Polycythemia clinic: common causes of hematology: relative increase, infectious secondary polycythemia: no cause, diagnosis, treatment, cause 1. Relative increase refers to the decrease of plasma volume and the relative increase of red blood cell volume. It can be seen in severe vomiting, diarrhea, profuse sweating, extensive burns, chronic adrenocortical hypofunction, diabetes insipidus, hyperthyroidism and diabetic ketoacidosis. 2. Secondary polycythemia is caused by the increase of erythropoietin in blood, and the increase of EPO can be congenital or acquired. The common causes of (1) acquired EPO increase are: ① compensatory increase of erythropoietin: it is caused by decreased oxygen saturation. The degree of erythrocytosis is directly proportional to the degree of hypoxia. The compensatory increase of physiological erythropoietin in fetus, newborn and residents in plateau area. Pathological increase can be seen in severe chronic cardiopulmonary diseases such as obstructive emphysema, cor pulmonale, cyanotic congenital heart disease and abnormal hemoglobin diseases with low oxygen carrying capacity. ② Uncompensated increase of erythropoietin: The increase of erythropoietin is related to some tumors or kidney diseases, such as renal cancer, hepatocellular carcinoma, ovarian cancer, renal embryo cancer, adrenal cortical adenoma, hysteromyoma, hydronephrosis and polycystic kidney. (2) Congenital increase of EPO is mainly caused by congenital high affinity hemoglobin production and spontaneous production of congenital excess EPO. 3. Primary polycythemia (1) Congenital primary polycythemia is an increase in erythropoiesis caused by mutation of EPO receptor gene. (2) Acquired primary polycythemia (polycythemia vera) is a myeloproliferative tumor with polycythemia as the main factor, which is currently thought to be caused by the mutation of pluripotent hematopoietic stem cell JAK2-V6 17F. The red blood cell count of adult male was >: 6.0× 10 12 /L, hemoglobin >; 170g/L, adult female red blood cell count >: 5.5× 10 12 /L, hemoglobin >; 160g/L is considered as polycythemia, but it is the key to further clarify the etiology and classification of polycythemia. The treatment is aimed at secondary acquired polycythemia, and the treatment mainly starts from the etiology. For polycythemia vera, the main goal of treatment is to avoid and reduce thrombotic events, followed by avoiding and delaying the progression of the disease to myelofibrosis and acute leukemia. So the usual treatment measures are as follows: 1. Long-term oral low-dose aspirin can significantly reduce thrombotic events. 2. Venous bloodletting can not only reduce the hemoglobin level rapidly, but also slow down the progress of long-term patients to myelofibrosis and acute leukemia. Ordinary bloodletting or red blood cell apheresis can be used. Venous bloodletting is not the fundamental solution to polycythemia vera, and it needs long-term persistence or combination with other treatment methods. 3. Cell inhibition therapy Long-term oral administration of hydroxyurea is the most commonly used method, and interferon can also be used alone or in combination. Maryland and isotope 32P are also used to reduce the number of red blood cells, but after long-term use, the risk of patients turning to myelofibrosis and acute leukemia increases, so they are not recommended in recent years. In recent years, it has been found that after cell inhibition therapy, if the hematocrit is lower than 45%, the thrombotic events of patients will be significantly reduced. 4.JAK2 inhibitor Because the onset of polycythemia vera is closely related to the activation of JAK2 pathway, the targeted therapeutic drugs designed and studied for this pathway have achieved great success in recent years, among which Ruxolitinib, which was first marketed, has shown good efficacy in clinical research, which not only significantly reduced the hemoglobin level, but also significantly improved the quality of life of patients and reduced the risk of thrombotic events, thus enabling patients to live longer.