Cancer anaemia can be of various origins:
Very classical anaemia occurring for many digestive or uterine cancers.
Microcytic hypochromic anaemia (with a Mean Globular Volume or VGM < 80 μ3) and presence of reticulocytes. Serum iron is diminished (< 13 μmol/l), the fixation capacity of transferrin is increased (> 70 μmol/l), and serum ferritin decreased (< 20 μg/l).
Such anaemia is the reflection of the severe degradation of the patient’s general status.
Its main characteristics are: diminished serum iron (< 13 μmol/l), but a fixation capacity of transferrin which is below normal values (< 70 μmol/l) and a normal or increased (> 20 μg/l) serum ferritin.
It is generally accepted that iron is confined by macrophages.
However, more recent knowledge about the self-regulation mechanisms of erythropoiesis, in particular the role of death receptors for apoptosis (Fas/ Fas-L) could explain anaemia by a superexpression of these Fas factors (for instance for multiple myeloma).
Tumour Necrosis Factor (TNF-α) and Interferon-γ are also factors which can induce erythroblast apoptosis.
These forms appear in the form of macrocytic anaemia with a Mean Globular Volume (VGM) greater than 100 μ3. Deficiency in vitamin B12 can be observed in gastric carcinoma. Folate deficiency is more common, particularly since cachexia and treatment interfere with folic acid.
These forms of anaemia are frequent in cases of renal insufficiency but also after nephrotoxic chemotherapy. Erythropoietin is synthesised by juxtaglomerular cells. Each nephrotoxic chemotherapy or event (ureteral compression) induces a deficiency in erythropoietin synthesis.
Moreover, when patients suffer from inflammatory anaemia with its increased erythroblast apoptosis, a relative deficiency in erythropoietin synthesisis is observed: in order to correct inflammatory anaemia, a supraphysiological level of erythropoietin would appear to be necessary.