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Patients are prone to developing thrombosis. Thrombosis can occur in most vessels, leading to strokes, transient ischemic attacks, or Budd-Chiari syndrome. In the past, experts believed that increased blood viscosity was a risk factor for thrombosis. Recent studies indicate that the risk of thrombosis may primarily depend on the severity of leukocytosis. However, this hypothesis remains to be tested in prospective studies specifically designed for this purpose.

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Platelet function may be impaired, increasing the risk of bleeding. Increased cell turnover can cause uric acid levels to buy differin cream, thereby increasing the risk of gout and kidney stones. Genetic factors. Clonal hematopoiesis is a hallmark of PV. This indicates that the cause of proliferation is a mutation in hematopoietic stem cells. The JAK2 V617F mutation (or one of several other rarer JAK2 gene mutations) is found in almost all patients with PV. However, it can be said with almost complete certainty that there are other mutations that underlie the disease. They maintain JAK2 protein in a state of constant activity, which leads to excessive cell proliferation regardless of erythropoietin concentration.

Polycythemia vera is often asymptomatic. Sometimes an increase in the number of circulating red blood cells and an increase in viscosity are accompanied by weakness, lightheadedness, blurred vision, fatigue and shortness of breath. A common symptom is itching, especially after a shower. There may be facial flushing and dilated retinal veins, as well as redness and tenderness of the palms and soles, sometimes accompanied by digital ischemia (erythromelalgia). Hepatomegaly is often observed; splenomegaly (sometimes pronounced) occurs in 75% of patients.

Signs and symptoms of polycythemia vera. It is detected either by chance by high hemoglobin or by symptoms of increased viscosity, such as fatigue, loss of concentration, headaches, dizziness, dark vision, itchy skin, nosebleeds. Sometimes it manifests itself as diseases of the peripheral arteries or damage to the blood vessels of the brain. Patients are often plethoric, and most have a palpable enlarged spleen. Thrombosis and often peptic ulcers, sometimes complicated by bleeding, may occur.

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Thrombosis can cause symptoms in the affected area (for example, neurological pathology due to stroke or tranacute ischemic attacks, pain in the legs, swelling of the legs or both with thrombosis of the vessels of the lower extremities, unilateral loss of vision with thrombosis of the retinal vessels). Bleeding occurs in 10% of differin. Accelerated metabolism can cause low-grade fever and lead to weight loss, which indicates the transition of the disease to the wasting phase. The latter is clinically indistinguishable from primary myelofibrosis.

Suspicion of PV often arises already at the stage of a complete blood count, but it should also arise in the presence of corresponding symptoms, in particular Budd-Chiari syndrome (it is worth noting, however, that in some patients Budd-Chiari syndrome develops before the hematocrit rises). Neutrophilic leukocytosis and thrombocytosis are common but not obligatory manifestations. Patients with an isolated increase in hemoglobin or erythrocytosis may also have PV, but in such cases secondary erythrocytosis should be ruled out first. PV may also be suspected in some patients with normal hemoglobin levels but microcytosis and signs of iron deficiency. This combination of features may occur when hematopoiesis occurs in the presence of limited iron stores, which is a hallmark of some cases of PV.

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WHO has developed new diagnostic criteria. Therefore, patients suspected of adapalene cream should usually be tested for JAK2 gene mutations. Testing a bone marrow sample is not always necessary. In cases where it is carried out, panmyelosis, large size and crowding of megakaryocytes usually attract attention in the bone marrow. In some cases, reticulin fibers are found. However, no changes in the bone marrow make it possible to distinguish PV with absolute certainty from other pathological conditions (for example, congenital familial polycythemia) accompanied by erythrocytosis.

Plasma erythropoietin concentrations in patients with PV are usually low or at the lower limit of normal. An increased concentration indicates the secondary nature of erythrocytosis. In some cases, endogenous colony formation of erythroid cells is tested in vitro (red blood cell precursors taken from the peripheral blood or bone marrow of patients with PV, unlike those from healthy people, can form erythroid cells in culture without the addition of erythropoietin).

Nonspecific abnormalities in laboratory parameters that may be observed in PV include an increase in the concentration of vitamin B 12 and an increase in B 12 binding capacity, as well as hyperuricemia and hyperuricosuria (present in > 30% of patients), increased expression of the PRV-1 gene in leukocytes, decreased expression of the C-mpl gene (thrombopoietin receptor) in megakaryocytes and platelets. These tests are not necessary to buy adapalene online. Prognosis of polycythemia vera.