Below are blood reference ranges for various types leucocytes/WBCs. The 97.5 percentile (right limits in intervals in image, showing 95% prediction intervals) is a common limit for defining leukocytosis.

A normal eosinophil count is considered to be less than 0.65/L. Eosinophil counts are higher in newborns and vary with age, time (lower in the morning and higher at night), exercise, environment, and exposure to allergens. Eosinophilia is never a normal lab finding. Efforts should always be made to discover the underlying cause, though the cause may not always be found.

The complete blood cell count is a blood panel that includes the overall WBC count and various subsets such as the absolute neutrophil count. Reference ranges for blood tests specify the typical counts in healthy people.

TLC- (Total leucocyte count):

Normal TLC in an adult person is 6000-8000WBC/mm^3 of blood.

DLC- (Differential leucocyte count):

Number/ (%) of different type of leucocyte in per cubic mm. of blood.

Lymphocytopenia is diagnosed when the complete blood count shows a lymphocyte count lower than the age-appropriate reference interval (for example, below 1.0 x 10(9)/L in an adult).

Lymphocytopenia caused by Feline Leukemia Virus and Feline immunodeficiency virus retroviral infections is treated with Lymphocyte T-Cell Immune Modulator.

Monocytosis is an increase in the number of monocytes circulating in the blood. Monocytes are white blood cells that give rise to macrophages and dendritic cells in the immune system.

In humans, 950/μL is regarded as at the upper limit of normal; monocyte counts above this level are regarded as monocytosis.

Monocytosis has sometimes been called mononucleosis, but that name is usually reserved specifically for infectious mononucleosis.

Monocytosis often occurs during chronic inflammation. Diseases that produce such a chronic inflammatory state:

- Infections: tuberculosis, brucellosis, listeriosis, subacute bacterial endocarditis, syphilis, and other viral infections and many protozoal and rickettsial infections (e.g. kala azar, malaria, Rocky Mountain spotted fever).

- Blood and immune causes: chronic neutropenia and myeloproliferative disorders.

- Autoimmune diseases and vasculitis: systemic lupus erythematosus, rheumatoid arthritis and inflammatory bowel disease.

- Malignancies: Hodgkin's disease and certain leukaemias, such as chronic myelomonocytic leukaemia (CMML) and monocytic leukemia.

- Recovery phase of neutropenia or an acute infection.

- Obesity (cf. Nagareddy et al. (2014), Cell Metabolism, Vol. 19, pp 821-835)

- Miscellaneous causes: sarcoidosis and lipid storage disease.

Leukocytosis is very common in acutely ill patients. It occurs in response to a wide variety of conditions, including viral, bacterial, fungal, or parasitic infection, cancer, hemorrhage, and exposure to certain medications or chemicals including steroids.

For lung diseases such as pneumonia and tuberculosis, WBC count is very important for the diagnosis of the disease, as leukocytosis is usually present.

The mechanism that causes leukocytosis can be of several forms: an increased release of leukocytes from bone marrow storage pools, decreased margination of leukocytes onto vessel walls, decreased extravasation of leukocytes from the vessels into tissues, or an increase in number of precursor cells in the marrow.

Certain medications, including corticosteroids, lithium and beta agonists, may cause leukocytosis.

About 10% of people who present a clinical picture of infectious mononucleosis do not have an acute Epstein–Barr-virus infection. A differential diagnosis of acute infectious mononucleosis needs to take into consideration acute cytomegalovirus infection and "Toxoplasma gondii" infections. Because their management is much the same, it is not always helpful, or possible, to distinguish between Epstein–Barr-virus mononucleosis and cytomegalovirus infection. However, in pregnant women, differentiation of mononucleosis from toxoplasmosis is important, since it is associated with significant consequences for the fetus.

Acute HIV infection can mimic signs similar to those of infectious mononucleosis, and tests should be performed for pregnant women for the same reason as toxoplasmosis.

People with infectious mononucleosis are sometimes misdiagnosed with a streptococcal pharyngitis (because of the symptoms of fever, pharyngitis and adenopathy) and are given antibiotics such as ampicillin or amoxicillin as treatment.

Other conditions from which to distinguish infectious mononucleosis include leukemia, tonsillitis, diphtheria, common cold and influenza (flu).

