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. 2021 Dec 10;2021(1):504-513. doi: 10.1182/hematology.2021000285

Table 3.

Characteristics of neutropenia in IEI commonly encountered by hematologists

IEI Frequency of neutropenia Proposed mechanism of neutropenia Neutropenia-directed therapy Comments
Chediak-Higashi syndrome Common57 -Accelerated granulocyte turnover secondary to intramedullary granulocyte destruction compounded by hypersplenism.9
-Abnormal bone marrow reserves with defective granulocyte mobilization from the marrow space.9
G-CSF
Antimicrobials
HSCT58
-Phagocyte intracellular killing and NK cytotoxicity is impaired.
CVID 1%-8.4%10,12 -Autoimmune clearance as supported by the identification of antineutrophil antibodies and evidence of hyperplastic yet inefficient germinal center responses.11,59
-Hypersplenism
-Postinfectious
-Drug-related
Corticosteroids
G-CSF
Rapamycin
-Neutropenia does not improve with IgG replacement
-Neutropenia is associated with increased infections, increased polyclonal lymphoproliferation, and autoimmunity.12
-Increased mortality rate associated with neutropenia in CVID patients.11,12
DADA2 7%-15%14,60 -Decreased ADA2 protein function in severely deleterious variants is proposed to lead to decreased marrow production.17
-Immune-mediated destruction is also hypothesized.
Corticosteroids
Rituximab
Anti-TNF agents
HSCT61
-ADA2 is highly expressed in myeloid cells and produced by activated macrophages, monocytes, and dendritic cells when stimulated by an inflammatory response.14
Hyper IgM syndrome 41%18 -Decreased CD16 expression and dysregulated transcriptome resulting in impaired differentiation.62
-Disrupted cytokine or growth factor support in the bone marrow.63
G-CSF -Neutropenia may be chronic or intermittent.
-Bone marrow evaluation may demonstrate maturation arrest.62
GATA2 haploinsufficiency 47%21 -Reduction of the primitive HSC pool20 G-CSF
HSCT
-Mild chronic neutropenia may be the first manifestation of disease with other clinical features, eg, monocytopenia or MDS/AML presenting later.
-Maturation of neutrophils in the bone marrow is generally preserved.20
WHIM syndrome Near universal -Diminished egress from the bone marrow secondary to gain of function mutations in CXCR423 G-CSF
CXCR4
antagonists
-Bone marrow is hypercellular with full maturation and classic pyknotic nuclei.
XLA 10%-26%64-66 -Decreased bone marrow precursors25
-Decreased maturation of myeloid precursors secondary to changes in BTK-related signal transduction25
-Decreased cytokine/chemokine production from monocytes, esp decreased IL-1825
G-CSF
IVIG
-BTK expressed in myeloid and B-cell differentiation (limited to hematopoietic cells).
-Neutropenia may be a presenting sign of XLA.
-Neutropenia generally resolves with initiation of IVIG, allowing G-CSF withdrawal.
-Neutropenia generally documented only in conjunction with an active infection.

AML, acute myeloid leukemia; MDS, myelodysplastic syndrome.