Platelet Changes in Cases of Iron Overload Clinical Trial
Official title:
Platelet Changes in Cases of Chronic Iron Over Load
Iron demand: The average daily demand to fit the cell biological metabolism is balanced between intake and lost which about 1-2 mg.
Iron demand: The average daily demand to fit the cell biological metabolism is balanced
between intake and lost which about 1-2 mg. One unit of packed red blood cells contains
approximately 200-250 mg of iron.Thus, patients who arereceiving an average of 2 to 4 units
of blood monthly willhave an iron intake of 5000to 10 000 mg of iron per year. Iron
overload(IO) A condition in which the body takes up and stores more iron than it needs from
any cause. Iron overload constitutes a major problem in patients receivingregular blood
transfusion. Patients with β-thalassemia,sickle cell anemia, and congenital and refractory
anemiasonchronic transfusion programs accumulate iron in variousbody organs. Untreated iron
overload will eventually lead todamage of the liver, endocrine organs, and most seriously
theheart(1).Acquired platelet function defect might be one of thecomplications of iron
overload. This could occur indirectlythrough the effect of iron load on the liver and other
organsor might occur due to effect of iron load on platelet functiondirectly.
Dleteriouscomlications contributed by chemical reactive deregulated iron may affect cellular
homeostasis systematically lead to tissue and organ damage when this toxicity occurred in
blood cells ,alteration of peripheral hematological profile concerning erythrocyte,leucocyte
and Platelet. On the other hand, acquired platelet function defects are classified broadly
into defects that are intrinsic or extrinsic to the platelets. Acquired platelets defect are
due to medications, medical conditions, underlying hematologic diseases, and are more
frequent than inherited causes of platelets defects. (2) Platelet function is also influenced
by changes in membranefluidity that has an important role in the expressionof platelet
receptors and in modulating the activity ofproteins like phospholipase C or proteinkinase
C(3). Ithas been shown (4) that changes in membrane fluidityare associated to altered
aggregation/agglutination functionof freshly prepared platelets. The platelet
aggregationresponse is modified by monovalent cations (whichalter fibrinogen binding) and
monovalent anions thatenhance hydroxyl radicals production of platelets inducing platelet
activation (5) Reactive oxygen species(ROS) are involved in integrin aIIbb3 activation(6,7).
Moreover, bursts of ROS are generated in platelets exposed to thrombin (8). We herein report
the case of a patient with acquired plateletfunction defect associated with iron overload as
a consequenceof chronic blood transfusion. Therefore, we emphasizethe necessity of further
studies to confirm directcorrelation between iron overload as a causative agent andplatelets
dysfunction. And we recommend screening forplatelet function in patients receiving chronic
blood transfusionaiming at possible prevention of any lifethreateningbleeding.
One of the most commonly used laboratorymarkers to early characterize platelet functionis the
mean platelet volume (MPV). Increasedplatelet volume mayindicate its greater content
ingranules, showing a platelet activation also betteraggregation and more reactive than the
ordinarysize one. Limited study and the inconsistent resultare available regarding the
platelet function studyin IO complicated condition. Higher MPV wasidentified in heterozygous
beta-thalassemiapatientswith no correlation with cardiovascularrelatedrisks( 9). However, but
in line with this study, adefect in platelet aggregation indicated by ahyporeactivityof
platelet after induction withADP, ristocetin, and collagen was showed in majorthalassemia
children patients
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| Status | Clinical Trial | Phase | |
|---|---|---|---|
| Not yet recruiting |
NCT04329377 -
Platelet Changes in Cases of Iron Overload(IO)
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