The heterophile antibody test works by agglutination of red blood cells from guinea pig, sheep and horse. This test is specific but not particularly sensitive (with a false-negative rate of as high as 25% in the first week, 5–10% in the second, and 5% in the third). About 90% of patients have heterophile antibodies by week 3, disappearing in under a year. The antibodies involved in the test do not interact with the Epstein–Barr virus or any of its antigens.

The monospot test is not recommended for general use by the CDC due to its poor accuracy.

White blood counts exceeding 100 x 10^9 / L (100,000 / microL) present symptoms of tissue hypoxia and may signal possible neurological and respiratory distress. Continuing research has shown that patients have suffered from hypoxia at leukocyte levels below 100 x 10^9 / L (100,000 / microL), therefore patients with leukemia need regular neurological and respiratory monitoring when leukocyte counts are approaching 100 x 10^9 / L (100,000 / microL) to decrease chances of tissue hypoxia. Biopsy's acquired are examined for damage to microvasculature, which serves as evidence of hypoxia through the identification of leukocyte blockage within the tissue. Due to a biopsy's invasive nature and the risks associated with the procedure, it is only used when deemed necessary.

Measurements for arterial pO2 have shown to be falsely decreased in patients with hyperleuckocytosis because of white blood cells ability to utilize oxygen. Pulse oximetry should be used to more accurately assess pO2 levels of a patient suspected to be suffering from leukocytosis.

Automated blood cell counters may be inaccurate due to fragments of blast cells being labeled on blood smears as platelets. The most accurate form of confirming platelet counts is by using a manual platelet count and review of a peripheral smear.

Serum potassium levels may also be artificially elevated caused by a release from leukemic blasts during in vitro clotting process, therefore serum potassium levels should be monitored by herparinized (the addition of herapin prevents coagulation) plasma samples in order to obtain accurate results of potassium levels.

Disseminated intravascular coagulation may occur in a significant amount of patients with presentation of various degrees of thrombin generation, followed by decreased fibrinogen and increased fibrinolysis.

Spontaneous tumor lysis syndrome is present in approximately 10 percent of patients with leuckostasis, lab tests are used to measure the potential of elevated serum concentrations such as uric acid, potassium, phosphate, and hyocalcemia.

Disseminated intravascular coagulation and spontaneous tumor lysis syndrome have the ability to develop before and after chemotherapy treatment. Patients undergoing this type of therapy need to be closely monitored before and after in addition to undergoing prophylactic measures to prevent possible complications.

Investigators at the National Institute of Allergy and Infectious Diseases at the US National Institutes of Health currently have clinical protocols to study new approaches to the diagnosis and treatment of this disorder.

Most patients with "ETV6-ACSL6"-related disease present with findings similar to eosinophilia, hypereosinophila, or chronic eosinophilic leukemia; at least 4 cases presented with eosinophilia plus findings of the red blood cell neoplasm, polycythemia vera; three cases resembled acute myelogenous leukemia; and one case presented with findings of a combined Myelodysplastic syndrome/myeloproliferative neoplasm. Best treatments for "ETV6-ACSL6"-related disease are unclear. Patients with the polycythemia vera form of the disease have been treated by reducing the circulating red blood cell load by phlebotomy or suppressing red blood cell formation using hydroxyurea. Individual case studies report that "ETV6-ACSL6"-associated disease is insensitive to tyrosine kinase inhibitors. Best treatment currently available, therefore, may involve chemotherapy and bone marrow transplantion.

Monocytes are a type of "leukocyte", or white blood cell. They are the largest type of leukocyte and can differentiate into macrophages and myeloid lineage dendritic cells. As a part of the vertebrate innate immune system monocytes also influence the process of adaptive immunity. There are at least three subclasses of monocytes in human blood based on their phenotypic receptors.

A "monocyte count" is part of a complete blood count and is expressed either as a percentage of monocytes among all white blood cells or as absolute numbers. Both may be useful but these cells became valid diagnostic tools only when monocyte subsets are determined.

It is an acute syndrome requiring aggressive cytoreductive including chemotherapy and/or leukapheresis to both reduce the number of circulating leukocytes and to break apart any aggregates that have already formed. Such rapid and massive lysis of tissue poses risk of complications (tumor lysis syndrome), but it is necessary to avoid stroke.

