According to etiology, erythrocytosis is divided into acquired and hereditary. In accordance with pathogenesis it is divided into true (absolute, which is caused by erythropoiesis activation in the bone marrow and an increase of circulating erythrocyte mass) and false — relative and hemoconcentration (results from plasma volume decrease and thus is not accompanied by an increase of circulating erythrocytes mass). Absolute erythrocytosis in its turn is subdivided into primary (as an independent disease) and secondary (symptomatic), the latter — into physiological ('compensatory) and pathological. Primary absolute erythrocytosis is caused by tumorous transformation of
erythrocytic stem cells with intensification of their proliferation independently from erythropoietin. It is true polycythemia (erythremia, or Vaquez disease), which is a variety of chronic leukemia. Hereditary absolute erythrocytosis may result from a genetically determined deficit of 2,3-diphosphoglycerate (regulator of hemoglobin oxygenation and deoxygenation) in erythrocytes. The affinity of hemoglobin to oxygen increases and its return to tissues decreases. Tissue hypoxia develops, erythropoietin production increases, erythropoiesis activates.