Agranulocytosis

 

Alternative Names

Granulocytopenia; Granulopenia

Definition

Agranulocytosis is a condition in which the bone marrow does not make enough of a certain type of mature white blood cells (neutrophils). Bone marrow is the soft tissue inside bones that helps form blood cells.

Causes

Agranulocytosis may be caused by:

  • Autoimmune disorders
  • Bone marrow diseases, such as myelodysplasia or large granular lymphocyte (LGL) leukemia
  • Certain medicines used to treat diseases
  • Certain street drugs
  • Chemotherapy
  • Poor nutrition
  • Preparation for bone marrow transplant
  • Problem with genes

Agranulocytosis results in a person not having enough of a specific type of white blood cells, called neutrophils or granulocytes. A low neutrophil count (neutropenia) may also occur when white blood cells are destroyed faster than they can be produced.

Symptoms

Persons with this condition are more likely to have fevers and infections.

Exams and Tests

A blood differential test will be done to measure the percentage of each type of white blood cell in your blood.

Treatment

Treatment depends on the cause of agranulocytosis. For example, if a medicine is the cause, stopping or changing to another drug may help. In other cases, medicines to help the body make more white blood cells will be used.

Outlook (Prognosis)

Treating or removing the cause usually results in a good outcome.

Prevention

If you are having treatment or taking medicine that could cause agranulocytosis, your health care provider will use blood tests to monitor you.

References

Maciejewski JP, Tiu RV. Acquired disorders of red cell, white cell, and platelet production. In: Hoffman R, Benz EJ Jr, Silberstein LE, et al., eds. Hematology: Basic Principles and Practice. 6th ed. Philadelphia, PA: Elsevier Saunders; 2012:chap 30.


Review Date: 5/29/2014
Reviewed By: Yi-Bin Chen, MD, Leukemia/Bone Marrow Transplant Program, Massachusetts General Hospital, Boston, MA. Also reviewed by David Zieve, MD, MHA, Isla Ogilvie, PhD, and the A.D.A.M. Editorial team.

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