Leukostasis is different from leukemic infiltration which is a neoplastic process where leukemic cells invade organs.

Blood films display a range of abnormalities. A monocyte count of >1x10/L is essential for a diagnosis of CMML. Other features may include; leukocytosis (50% of cases); left shift and dysplasia of monocytes and granulocytes; presence of metamyelocytes, myelocytes and promonocytes; monocytes with hypersegmented/abnormal shaped nuclei, increased cytoplasmic basophilia and/or the presence of cytoplasmic granules; eosinophilia (in cases of CMML with eosinophilia); and spherocytosis (in cases of DCT positive haemolytic anaemia). Platelet counts may be reduced, increased or normal. Haemoglobin levels are usually reduced with normocytic and normochromic red blood cells. Autoantibodies and cold agglutinins may be present and 10% of CMML is DCT positive.

Bone marrow aspirates will display hypercellularity with increased counts of granulocytic and monocytic cells. Bone marrow core biopsies may show a predominance of myelocytic and monocytic cells, abnormal localisation of immature precursors and dysplastic megakaryocytes. Monocytic nodules are a common feature in biopsies.

The phenotypical characteristics of CMML are; CD11b, CD11c, CD14, CD33, CD45 and CD64 seen in 100% of cases; CD13 found in 95% of cases; CD4 found in 76% of cases; HLA-DR found in 71% of cases; CD56 found in 53% of cases; CD2 found in 34% of cases; CD16 found in 29% of cases; CD10 found in 28% of cases; CD23 and CD7 found in 9% of cases; and CD117 found in 5% of cases.

The FAB criteria for diagnosis are as follows:

- Monocyte count >1x10/L

- 0–19% blasts in bone marrow

- <5% blasts in peripheral blood

The FAB also arbitrarily categorises CMML into myelodysplastic-like and myeloproliferative-like groups. A white blood count of 13x10 is used as a cut-off to differentiate the two.

Lymphocyte-variant hypereosinophilia is a rare disease in which eosinophilia is caused by aberrant T cell lymphocytes which secrete cytokines (e.g. interleukin-5) that stimulate the proliferation of eosinophil precursor cells. The disease, which occasionally proceeds to a malignant lymphocytic phase, clearly reflects a clonal disturbance in lymphocytes, not eosinophils, and therefore is not a clonal hypereosinophilia. Similar non-clonal eosinophilia due to eosinophil precursor cell stimulation by clonal malignant cells is sometimes seen in cases of Hodgkin disease, B-cell lymphoma, T-cell lymphomas, T cell leukemias, and Langerhans cell histiocytosis. Other hematological diseases are associated with eosinophilia but regarded as clonal eosinophilia associated with a more important clonal malignancy in another cell type. For example, eosinophilia occurs in 20% to 30% of patients with systemic mastocytosis. Also referred to as SM-eo (systemic mastocytosis with eosinophilia) or SM-SEL (systemic mastocytosis with chronic eosinophilic leukemia), this disease's clonal eosinophils bear the same driving mutation, D816V in the"KIT" gene, as the clonal mast cells.

RALD patients show normal to modestly decreased total lymphocytes, mild to no elevation in αβ-double negative T cells, a relative expansion of B cells, and elevated granulocytes and monocytes. The absolute or relative monocytosis in particular is an important characteristic of this disorder and help differentiate it from ALPS. Autoantibodies are also common.

JMML accounts for 1-2% of childhood leukemias each year; in the United States, an estimated 25-50 new cases are diagnosed each year, which also equates to about 3 cases per million children. There is no known environmental cause for JMML. Since about 10% of patients are diagnosed before 3 months of age, it is thought that JMML is a congenital condition in these infants

Prognosis refers to how well a patient is expected to respond to treatment based on their individual characteristics at time of diagnosis. In JMML, three characteristic areas have been identified as significant in the prognosis of patients:

Without treatment, the survival [5 years?] of children with JMML is approximately 5%. Only Hematopoietic Stem Cell Transplantation (HSCT), commonly referred to as a bone marrow or (umbilical) cord blood transplant, has been shown to be successful in curing a child of JMML. With HSCT, recent research studies have found the survival rate to be approximately 50%. Relapse is a significant risk after HSCT for children with JMML. It is the greatest cause of death in JMML children who have had stem cell transplants. Relapse rate has been recorded as high as 50%. Many children have been brought into remission after a second stem cell transplant.

