Sandbox:mani karimzade
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief:
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Template:DiseaseDisorder infobox
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [2]; Associate Editor(s)-In-Chief: Varun Kumar, M.B.B.S. [3]
Overview
Monocytosis is a common nonspecific finding usually representing the reactive innate immunity.[1] Circulating Monocytes ( with 1-3 day half life for classical monocytes )[2] are precursors of Macrophages and myeloid dendritic cells which can also act as an antigen presenting cells to other lymphocytes.[3] Monocytosis can also occur Among morbid pathological conditions like inflammatory diseases or neoplasms, so it could be clinically challenging for physicians to evaluate Monocytosis.[1] underlying Protozoa infections were known to be the main cause of Monocytosis.[4] Since Leukocytes traffic are mainly controlled by different ChemoKine's; Understanding this versatile and dynamic interaction of ChemoKine's with Monocytes may help to have a more complete picture of monocytosis.[5] Angiotensin-II/AGTR1A-signaling pathway helps the monocytes to move into the blood circulation. Inflammation can also stimulate the bone marrow to signal the monocytes to enter the circulation; persistent stimulation of bone marrow may alter the receptor distribution on monocytes surface which can lead to a sudden egress of monocytes into circulation.[6]
There are three major Monocytes ( Classical, Intermediate, and nonclassical ) including other subtypes. Today Singel-cell RNA sequencing (scRNA-seq ) is used for monocytes transcriptomic analysis but The high plasticity of monocytes subpopulations makes it difficult to distinct them. pathway analyzing is another promising method to understand monocytes and monocytosis.[7]
Clinicians should always look for other causes of monocytosis after excluding reactive monocytosis.[8] for example to differentiate CMML (Chronic myelomonocytic leukemia) with reactive monocytosis clinicians used Classical monocytes ( CD14++/CD16−) count as a biomarker which today is not correlated with CMML diagnosis.[9][10] Although for diagnosis of CMML we can use this biomarker ( with help of OKM5 monoclonal antibody which binds to monocyte membrane protein and platelet membrane protein ) for flow Cytometry but these monocyte-like cells lack nonspecific Esterase. [11] So it is also important to consider whether the Monocytosis is persistent or not.[2] Monocyte count is not correlated with survival in CMML transformation to Acute Leukemia which is a rare and aggressive form classified as acute myeloid leukemia with myelo-dysplasia-related changes [12] ( but increased marrow blasts count is correlated with decreased survival ( confirmed with CD34 )).[13]
Not only evaluating the Monocytes population with flow cytometry is necessary in the case of myeloid neoplasm speculation; but also it is important to evaluate the Monocytes population morphology, due to various atypical expressions of its CD markers ( Cluster of Differentiation ).[2]
Monocytosis is correlated with an increased risk of DVT ( Deep vein thrombosis ) and Cerebral infarcts and Subarachnoid hemorrhage, which emphasizes their role in coagulation cascade. [14][15]
Historical Perspective
[Disease name] was first discovered by [name of scientist], a [nationality + occupation], in [year]/during/following [event]. Monocytes name was suggested by one of the most Epic and enigmatic pathologist " James Homer Wright ". [4][16] 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].
There have been several outbreaks of [disease name], including -----.
In [year], [diagnostic test/therapy] was developed by [scientist] to treat/diagnose [disease name].
Classification
Based on CMML diagnostic Criteria; PB monocytosis ≥1 × 109/L, with monocytes accounting for ≥10% of the WBC count is considered as Monocytosis. [17][18]
After Discovery of flow cytometry and monoclonal antibodies in 1989 scientists start to classify Monocytes subpopulations, Then a panel of experts finally categorized these subpopulations to 3 groups ( classical, intermediate, non-classical ). The newer approach to classify Monocytes population is to also consider the expression of "slan" which is a carbohydrate modification of p-selectin glycoprotein ligand 1 ( PSGL-1 ). It is believed "slan" plays an important role in monocytes migration and is a good marker in the expanding list of markers to evaluate monocytes subpopulations.[19]
There is no established system for the classification of [disease name].
