Summary
Neutrophilia may occur with or without an elevated white blood cell (WBC) count. Neutrophilia without leukocytosis is defined as an elevated circulating neutrophil count (>7.7×10⁹/L) in adults with a normal total WBC count of <11×10⁹/L.[1] An elevated total WBC count (>11×10⁹/L) and an absolute neutrophil count >7.7×10⁹/L is defined as a neutrophilic leukocytosis.[1]
The absolute neutrophil count can be estimated by multiplying the total WBC count by the percentage of polymorphonuclear cells and band forms (immature neutrophils have a band-shaped nucleus).[2]
The terms granulocytosis and neutrophilia are often used interchangeably, although granulocytosis also includes elevations in eosinophils and basophils.
The terms hyperleukocytosis and leukaemoid reaction are reserved for total leukocyte counts of >50×10⁹/L. Leukaemoid reaction may mimic leukaemia, but has a non-malignant aetiology.
Neutrophilia results from:
Increased production of neutrophils
Demargination (process of neutrophils entering the peripheral circulation from areas of intravascular marginated polymorphonuclear cell pools), or
Decreased egress (outwards migration) of neutrophils from peripheral circulation to the tissues.
[Figure caption and citation for the preceding image starts]: NeutrophiliaFrom the collection of T. George, MD [Citation ends].
Epidemiology
Many diverse factors contribute to the development of neutrophilia, so defining the population at risk is difficult. Leukocyte and neutrophil counts in health exhibit some racial differences. Hispanic people in the US have been shown to have a higher leukocyte count (mean difference 0.16×10⁹/L) and higher neutrophil count (mean difference 0.11×10⁹/L) relative to white people.[3]
The neutrophil count changes with age, with the highest counts seen in the first few days after birth, then decreasing rapidly. Neutrophil counts approach adult levels around age 10. Lifestyle factors, including exercise levels, stress, and smoking status, influence the risk of neutrophilia.
Differentials
Common
- Infection
- Inflammatory conditions
- Chronic myeloid leukaemia (CML)
- Essential thrombocythaemia
- Polycythaemia vera
- Primary myelofibrosis
- Pregnancy
Uncommon
- Platelet clumping
- Cryoglobulinaemia
- Anaemia
- Solid tumour malignancy
- Bone marrow infiltration
- Heat stroke
- Chronic bone marrow stimulation
- Asplenia
- Sweet's syndrome
- Drug-induced haematopoiesis
- Chronic neutrophilic leukaemia
- Myelodysplastic syndrome
- Acute myeloid leukaemia
- Hereditary neutrophilia
- Pelger-Huet abnormality
- Amegakaryocytic thrombocytopenia
- Trisomy 21 (Down's syndrome)
- Leukocyte adhesion deficiency type I
- Familial cold autoinflammatory syndrome
- Chronic idiopathic neutrophilia
- Stress-induced demargination
- Drug-induced demargination
- Drug-induced decreased egress
Contributors
Authors
Devon Chabot-Richards, MD
Assistant Professor of Pathology
University of New Mexico Health Sciences Center
Albuquerque
NM
Disclosures
DCR declares that she has no competing interests.
Tracy I. George, MD
Professor of Pathology
University of New Mexico Health Sciences Center
Albuquerque
NM
Disclosures
TIG declares that she has received consulting fees from Wiley Blackwell as coeditor-in-chief for the International Journal of Laboratory Hematology, royalties from Wolters Kluwer for an atlas on peripheral blood smears, royalties from UpToDate, Inc. for an online chapter on automated hematology, and consulting fees from Roche Hematology.
Acknowledgements
Dr Devon Chabot-Richards and Dr Tracy I. George would like to gratefully acknowledge Dr Holbrook Kohrt, a previous contributor to this topic.
Disclosures
HK declares that he has no competing interests.
Peer reviewers
Carla Wilson, MD, PhD
Professor
Department of Pathology
University of New Mexico Health Sciences Center
Albuquerque
NM
Disclosures
CW declares that she has no competing interests.
Sherrie Perkins, MD, PhD
Professor of Pathology
Medical Director of Hematopathology
University of Utah Health Sciences and ARUP Laboratories
Salt Lake City
UT
Disclosures
SP declares that she has no competing interests.
John Reilly, BSc, MD, FRCP, FRCPath
Consultant Haematologist
Royal Hallamshire Hospital
Professor
University of Sheffield
Sheffield
UK
Disclosures
JR declares that he has no competing interests.
Priyanka Mehta, MD, MRCP, FRCPath
Consultant Haematologist
University Hospital Bristol
Bristol
UK
Disclosures
PM declares that she has no competing interests.
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