrand factor depends on its molecular weight, the greatest thrombogenic potential is observed in the largest multimers.
Willebrand disease is a genetically determined pathology caused by mutations of the gene for the VWF factor, which is located on chromosome 12. The inheritance of Willebrand disease type I and II is autosomal dominant with incomplete penetrance (patients are heterozygotes), type III is autosomal recessive (patients are homozygotes). In type III Willebrand disease, there are deletions of large portions of the VWF gene, mutations, or a combination of these defects. Moreover, both parents usually have a mild course of type I disease.
Acquired forms of von Willebrand disease can occur as a complication after multiple blood transfusions, against the background of systemic (SLE, rheumatoid arthritis), cardiac (aortic stenosis), cancer (nephroblastoma, Wilms tumor, macroglobulinemia) diseases. These forms of von Willebrand disease are associated with the formation of autoantibodies to VWF, the selective absorption of oligomers by tumor cells or defects in platelet membranes.
Prognosis and prevention of von Willebrand disease
In the case of adequate hemostatic treatment, Willebrand disease usually proceeds relatively favorably. Severe Willebrand disease can lead to severe post-hemorrhagic anemia, fatal bleeding after childbirth, serious injuries and surgeries, sometimes subarachnoid hemorrhage and hemorrhagic stroke. In order to prevent Willebrand disease, it is necessary to exclude marriages between patients (including relatives), in the presence of a diagnosis, exclude the use of NSAIDs, antiplatelet drugs, avoid injuries, accurately follow the doctor's recommendations.