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[Disease name] may be classified according to [classification method] into [number] subtypes/groups: [group1], [group2], [group3], and [group4].
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[Disease name] may be classified into [large number > 6] subtypes based on [classification method 1], [classification method 2], and [classification method 3]. [Disease name] may be classified into several subtypes based on [classification method 1], [classification method 2], and [classification method 3].
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Based on the duration of symptoms, [disease name] may be classified as either acute or chronic.
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If the staging system involves specific and characteristic findings and features: According to the [staging system + reference], there are [number] stages of [malignancy name] based on the [finding1], [finding2], and [finding3]. Each stage is assigned a [letter/number1] and a [letter/number2] that designate the [feature1] and [feature2].
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The staging of [malignancy name] is based on the [staging system].
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There is no established system for the staging of [malignancy name].
Pathophysiology
Monocytosis arises from monocytes which have diverse roles. Monocytes ( with 12-20 μm diameter ) are similar with Neutrophils in terms of tissue penetration; their bi-lobed kidney shaped nucleus helps them to have more chromatin flexibility and deformation and they constitue 5% of nucleated circulating blood cell population.[20][21] Monocytes as a part of innate immunity; could respond to PAMP ( pathogen-associated molecular patterns ) and DAMP ( danger-associated molecular patterns ) with PRR ( pattern-recognition receptors ) and can activate inflammasome ( through TLR's and MYD88 which results in secretion of interferon-β and the consequent pro-inflammatory mediators like IL-1β ). [22] Inflammasome can activate pyroptosis in different cell populations.[23]
There are 3 major types of monocytes: classical ( CD14++CD16− ), intermediate ( CD14++CD16+ ) and non‐classical ( CD14+CD16++). Classical type usually consist 85-90 percent of the monocyte population in the body. The Classical monocytes is released from bone marrow and then it could be transformed to the intermediate monocyte first and then it could transform to the non-classical monocyte sub-population. Non-classical monocytes are known as protector of vasculature ( with 7.4 day circulation duration in the blood ). [24] During inflammation non-classical monocytes count increases rapidly and contributes to ROS production and phagocytosis.[25]Classical Monocytes are known to react in bacterial infection and inflammation through NLRP3 inflammasome signaling pathways. [7] It was believed that Monocytes sub-populations mainly react to the tissue responses to mobilize and control the further local mono-nuclear phagocytic population in the tissues, but today it is known that Monocytes give rise to dendritic cells and Macrophages are replenished in the tissue by their own ( in artery wall ). [26]
The exact pathogenesis of Monocytosis is not fully understood. Rapid early migration of monocytes to the tissue is dependent on MCP-1.[27] The trans-endothelial migration of Monocytes starts with monocytes tethering to the endothelium and then through contact of Selectin's and Integrin's with VCAM-1 and ICAM-1, ICAM-2 and then finally with PECAM during Diapedesis.[28]
The more Monocytes circulate in the blood, the more Monocytes interact with the artery wall. For example, in animal models, it was shown that cholesterol can induce Monocytosis from bone marrow and lead to a pro-inflammatory state ( not inflammatory state ) in arteries and disrupt the usual macrophage balance in the artery wall. The imbalance of monocytes and macrophages which are not completely understood will result in more lipo-toxic events in macrophages resides in the artery wall due to macrophage reduced mobility; thus more Necrotic lesions are formed in atherosclerotic situations.[29]
It is known that intermediate monocytes can produce a lot of IL-6, TNF-α, and IL-1β in response to LPS ( which can interact with CD14 ) but our understanding of each subpopulation in Human models is limited and needs further investigations. For example, it is hard to distinguish the role of non-classical subpopulation vs intermediate subpopulation in cytokine production. Monocytes expressing CD16+ could increase CD8+ T cells responses. Thus maybe in COVID-19 patients when there is a shift toward the non-classical population and the T cell exhaustion; this transformation of intermediate to non-classical is happening catastrophically and limits the intermediate type to balance the CD8+ T cell population. It seems that the more mature monocytes become, The more shift toward an inflammatory state could be expected.[30]
One of the major pathways activated during the inflammatory state in monocytes is the NFKB pathway, which is directly correlated with TNF-α production in their environment and results in more inflammatory cytokine production.[31]
Causes
The most common cause of Monocytosis is nonspecific, and its usually reactive to a secondary cause ( reactive Monocytosis ).[1]
some causes of peripheral Monocytosis are : chronic stress, chronic infections ( sub-acute bacterial endocarditis, malaria, congenital syphilis, pertussis infection ) , Immune disorders and inflammatory disorders, post-splenectomy, Neutropenia and Bone marrow recovery, hemolytic anemia's and iatrogenic causes (eg, radiation therapy), Solid tumors, Myocardial infarction, Myeloid or lymphoid or plasma cell malignancies and Cutaneous myeloid dendritic cell dyscrasia and atherosclerosis . [1][25][32]
After excluding all possible secondary causes a physician should look for Neoplastic causes. The most important one is CMML ( chronic myelomonocytic leukemia ) a type of myelodysplastic/myeloproliferative neoplasm (MDS/MPN). The main neoplastic entities with Monocytosis are :
1. Myelodysplastic/Myeloproliferative neoplasms ( represent with monocytopenia which is correlated with more adverse outcome ) [33]
2. Acute myeloid leukemia with Monocytic differentiation
3. Myeloproliferative neoplasms
4. Myeloid/lymphoid neoplasms with PDGFRA, PDGFRB, or FGFR1 rearrangement or PCM1-JAK2 fusion[1]
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Differentiating ((Page name)) from other Diseases
[Disease name] must be differentiated from other diseases that cause [clinical feature 1], [clinical feature 2], and [clinical feature 3], such as [differential dx1], [differential dx2], and [differential dx3].
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[Disease name] must be differentiated from [[differential dx1], [differential dx2], and [differential dx3].
Epidemiology and Demographics
The incidence/prevalence of [disease name] is approximately [number range] per 100,000 individuals worldwide.
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In [year], the incidence/prevalence of [disease name] was estimated to be [number range] cases per 100,000 individuals worldwide.
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In [year], the incidence of [disease name] is approximately [number range] per 100,000 individuals with a case-fatality rate of [number range]%.
Patients of all age groups may develop [disease name].
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The incidence of [disease name] increases with age; the median age at diagnosis is [#] years.
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[Disease name] commonly affects individuals younger than/older than [number of years] years of age.
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[Chronic disease name] is usually first diagnosed among [age group].
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[Acute disease name] commonly affects [age group].
There is no racial predilection to [disease name].
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[Disease name] usually affects individuals of the [race 1] race. [Race 2] individuals are less likely to develop [disease name].
[Disease name] affects men and women equally.
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[Gender 1] are more commonly affected by [disease name] than [gender 2]. The [gender 1] to [gender 2] ratio is approximately [number > 1] to 1.
The majority of [disease name] cases are reported in [geographical region].
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[Disease name] is a common/rare disease that tends to affect [patient population 1] and [patient population 2].
Risk Factors
There are no established risk factors for [disease name].
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The most potent risk factor in the development of [disease name] is [risk factor 1]. Other risk factors include [risk factor 2], [risk factor 3], and [risk factor 4].
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Common risk factors in the development of [disease name] include [risk factor 1], [risk factor 2], [risk factor 3], and [risk factor 4].
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Common risk factors in the development of [disease name] may be occupational, environmental, genetic, and viral.
Screening
There is insufficient evidence to recommend routine screening for [disease/malignancy].
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According to the [guideline name], screening for [disease name] is not recommended.
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According to the [guideline name], screening for [disease name] by [test 1] is recommended every [duration] among patients with [condition 1], [condition 2], and [condition 3].
Natural History, Complications, and Prognosis
If left untreated, [#]% of patients with [disease name] may progress to develop [manifestation 1], [manifestation 2], and [manifestation 3].
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Common complications of [disease name] include [complication 1], [complication 2], and [complication 3].
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Prognosis is generally excellent/good/poor, and the 1/5/10-year mortality/survival rate of patients with [disease name] is approximately [#]%.
