Leukemoid reaction
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
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Overview
- The term leukemoid reaction, also referred to as transient myeloproliferative disorder, describes an elevated white blood cell count, or leukocytosis, that is a physiologic response to stress or infection (as opposed to a primary blood malignancy, such as leukemia).
Historical Perspective
- [Disease name] was first discovered by [name of scientist], a [nationality + occupation], in [year]/during/following [event].
- The association between [important risk factor/cause] and [disease name] was made in/during [year/event].
- In [year], [scientist] was the first to discover the association between [risk factor] and the development of [disease name].
- In [year], [gene] mutations were first implicated in the pathogenesis of [disease name]
Classification
Leukemoid reaction can be classified according to the course of the disease and the type of hematopoietic lineage of the bone marrow.
- According to the course of the disease:
- Phase of expressed manifestations
- Phase of recession
- Phase of normalization with trace reactions.
- According to the type of hematopoietic lineage of the bone marrow :
1. Reactions of myeloid type
1.1. Neutrophilicleukemoid reactions
1.2. Eosinophilic leukemoid reactions
2. Reactions of lymphoid type
2.1. Lymphomonocytic leukemoid reactions
2.2. Lymphocytic leukemoid reactions
2.3. Plasmocyticleukemoid reactions
2.4. Leukemoid reaction with blast cells
3. Secondary (reactive) thrombocytosis
4. Secondary erythrocytosis
5. Mixed forms of leukemoid reactions
6. Rare forms of leukemoid reaction
6.1. Cytopenia
6.2. Leukemoid reactions of basophilic type.
Pathophysiology
Causes
As noted above, a leukemoid reaction is typically a response to an underlying medical issue. Causes of leukemoid reactions include:
- Hemorrhage
- Drugs
- Use of glucocorticoids
- Use of G-CSF or related growth factors
- All-trans retinoic acid (ATRA)
- Infections (e.g. tuberculosis, pertussis)
- As a feature of Trisomy 21 in infancy (incidence of ~10%)
- As a paraneoplastic phenomenon (rare)
Differentiating Leukemoid reaction from Other Diseases
Epidemiology and Demographics
Risk Factors
Screening
Natural History, Complications, and Prognosis
Natural History
Complications
Prognosis
Diagnosis
Diagnostic Criteria
History and Symptoms
Physical Examination
Laboratory Findings
Conventionally, a leukocytosis exceeding 50,000 WBC/mm3 with a significant increase in early neutrophil precursors is referred to as a leukemoid reaction.[1] The peripheral blood smear may show myelocytes, metamyelocytes, promyelocytes, and even myeloblasts; however, there is a mix of early mature neutrophil precursors, in contrast to the immature forms typically seen in acute leukemia. The bone marrow in a leukemoid reaction, if examined, may be hypercellular but is otherwise typically unremarkable.
Leukemoid reactions are generally benign and are not dangerous in and of themselves, although they are often a response to a significant disease state (see Causes below). However, leukemoid reactions can resemble more serious conditions such as chronic myelogenous leukemia (CML), which can present with identical findings on peripheral blood smear.
Historically, various clues including the leukocyte alkaline phosphatase score and the presence of basophilia were used to distinguish CML from a leukemoid reaction. However, at present the test of choice in adults to distinguish CML is an assay for the presence of the Philadelphia chromosome, either via cytogenetics and FISH, or via PCR for the Bcr/abl fusion protein. The LAP (Leukocyte Alkaline Phosphatase) score is high in reactive states but is low in CML. In cases where the diagnosis is uncertain, a qualified hematologist or oncologist should be consulted.
Electrocardiogram
X-Ray
Echocardiograph and Ultrasound
CT
MRI
Imaging Findings
Other Diagnostic Studies
Treatment
Medical Therapy
Surgery
Primary Prevention
Secondary Prevention
See also
References
- ↑ Ronald Hoffman; et al. (2005). Hematology: basic principles and practice. St. Louis, Mo: Elsevier Churchill Livingstone. ISBN 0-443-06628-0. p. 803.