Ignite Creation Date:
2025-12-24 @ 12:03 PM
Ignite Modification Date:
2025-12-24 @ 12:03 PM
Study NCT ID:
NCT04104061
Status:
UNKNOWN
Last Update Posted:
2019-09-26
First Post:
2019-09-24
Is Possible Gene Therapy:
False
Has Adverse Events:
False
Brief Title:
Iron Profile in Patients With Congenital Cyanotic Heart Disease
Sponsor:
Assiut University
Organization:
Study Overview
Official Title:
Iron Profile in Patients With Congenital Cyanotic Heart Disease
Status:
UNKNOWN
Status Verified Date:
2019-09
Last Known Status:
NOT_YET_RECRUITING
Delayed Posting:
No
If Stopped, Why?:
Not Stopped
Has Expanded Access:
False
If Expanded Access, NCT#:
N/A
Has Expanded Access, NCT# Status:
N/A
Acronym:
None
Brief Summary:
Iron is a vital substrate for hemoglobin production and sufficient iron stores are necessary to achieve and maintain adequate levels of hemoglobin.
Detailed Description:
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.
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.
Study Oversight
Has Oversight DMC:
None
Is a FDA Regulated Drug?:
False
Is a FDA Regulated Device?:
False
Is an Unapproved Device?:
None
Is a PPSD?:
None
Is a US Export?:
None
Is an FDA AA801 Violation?: