Leukopenia and agranulocytosis Causes

Bone marrow damage, neutrophil generation reduction. Normal adult bone marrow to generate daily at many of neutrophils about 1011 or more colony-stimulating factor IL-3, GM-CSF can induce G0 period of hematopoietic stem cells into the cell cycle, proliferation in the bone marrow pool of G-CSF specifically induced by granulocyte progenitor cell proliferation and differentiation further. late promyelocyte cells stopped proliferation, differentiation and maturation continues for the rod-shaped nucleus and a neutral sub-leaf cells. these cells into the peripheral blood before can stay in the bone marrow storage pool of about five days. because of some pathogenic factors cause direct injury of bone marrow CFU-GM number of abnormalities or hematopoietic dysfunction often neutropenia are the most common causes:

1. Drug-induced injury: anti-cancer drugs and immunosuppressive agents can be directly anti-proliferative cells. Substances inhibit or interfere with nucleic acid synthesis of granulocyte affect cell metabolism, impeding cell division. Drug directly caused by the toxic effects of neutropenia and Drug dose-related. many other types of drugs can also have direct cytotoxicity or through immune mechanisms that enable cells to reduce the tablets.

2. Chemical toxicology and radiation: the chemical benzene and its derivatives, two p-Nitrophenol, arsenic, bismuth, such as hematopoietic toxic role of stem cells. X-ray, γ-ray and neutron can directly damage blood stem cell and bone marrow micro-environment, resulting in acute or chronic radiation damage, there neutropenia.

3. immunological factors: autoimmune neutropenia are autoantibodies, T lymphocytes or natural killer cell function in granulocyte differentiation at different stages of injury-induced bone marrow cells impede tablets. common in rheumatology and autoimmune diseases. certain drugs for the hapten into the sensitive membrane proteins in vivo and in combination tablets or with the plasma protein binding antigen Chengquan Absorption in granulocyte cell surface. These are all antigen to stimulate the body to produce anti-granulocyte antibody IgG or IgM. When duplicate medication caused by granulocyte agglutination and destruction. This is called autoimmune drug-induced granulocyte cell deficiency. have some patients for certain drugs (sulfonamides, antipyretic analgesics, antibiotics, etc.) an allergic reaction, in addition to cause neutropenia, but also there is often accompanied by rash, urticaria, asthma, allergic manifestations such as edema. caused by autoimmune neutropenia has nothing to do with dosage.

4. systemic infection: bacterial infections such as mycobacteria (especially Mycobacterium tuberculosis) and viral infections such as hepatitis viruses.

5. abnormal cell infiltration of bone marrow: bone marrow cancer metastasis, hematopoietic malignant disease and bone marrow fibrosis causing bone marrow hematopoiesis failure.

6. sophisticated obstacle cells - hematopoietic invalid: such as lack of folic acid and vitamin B12, affecting DNA synthesis. bone marrow hematopoietic activity, but stagnation and sophisticated cell damage in bone marrow . certain congenital agranulocytosis and acute non-lymphocytic leukemia, myelodysplastic syndrome, paroxysmal nocturnal hemoglobinuria sophisticated barriers also exist, due to neutropenia.

Peripheral circulation in the distribution of granulocyte abnormalities. Entered the blood within the neutrophils only 1 / 2 at cycle pool, that is, with the blood circulation, the other 1 / 2 neutrophils immediately after the capillaries and small veins capillaries endothelial cells (marginal pool), not with the blood circulation, it should not in white blood cell count was detected.circle the edge of ponds and pools can be between the myeloid conversion. injection of adrenaline or stress conditions, may be marginal granulocyte Chi Chi rapidly into circulation, so that significantly higher neutrophil counts. myeloid pools such as the edge of a relatively substantial increase in volume can cause pseudo-neutropenia when neutrophil production and use were normal. systemic infection and allergic reactions can be caused by reactive pseudo-acquired agranulocytosis.

Vascular tissue neutrophil increased demand for consumption accelerated at intravascular neutrophil general only a few hours (half of them stay for 6h) that is moved YOU to extravascular into organizations, to carry out its defense and removal of "waste" of the function, about 1 ~ 2 days of death. in bacteria, fungi, viruses or rickettsiae infections, allergic reactions and other circumstances, by the myeloid growth factor GM-CSF and Regulation of G-CSF, granulocyte-generation rate of increase in the release from bone marrow to peripheral blood and enter the organization increased neutrophil and phagocytosis and bactericidal activity. However, serious infections when the body fluids of normal stimulation, lack of adequate response, simultaneously on a number of neutrophil leukocyte adhesion molecules (CD11/CD18, etc.) and vascular endothelial cells on the adhesion molecule (ICAM-1) were activated by inflammatory mediators, so that leukocyte adhesion in the vessel wall easily and transfer across the endothelial cells to Organize. finally we can see the blood still has short-term neutropenia. autoimmune neutropenia and hypersplenism in patients with myeloid consumption may exceed the capacity of bone marrow formation, can occur neutropenia.