Diagnosis
Diagnostic Study of Choice
The diagnosis of [disease name] is made when at least [number] of the following [number] diagnostic criteria are met: [criterion 1], [criterion 2], [criterion 3], and [criterion 4].
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The diagnosis of [disease name] is based on the [criteria name] criteria, which include [criterion 1], [criterion 2], and [criterion 3].
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The diagnosis of [disease name] is based on the [definition name] definition, which includes [criterion 1], [criterion 2], and [criterion 3].
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There are no established criteria for the diagnosis of [disease name].
History and Symptoms
The majority of patients with [disease name] are asymptomatic.
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The hallmark of [disease name] is [finding]. A positive history of [finding 1] and [finding 2] is suggestive of [disease name]. The most common symptoms of [disease name] include [symptom 1], [symptom 2], and [symptom 3]. Common symptoms of [disease] include [symptom 1], [symptom 2], and [symptom 3]. Less common symptoms of [disease name] include [symptom 1], [symptom 2], and [symptom 3].
Physical Examination
Patients with [disease name] usually appear [general appearance]. Physical examination of patients with [disease name] is usually remarkable for [finding 1], [finding 2], and [finding 3].
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Common physical examination findings of [disease name] include [finding 1], [finding 2], and [finding 3].
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The presence of [finding(s)] on physical examination is diagnostic of [disease name].
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The presence of [finding(s)] on physical examination is highly suggestive of [disease name].
Laboratory Findings
An elevated/reduced concentration of serum/blood/urinary/CSF/other [lab test] is diagnostic of [disease name].
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Laboratory findings consistent with the diagnosis of [disease name] include [abnormal test 1], [abnormal test 2], and [abnormal test 3].
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[Test] is usually normal among patients with [disease name].
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Some patients with [disease name] may have elevated/reduced concentration of [test], which is usually suggestive of [progression/complication].
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There are no diagnostic laboratory findings associated with [disease name].
Electrocardiogram
There are no ECG findings associated with [disease name].
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An ECG may be helpful in the diagnosis of [disease name]. Findings on an ECG suggestive of/diagnostic of [disease name] include [finding 1], [finding 2], and [finding 3].
X-ray
There are no x-ray findings associated with [disease name].
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An x-ray may be helpful in the diagnosis of [disease name]. Findings on an x-ray suggestive of/diagnostic of [disease name] include [finding 1], [finding 2], and [finding 3].
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There are no x-ray findings associated with [disease name]. However, an x-ray may be helpful in the diagnosis of complications of [disease name], which include [complication 1], [complication 2], and [complication 3].
Echocardiography or Ultrasound
There are no echocardiography/ultrasound findings associated with [disease name].
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Echocardiography/ultrasound may be helpful in the diagnosis of [disease name]. Findings on an echocardiography/ultrasound suggestive of/diagnostic of [disease name] include [finding 1], [finding 2], and [finding 3].
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There are no echocardiography/ultrasound findings associated with [disease name]. However, an echocardiography/ultrasound may be helpful in the diagnosis of complications of [disease name], which include [complication 1], [complication 2], and [complication 3].
CT scan
There are no CT scan findings associated with [disease name].
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[Location] CT scan may be helpful in the diagnosis of [disease name]. Findings on CT scan suggestive of/diagnostic of [disease name] include [finding 1], [finding 2], and [finding 3].
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There are no CT scan findings associated with [disease name]. However, a CT scan may be helpful in the diagnosis of complications of [disease name], which include [complication 1], [complication 2], and [complication 3].
MRI
There are no MRI findings associated with [disease name].
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[Location] MRI may be helpful in the diagnosis of [disease name]. Findings on MRI suggestive of/diagnostic of [disease name] include [finding 1], [finding 2], and [finding 3].
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There are no MRI findings associated with [disease name]. However, a MRI may be helpful in the diagnosis of complications of [disease name], which include [complication 1], [complication 2], and [complication 3].
Other Imaging Findings
There are no other imaging findings associated with [disease name].
OR
[Imaging modality] may be helpful in the diagnosis of [disease name]. Findings on an [imaging modality] suggestive of/diagnostic of [disease name] include [finding 1], [finding 2], and [finding 3].
