Vitamin B12 levels should be assessed at the same time due to the close relationship in metabolism.

Concern about excess folate level only occurs in the context of folic acid supplementation in pregnancy or the safety of dietary supplementation.

There is no clear consensus on the level of serum folate that indicates folate excess.

Conventionally, clinicians have used serum folate lower than 7 nmol/L (3 lg/L) as a guideline because the risk of megaloblastic anaemia greatly increases below this level.

There is no clear consensus on the level of serum folate that indicates folate deficiency.

If severe, there may be leukopenia and thrombocytopenia. The peripheral blood film shows macrocytes with hypersegmented polymorphs with six or more lobes in the nucleus.

FBC and blood film: features of megaloblastic anaemia: the mean corpuscular volume (MCV) is characteristically greater than 96 fL unless there is a co-existing microcytosis when there may be a dimorphic picture with a normal/low average MCV.

Mutations in the SLC46A1 gene, leading to proton-coupled folate transporter deficiency.

Trimethoprim may exacerbate pre-existing folate deficiency but does not cause megaloblastic anaemia.

Causing malabsorption of folate (eg, colestyramine, sulfasalazine, methotrexate).

With uncertain mechanism of action (eg, anticonvulsants and possibly alcohol and nitrofurantoin).

This includes, for example, congestive heart failure, acute liver damage and chronic dialysis.

Inflammation (eg, tuberculosis, Crohn's disease, malaria).

Blood disorders (eg, haemolytic anaemias, sickle cell anaemia, thalassaemia major, chronic myelosclerosis).

Malignancy (eg, leukaemia, carcinoma, lymphoma).

Physiological (eg, pregnancy, lactation, prematurity and infancy).

NB: goat's milk has a much lower folate concentration than cow's milk and infants fed exclusively on this may become deficient, unless commercial folic acid-fortified goat's milk is used.

Alcohol excess (also causes impaired utilisation).

Malabsorption (eg, coeliac disease, tropical sprue, congenital specific malabsorption, jejunal resection, inflammatory bowel disease).

Folate deficiency can occur for a number of reasons, including: The main cause of folate deficiency is poor intake, which may occur alone or in combination with excessive utilisation or malabsorption.

Folate deficiency may be associated with some types of cancer.

Low folate intake or low plasma folate concentration is associated with increased cardiovascular and stroke risk.

Folate is a vital regulator in the metabolic process of homocysteine, which is a risk factor of atherothrombotic events.

There is no simple relationship between maternal folate status and fetal abnormalities but folic acid supplements at the time of conception and in the first 12 weeks of pregnancy reduce the incidence of neural tube defects (NTDs).

Folate is also required for the development of a healthy fetus and plays an important role in the development of the fetus' spinal cord and brain.

The maturation of nuclei in megaloblastic cells is delayed while cytoplasmic development is normal. Neutrophils can be hypersegmented and megakaryocytes are abnormal. Erythrocytes are larger and have higher nuclear-to-cytoplasmic ratios compared to normoblastic cells.

Megaloblastic anaemias are a heterogeneous group of disorders sharing common morphological characteristics.

Insufficient folate can result in megaloblastic anaemia.Other useful sources include fortified breakfast cereals, beans, some bread and some fruit (such as oranges and bananas). Good food sources of folate include broccoli, Brussels sprouts, asparagus, peas, chickpeas and brown rice.Almost half of the body folate is found in the liver. The body's reserves of folate, unlike vitamin B12, are low and only sufficient for around four months. Folate is usually absorbed through the upper part of the small intestine. Folate (folic acid) is one of the B group of vitamins found in small amounts in many foods.

What is scid deficicency