Diagnosis of sarcoidosis is a matter of exclusion, as there is no specific test for the condition. To exclude sarcoidosis in a case presenting with pulmonary symptoms might involve a chest radiograph, CT scan of chest, PET scan, CT-guided biopsy, mediastinoscopy, open lung biopsy, bronchoscopy with biopsy, endobronchial ultrasound, and endoscopic ultrasound with fine-needle aspiration of mediastinal lymph nodes (EBUS FNA). Tissue from biopsy of lymph nodes is subjected to both flow cytometry to rule out cancer and special stains (acid fast bacilli stain and Gömöri methenamine silver stain) to rule out microorganisms and fungi.

Serum markers of sarcoidosis, include: serum amyloid A, soluble interleukin-2 receptor, lysozyme, angiotensin converting enzyme, and the glycoprotein KL-6. Angiotensin-converting enzyme blood levels are used in the monitoring of sarcoidosis. A bronchoalveolar lavage can show an elevated (of at least 3.5) CD4/CD8 T cell ratio, which is indicative (but not proof) of pulmonary sarcoidosis. In at least one study the induced sputum ratio of CD4/CD8 and level of TNF was correlated to those in the lavage fluid. A sarcoidosis-like lung disease called granulomatous–lymphocytic interstitial lung disease can be seen in patients with common variable immunodeficiency (CVID) and therefore serum antibody levels should be measured to exclude CVID.

Differential diagnosis includes metastatic disease, lymphoma, septic emboli, rheumatoid nodules, granulomatosis with polyangiitis, varicella infection, tuberculosis, and atypical infections, such as "Mycobacterium avium" complex, cytomegalovirus, and cryptococcus. Sarcoidosis is confused most commonly with neoplastic diseases, such as lymphoma, or with disorders characterized also by a mononuclear cell granulomatous inflammatory process, such as the mycobacterial and fungal disorders.

Chest radiograph changes are divided into four stages:

1. bihilar lymphadenopathy

2. bihilar lymphadenopathy and reticulonodular infiltrates

3. bilateral pulmonary infiltrates

4. fibrocystic sarcoidosis typically with upward hilar retraction, cystic and bullous changes

Although people with stage 1 radiographs tend to have the acute or subacute, reversible form of the disease, those with stages 2 and 3 often have the chronic, progressive disease; these patterns do not represent consecutive "stages" of sarcoidosis. Thus, except for epidemiologic purposes, this categorization is mostly of historic interest.

In sarcoidosis presenting in the Caucasian population, hilar adenopathy and erythema nodosum are the most common initial symptoms. In this population, a biopsy of the gastrocnemius muscle is a useful tool in correctly diagnosing the person. The presence of a noncaseating epithelioid granuloma in a gastrocnemius specimen is definitive evidence of sarcoidosis, as other tuberculoid and fungal diseases extremely rarely present histologically in this muscle.

Sarcoidosis may be divided into the following types:

- Annular sarcoidosis

- Erythrodermic sarcoidosis

- Ichthyosiform sarcoidosis

- Hypopigmented sarcoidosis

- Löfgren syndrome

- Lupus pernio

- Morpheaform sarcoidosis

- Mucosal sarcoidosis

- Neurosarcoidosis

- Papular sarcoid

- Scar sarcoid

- Subcutaneous sarcoidosis

- Systemic sarcoidosis

- Ulcerative sarcoidosis

Hemangiosarcoma can cause a wide variety of hematologic and hemostatic abnormalities, including anemia, thrombocytopenia (low platelet count), disseminated intravascular coagulation (DIC); presence of nRBC, schistocytes, and acanthocytes in the blood smear; and leukocytosis with neutrophilia, left shift, and monocytosis.

A definitive diagnosis requires biopsy and histopathology. Cytologic aspirates are usually not recommended, as the accuracy rate for a positive diagnosis of malignant splenic disease is approximately 50%. This is because of frequent blood contamination and poor exfoliation. Surgical biopsy is the typical approach in veterinary medicine.