Congenital; Cyanotic Heart Disease Clinical Trial
Official title:
Iron Profile in Patients With Congenital Cyanotic Heart Disease
Iron is a vital substrate for hemoglobin production and sufficient iron stores are necessary to achieve and maintain adequate levels of hemoglobin.
Iron is a vital substrate for hemoglobin production and sufficient iron stores are necessary
to achieve and maintain adequate levels of hemoglobin. Unfortunately, more than one third of
patients with cyanotic heart disease are iron-deficient (1),(2). In 1990, West et al, have
demonstrated that more than one-third of patients with congenital cyanotic heart diseases
(CCHD) had iron deficiency(3) In another study done by Olcay et al, the prevalence of iron
deficiency anemia (IDA) was found to be 52.2%(4).
Possible causes of iron deficiency include increased iron consumption through increased
erythropoiesis, inappropriate venesections, hemoptysis, bleeding from arteriovenous
malformations or collateral vessels, abnormal hemostasis, limited dietary intake or
absorption, and use of anticoagulants and antiplatelets (5).
Also congenital cyanotic heart lesions are associated with a state of constant hypoxia This
hypoxia triggers a physiological increase in erythropoietin release leading to stimulation of
the bone marrow to produce more red cells in an effort to increase the body's oxygen carrying
capacity, so as to improve oxygen delivery to the tissues. With persisting right to left
shunt, the arterial oxygen tensions remain perpetually low and so the production of more and
more red cells goes unabated leading to polycythemia. This seemingly noble physiological
response eventually leads to depletion of iron stores (6).
In these patients, the total haemoglobin is normal, high or slightly reduced compared to
aged-matched normal individuals without cyanosis. However, the MCV, MCH and serum ferritin
are usually comparatively lower than their peers as shown by Cemile et al - a phenomenon
known as relative anemia (7).
In fact, traditional diagnostic criteria for anemia do not apply to these patients, where
"appropriate" levels of hemoglobin may vary according to their oxygen saturations (8). Also,
other erythrocyte indices such as MCV and MCH are not sensitive indicators of iron deficiency
in cyanotic patients (9).
IDA aggravates hyperviscosity symptoms due to the presence of microcytic erythrocytes not
amenable to deformation in the microcirculation. Thus, presence of IDA in these children
further increases their chances of morbidity in the form of cerebrovascular events and
cyanotic spells (10).
The high incidence of iron deficiency among children with CCHD draws attention to the
importance of evaluating iron deficiency in this population.
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