Several mechanisms are involved in the pathophysiology of anaemia in CHF, including blunted erythropoietin production and/or erythropoietin resistance, further bone marrow dysfunction, gastrointestinal blood losses, and haemodilution, but, in the majority of patients, iron deficiency seems to play a role.
Indeed, the relationship between TL in stem cell progenitor cells and bone marrow dysfunction has been well established (Ball et al, 1998; Du et al, 2009), and abnormally short TL have been associated with myeloproliferative disorders such as aplastic anaemia (Ball et al, 1998).
SDS is clinically characterized by pancreatic insufficiency, skeletal abnormalities and bone marrow dysfunction.
A recent study found profound and general bone marrow dysfunction in CHF patients, another factor contributing to anaemia.
The patient eligibility criteria for this study were broadened to include patients with fewer transfusion requirements (as low as one transfusion within 24 months prior to initiating eculizumab treatment) and more severe bone marrow dysfunction (platelet counts as low as 30 × 10/l) (Hillmen et al, 2007; Brodsky et al, 2008).
Impaired proliferation, differentiation, mobilization, and iron incorporation in hematopoietic stem cells contribute to the bone marrow dysfunction [ 22].
Bone marrow dysfunction is common in severely injured trauma patients, with release of hematopoietic progenitor cells (HPC) into the peripheral blood.
While bone marrow dysfunction or liver cirrhosis can be found concurrently with pulmonary fibrosis, these diseases are frequently found in different individuals.
