Basophils are only occasionally seen in normal peripheral blood comprising < 1% of circulating white cells. However, they are the largest type of granulocyte. They have many dark cytoplasmic granules which overlie the nucleus and contain heparin and histamine. They have immunoglobulin E (IgE) attachment sites and their degranulation is associated with histamine release. Basophils are very similar in both appearance and function to mast cells.

Antinuclear antibodies (ANA) are autoantibodies to the cells’ nucleus.

The ANA test is the most sensitive diagnostic test for verifying the disease’s diagnosis.

Other autoantibodies that may be found in SLE patients include rheumatoid factor, antiphospholipid antibodies, and antimitochondrial antibodies.

Acute lymphoblastic leukaemia (ALL) is caused by an accumulation of lymphoblasts in the bone marrow and is the most common malignancy of childhood. The incidence of ALL is highest at 3 – 7 years, with 75% of cases occurring before the age of 6. 85% of cases are of B-cell lineage. Haematological investigations reveal a normochromic normocytic anaemia with thrombocytopenia in most cases. There is great variation in the chance of individual patients achieving a long-term cure based on a number of biological variables. Approximately 25% of children relapse after first-line therapy and need further treatment but overall 90% of children can expect to be cured. The cure rate in adults drops significantly to less than 5% over the age of 70 years.

Acute myeloid leukaemia (AML) is the most common form of acute leukaemia in adults and becomes increasingly common with age, with a median onset of 65 years. It forms only a minor fraction (10 – 15%) of childhood leukaemia. The clinical features of AML typically presents with clinical features secondary to leukaemic infiltration of bone marrow and extramedullary sites:
Anaemia (lethargy, pallor and breathlessness)
Thrombocytopaenia (petechiae, bruising, epistaxis, haemorrhage) – often profound
Neutropenia (infections)
Hepatosplenomegaly
Gingival infiltration
Central nervous system involvement in AML is uncommon.
Leukaemia cutis is the infiltration of neoplastic leukocytes in the skin. It occurs in approximately 10% of patients with AML.Haematological investigations reveal a normochromic normocytic anaemia with thrombocytopenia in most cases. The total white cell count is usually increased and blood film examination typically shows a variable number of blast cells. The bone marrow is hypercellular and typically contains many blast cells.. The prognosis for patients with AML has been improving steadily, particularly for those under 60 years of age, and approximately one-third of patients of this group can expect to achieve long-term cure. For the elderly, the situation is poor and less than 10% of those over 70 years of age achieve long-term remission.
CML is commonly associated with the Philadelphia chromosome. The Philadelphia chromosome is present in only 1% of adults AML cases.
Lymphadenopathy is rare in AML.

Myocardial cells are unable to regenerate, they are unable to divide in response to tissue injury. The remain permanently in G0 and cannot progress to G1. If a segment of muscle dies, for example in myocardial infarction, this tissue will be replaced by scar tissue if the patient recovers. This scar tissue is non-contractile and therefore the remaining myocardium must work harder to maintain cardiac output. As a consequence the remaining undamaged myocardium undergoes compensatory hypertrophy without cell division.

B-cells (20% of lymphocytes) mature in the bone marrow and circulate in the peripheral blood until they undergo recognition of antigen. B-cell immunoglobulin molecules synthesised in the cell are exported and bound to the surface membrane to become the B-cell receptor (BCR) which can recognise and bind to a specific antigen (either free or presented by APCs). The BCR is also important for antigen internalisation, processing and presentation to T helper cells. Most antibody responses require help from antigen-specific T helper cells (although some antigens such as polysaccharide can lead to T-cell independent B-cell antibody production). When the B-cell is activated, the receptor itself is secreted as free soluble immunoglobulin and the B-cell matures into a memory B-cell or a plasma cell (a B-cell in its high-rate immunoglobulin secreting state). Plasma cells are non-motile and are found predominantly in the bone marrow or spleen. Most plasma cells are short-lived (1 – 2 weeks) but some may survive much longer. A proportion of B-cells persist as memory cells, whose increased number and rapid response underlies the augmented secondary response of the adaptive immune system.

Newborn babies have a higher concentration of red blood cells with shorter lifespan leading to higher bilirubin levels than in adults. This condition is short-lived and harmless but with potential serious causes that need to be assessed for if present.

The most obvious physical sign of jaundice is a yellow discolouration of the sclera, skin and mucous membranes. At a bilirubin level of 35 μmol/L or higher, the eye is affected. The bilirubin level will need to be higher than 255 μmol/L for the feet and extremities to be affected.

Megaloblastic anemia results from inhibition of DNA synthesis during red blood cell production. When DNA synthesis is impaired, the cell cycle cannot progress from the growth stage to the mitosis stage. This leads to continuing cell growth without division, which presents as macrocytosis, with an increase in mean corpuscular volume (MCV). The defect in red cell DNA synthesis is most often due to hypovitaminosis, specifically vitamin B12 deficiency or folate deficiency.
Folate is an essential vitamin found in most foods, especially liver, green vegetables and yeast. The normal daily diet contains 200 – 250 μg, of which about 50% is absorbed. Daily adult requirements are about 100 μg. Absorption of folate is principally from the duodenum and jejunum. Stores of folate are normally only adequate for 4 months and so features of deficiency may be apparent after this time.

Features include:
Anaemia
Jaundice (caused by unconjugated bilirubin in plasma, bilirubin is absent from urine)
Pigment gallstones
Splenomegaly
Ankle ulcers
Expansion of marrow with, in children, bone expansion e.g. frontal bossing in beta-thalassaemia major
Aplastic crisis caused by parvovirus

During or shortly after transfusion, febrile transfusion reactions, also known as non-haemolytic transfusion reactions, present with an unexpected temperature rise (38oC or 1oC above baseline, if baseline is 37oC). This is usually a one-off occurrence. The fever is sometimes accompanied by chills.

The most common type of transfusion reaction is febrile transfusion reactions, which occur in about 1 in every 8 transfusions.

The most common event leading to symptoms of febrile transfusion reactions is cytokine accumulation during storage of cellular components (especially platelet units). White cells secrete cytokines, and pre-storage leucodepletion has reduced this risk.

Recipient antibodies (raised as a result of previous transfusions or pregnancies) reacting to donor human leukocyte antigen (HLA) or other antigens can also cause febrile transfusion reactions. Donor lymphocytes, granulocytes, and platelets all contain these antigens.

Treatment is reassuring. Other causes should be ruled out, and antipyretics like paracetamol can help with fever relief. If another cause of fever is suspected, the transfusion should be stopped; however, if other causes of fever have been ruled out, it can be restarted at a slower rate.