Other Diagnostic Studies
There are no other diagnostic studies associated with [disease name].
OR
[Diagnostic study] may be helpful in the diagnosis of [disease name]. Findings suggestive of/diagnostic of [disease name] include [finding 1], [finding 2], and [finding 3].
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Other diagnostic studies for [disease name] include [diagnostic study 1], which demonstrates [finding 1], [finding 2], and [finding 3], and [diagnostic study 2], which demonstrates [finding 1], [finding 2], and [finding 3].
Treatment
Medical Therapy
There is no treatment for [disease name]; the mainstay of therapy is supportive care.
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Supportive therapy for [disease name] includes [therapy 1], [therapy 2], and [therapy 3].
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The majority of cases of [disease name] are self-limited and require only supportive care.
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[Disease name] is a medical emergency and requires prompt treatment.
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The mainstay of treatment for [disease name] is [therapy].
OR The optimal therapy for [malignancy name] depends on the stage at diagnosis.
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[Therapy] is recommended among all patients who develop [disease name].
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Pharmacologic medical therapy is recommended among patients with [disease subclass 1], [disease subclass 2], and [disease subclass 3].
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Pharmacologic medical therapies for [disease name] include (either) [therapy 1], [therapy 2], and/or [therapy 3].
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Empiric therapy for [disease name] depends on [disease factor 1] and [disease factor 2].
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Patients with [disease subclass 1] are treated with [therapy 1], whereas patients with [disease subclass 2] are treated with [therapy 2].
Surgery
Surgical intervention is not recommended for the management of [disease name].
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Surgery is not the first-line treatment option for patients with [disease name]. Surgery is usually reserved for patients with either [indication 1], [indication 2], and [indication 3]
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The mainstay of treatment for [disease name] is medical therapy. Surgery is usually reserved for patients with either [indication 1], [indication 2], and/or [indication 3].
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The feasibility of surgery depends on the stage of [malignancy] at diagnosis.
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Surgery is the mainstay of treatment for [disease or malignancy].
Primary Prevention
There are no established measures for the primary prevention of [disease name].
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There are no available vaccines against [disease name].
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Effective measures for the primary prevention of [disease name] include [measure1], [measure2], and [measure3].
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[Vaccine name] vaccine is recommended for [patient population] to prevent [disease name]. Other primary prevention strategies include [strategy 1], [strategy 2], and [strategy 3].
Secondary Prevention
There are no established measures for the secondary prevention of [disease name].
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Effective measures for the secondary prevention of [disease name] include [strategy 1], [strategy 2], and [strategy 3].
References
- ↑ 1.0 1.1 1.2 1.3 1.4 Lynch DT, Hall J, Foucar K (2018). "How I investigate monocytosis". Int J Lab Hematol. 40 (2): 107–114. doi:10.1111/ijlh.12776. PMID 29345409.
- ↑ 2.0 2.1 2.2 "StatPearls". 2021. PMID 32491550 Check
|pmid=value (help). - ↑ Tacke F (2009). "[Monocyte subpopulations in inflammation processes: principles and perspectives]". Dtsch Med Wochenschr. 134 (33): 1645–8. doi:10.1055/s-0029-1233994. PMID 19650028.
- ↑ 4.0 4.1 Dutton HR (1928). "The Diagnostic Value of a Monocytosis". Ind Med Gaz. 63 (11): 627–628. PMC 5235623. PMID 29011555.
- ↑ Baggiolini M (1998). "Chemokines and leukocyte traffic". Nature. 392 (6676): 565–8. doi:10.1038/33340. PMID 9560152.
- ↑ Teh YC, Ding JL, Ng LG, Chong SZ (2019). "Capturing the Fantastic Voyage of Monocytes Through Time and Space". Front Immunol. 10: 834. doi:10.3389/fimmu.2019.00834. PMC 6476989. PMID 31040854.
