Neutropenia

The neutropenia (syn. Neutropenia, granulocytopenia ) describes the reduction of neutrophils in the blood . It is the most common type of leukopenia , a decrease in the number of white blood cells ( leukocytes ).

The number of neutrophil granulocytes in the blood of a healthy person is variable and lies between 1,800 and approx. 8,000 cells per microliter. A decrease in neutrophil granulocytes to 1,000 per microliter is said to be a mild form of neutropenia, 500 to 1,000 neutrophils per microliter of a moderate form and a neutrophil count of less than 500 per microliter of a severe form of neutropenia.

A febrile neutropenia is an additional fever above 38 ° C that lasts longer than an hour or a single fever above 38.5 ° C.

Neutrophil granulocytes are important for the defense against infections and are part of the body's non-specific defense system. Therefore, infections are easy to develop in patients with neutropenia . The most severe form of neutropenia is agranulocytosis .

Pathogenesis and Associated Diseases

Decreased production of granulocytes

Bone marrow damage is the most important cause of educational disorders. Possible triggers are drugs ( side effects of diuretics , sulfonamides , griseofulvin , chloramphenicol and other antibiotics , as well as chemotherapy drugs ) as well as toxic chemicals and plants.

Also infectious ( parvoviruses , panleukopenia , the feline leukemia virus , Ehrlichia ) or neoplastic (z. B. in leukemia , myelofibrosis ) or immune-mediated bone marrow damage may be the cause. After stem cell transplantation , neutropenia occurs in the early post- transplant phase (before the middle post- transplant phase ).

The decrease in the number of neutrophils causes a temporary suppression of the immune system. The extent and duration of neutropenia and thus the risk of infection also depend on the type of damage.

Increased consumption of granulocytes

Neutrophils are extensively consumed in acute inflammation. If the demand exceeds the production capacity in the bone marrow, there is a decrease in the number of cells in the blood. At the same time, a shift to the left can occur because only immature neutrophils and metamyelocytes (precursor cells of neutrophils) are released.

Therefore, neutropenia occurs especially in the acute phase of very severe general diseases such as sepsis , peritonitis (peritonitis), metritis or gangrenous mastitis .

Dysgranulopoiesis

Disturbed neutrophil formation ( dysgranulopoiesis ) can also cause neutropenia. It can be caused by an arrested development cycle or by reduced bone marrow release despite sufficient formation. Possible causes of the disease are myelodysplasia , acute myeloid leukemia and viral infections ( AIDS , immunodeficiency syndrome in cats , feline leukemia ).

Congenital neutropenia

Congenital neutropenia occurs in Kostmann syndrome and glycogenosis type 1b .

Increased margination

A shift of neutrophils from the circulating part into the so-called marginal neutrophil pool ( neutrophils bound to the endothelial cells of small blood vessels ) can cause acute but temporary neutropenia. Possible triggers are anaphylaxis or endotoxins . Usually this neutropenia has already subsided before the doctor or veterinarian is consulted.

therapy

The therapy depends on the underlying disease. Granulocyte-colony-stimulating factors G-CSF are used symptomatically . G-CSF are growth factors for granulocytes. Under certain circumstances, is reverse isolation necessary.

A febrile neutropenia (see above) is generally treated immediately with antibiotics, whereby the type of antibiotic therapy depends on the patient's classification in one of three risk levels.

General measures

The development of neutropenia requires a number of preventive and therapeutic measures. General hygienic precautions should be taken. Patients with long-term neutropenia should only be treated with mouth and nose protection and disinfected hands. If necessary, is isolated accommodation in a single room required.

Use of growth factors

G-CSF is a specific growth factor that stimulates the maturation of neutrophil granulocytes. As a medicinal substance, G-CSF is produced recombinantly either from E. coli ( filgrastim ) or from mammalian cells ( CHO cells , lenograstim ). The amino acid sequence of filgrastim and lenograstim is identical. In addition, G-CSF also exists in PEGylated form ( pegfilgrastim ).

G-CSF is used in supportive cancer therapy to prevent neutropenic infections or to support antibiotic therapy in the event of a severe infection. The four leading medical societies DGHO , NCCN , ASCO and EORTC recommend preventive, primary prophylactic G-CSF treatment if the risk of febrile neutropenia is 20 percent. G-CSF is also given so that chemotherapy can be administered on time and in accordance with the protocol. An algorithm outlined in the guidelines suggests GCSF administration in certain cases (comorbidities, poor general condition, female gender) even if the risk is between 10 and 20 percent. As a secondary prophylactic measure, the use of G-CSF is recommended in the following cycles after the occurrence of fever in the neutropenic phase of the previous chemotherapy cycle, if the maintenance of the dose intensity and the timely administration of the chemotherapy are decisive for the success of the treatment.

The more intense the chemotherapy administered, the longer the neutropenia phase lasts. The use of growth factors such as G-CSF shortens the time of neutropenia by several days. Compliance with the intervals between chemotherapy cycles can also be positively influenced by the preventive administration of G-CSF.

Web links

• Handbook "Severe Chronic Neutropenia" (PDF file; 1015 kB)

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1. ↑ Hoff Brand AV (2003) Basic course Hämatologie.Blackwell publishing.
2. ^ H. Link et al .: Infections in Neutropenia - Diagnosis and Therapy. Recommendations for practice. Working Group on Infections in Hematology and Oncology (AGIHO) of the DGHO, 2006.
3. ^ Marianne Abele-Horn: Antimicrobial Therapy. Decision support for the treatment and prophylaxis of infectious diseases. With the collaboration of Werner Heinz, Hartwig Klinker, Johann Schurz and August Stich, 2nd, revised and expanded edition. Peter Wiehl, Marburg 2009, ISBN 978-3-927219-14-4 , p. 46.
4. ↑ R. Kostmann: Infantile genetic agranulocytosis; agranulocytosis infantilis hereditaria. In: Acta Pediatr Suppl. 1956 Feb; 45 (Suppl 105), pp. 1-78. PMID 13326376 .
5. ↑ Glycogenosis type 1b at orpha.net.
6. ^ Marianne Abele-Horn: Antimicrobial Therapy. Decision support for the treatment and prophylaxis of infectious diseases. With the collaboration of Werner Heinz, Hartwig Klinker, Johann Schurz and August Stich, 2nd, revised and expanded edition. Peter Wiehl, Marburg 2009, ISBN 978-3-927219-14-4 , s. 41–44 ( fever in leukopenia ).
7. ↑ DGHO: Treatment with haematopoietic growth factors (008) .
8. ^ Bavarian Cancer Society eV: Neutropenia. Undesirable side effect of chemotherapy. A guide for cancer patients in chemotherapy .

This article is about a health issue. It is not used for self-diagnosis and does not replace a diagnosis by a doctor. Please note the information on health issues !