- ↑ 7.0 7.1 Cormican S, Griffin MD (2020). "Human Monocyte Subset Distinctions and Function: Insights From Gene Expression Analysis". Front Immunol. 11: 1070. doi:10.3389/fimmu.2020.01070. PMC 7287163 Check
|pmc=value (help). PMID 32582174 Check|pmid=value (help). - ↑ Mangaonkar AA, Tande AJ, Bekele DI (2021). "Differential Diagnosis and Workup of Monocytosis: A Systematic Approach to a Common Hematologic Finding". Curr Hematol Malig Rep. doi:10.1007/s11899-021-00618-4. PMC 8057007 Check
|pmc=value (help). PMID 33880680 Check|pmid=value (help). - ↑ Murali A, Cross D, Mollee P (2021). "The use of monocyte subset repartitioning by flow cytometry for diagnosis of chronic myelomonocytic leukaemia". Blood Cancer J. 11 (1): 6. doi:10.1038/s41408-020-00401-3. PMC 7791046 Check
|pmc=value (help). PMID 33414421 Check|pmid=value (help). - ↑ Cazzola M (2019). "Clonal monocytosis of clinical significance". Blood. 133 (12): 1271–1272. doi:10.1182/blood-2019-01-896084. PMID 30898774.
- ↑ Takahashi K, Mishima K, Ichikawa Y, Watanabe K, Komatsuda M, Arimori S (1987). "Report of a case with chronic myelomonocytic leukemia: demonstration of leukemic monocytes lacking nonspecific esterase by flow cytometry using monoclonal antibodies". Tokai J Exp Clin Med. 12 (5–6): 275–81. PMID 3508652.
- ↑ Courville EL, Wu Y, Kourda J, Roth CG, Brockmann J, Muzikansky A; et al. (2013). "Clinicopathologic analysis of acute myeloid leukemia arising from chronic myelomonocytic leukemia". Mod Pathol. 26 (6): 751–61. doi:10.1038/modpathol.2012.218. PMID 23307061.
- ↑ Storniolo AM, Moloney WC, Rosenthal DS, Cox C, Bennett JM (1990). "Chronic myelomonocytic leukemia". Leukemia. 4 (11): 766–70. PMID 2232890.
- ↑ Maldonado-Peña J, Rivera K, Ortega C, Betancourt M, Lugo JE, Camargo E (2016). "Can monocytosis act as an independent variable for predicting deep vein thrombosis?". Int J Cardiol. 219: 282–4. doi:10.1016/j.ijcard.2016.06.020. PMID 27343421.
- ↑ Unda SR, Birnbaum J, Labagnara K, Wong M, Vaishnav DP, Altschul DJ (2020). "Peripheral Monocytosis at Admission to Predict Cerebral Infarct and Poor Functional Outcomes in Subarachnoid Hemorrhage Patients". World Neurosurg. 138: e523–e529. doi:10.1016/j.wneu.2020.02.170. PMID 32151773 Check
|pmid=value (help). - ↑ Lee RE, Young RH, Castleman B (2002). "James Homer Wright: a biography of the enigmatic creator of the Wright stain on the occasion of its centennial". Am J Surg Pathol. 26 (1): 88–96. doi:10.1097/00000478-200201000-00011. PMID 11756774.
- ↑ Vardiman JW, Thiele J, Arber DA, Brunning RD, Borowitz MJ, Porwit A; et al. (2009). "The 2008 revision of the World Health Organization (WHO) classification of myeloid neoplasms and acute leukemia: rationale and important changes". Blood. 114 (5): 937–51. doi:10.1182/blood-2009-03-209262. PMID 19357394.
- ↑ Arber DA, Orazi A, Hasserjian R, Thiele J, Borowitz MJ, Le Beau MM; et al. (2016). "The 2016 revision to the World Health Organization classification of myeloid neoplasms and acute leukemia". Blood. 127 (20): 2391–405. doi:10.1182/blood-2016-03-643544. PMID 27069254.
- ↑ Ancuta P (2015). "A slan-based nomenclature for monocytes?". Blood. 126 (24): 2536–8. doi:10.1182/blood-2015-10-675470. PMID 26635407.
- ↑ Prinyakupt J, Pluempitiwiriyawej C (2015). "Segmentation of white blood cells and comparison of cell morphology by linear and naïve Bayes classifiers". Biomed Eng Online. 14: 63. doi:10.1186/s12938-015-0037-1. PMC 4485641. PMID 26123131.
- ↑ Skinner BM, Johnson EE (2017). "Nuclear morphologies: their diversity and functional relevance". Chromosoma. 126 (2): 195–212. doi:10.1007/s00412-016-0614-5. PMC 5371643. PMID 27631793.
- ↑ Santoni G, Cardinali C, Morelli MB, Santoni M, Nabissi M, Amantini C (2015). "Danger- and pathogen-associated molecular patterns recognition by pattern-recognition receptors and ion channels of the transient receptor potential family triggers the inflammasome activation in immune cells and sensory neurons". J Neuroinflammation. 12: 21. doi:10.1186/s12974-015-0239-2. PMC 4322456. PMID 25644504.
- ↑ Walsh JG, Muruve DA, Power C (2014). "Inflammasomes in the CNS". Nat Rev Neurosci. 15 (2): 84–97. doi:10.1038/nrn3638. PMID 24399084.
- ↑ Patel AA, Zhang Y, Fullerton JN, Boelen L, Rongvaux A, Maini AA; et al. (2017). "The fate and lifespan of human monocyte subsets in steady state and systemic inflammation". J Exp Med. 214 (7): 1913–1923. doi:10.1084/jem.20170355. PMC 5502436. PMID 28606987.
- ↑ 25.0 25.1 Chistiakov DA, Grechko AV, Myasoedova VA, Melnichenko AA, Orekhov AN (2018). "The role of monocytosis and neutrophilia in atherosclerosis". J Cell Mol Med. 22 (3): 1366–1382. doi:10.1111/jcmm.13462. PMC 5824421. PMID 29364567.
- ↑ Yona S, Jung S (2010). "Monocytes: subsets, origins, fates and functions". Curr Opin Hematol. 17 (1): 53–9. doi:10.1097/MOH.0b013e3283324f80. PMID 19770654.
- ↑ Henderson RB, Hobbs JA, Mathies M, Hogg N (2003). "Rapid recruitment of inflammatory monocytes is independent of neutrophil migration". Blood. 102 (1): 328–35. doi:10.1182/blood-2002-10-3228. PMID 12623845.
- ↑ Maslin CL, Kedzierska K, Webster NL, Muller WA, Crowe SM (2005). "Transendothelial migration of monocytes: the underlying molecular mechanisms and consequences of HIV-1 infection". Curr HIV Res. 3 (4): 303–17. doi:10.2174/157016205774370401. PMID 16250878.
- ↑ Kanter JE, Hsu CC, Bornfeldt KE (2020). "Monocytes and Macrophages as Protagonists in Vascular Complications of Diabetes". Front Cardiovasc Med. 7: 10. doi:10.3389/fcvm.2020.00010. PMC 7033616 Check
|pmc=value (help). PMID 32118048 Check|pmid=value (help). - ↑ Ożańska A, Szymczak D, Rybka J (2020). "Pattern of human monocyte subpopulations in health and disease". Scand J Immunol. 92 (1): e12883. doi:10.1111/sji.12883. PMID 32243617 Check
|pmid=value (help). - ↑ Dichamp I, Bourgeois A, Dirand C, Herbein G, Wendling D (2007). "Increased nuclear factor-kappaB activation in peripheral blood monocytes of patients with rheumatoid arthritis is mediated primarily by tumor necrosis factor-alpha". J Rheumatol. 34 (10): 1976–83. PMID 17896809.
- ↑ Carbonetti NH (2016). "Pertussis leukocytosis: mechanisms, clinical relevance and treatment". Pathog Dis. 74 (7). doi:10.1093/femspd/ftw087. PMC 5761200. PMID 27609461.
- ↑ Saeed L, Patnaik MM, Begna KH, Al-Kali A, Litzow MR, Hanson CA; et al. (2017). "Prognostic relevance of lymphocytopenia, monocytopenia and lymphocyte-to-monocyte ratio in primary myelodysplastic syndromes: a single center experience in 889 patients". Blood Cancer J. 7 (3): e550. doi:10.1038/bcj.2017.30. PMC 5380913. PMID 28362440.