Clinical Trial Details
— Status: Not yet recruiting
Administrative data
| NCT number |
NCT04329377 |
| Other study ID # |
pcicoio |
| Secondary ID |
|
| Status |
Not yet recruiting |
| Phase |
|
| First received |
|
| Last updated |
|
| Start date |
April 1, 2020 |
| Est. completion date |
April 1, 2022 |
Study information
| Verified date |
March 2020 |
| Source |
Assiut University |
| Contact |
n/a |
| Is FDA regulated |
No |
| Health authority |
|
| Study type |
Observational
|
Clinical Trial Summary
Iron demand: The average daily demand to fit the cell biological metabolism is balanced
between intake and lost which about 1-2 mg.
Description:
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
life-threateningbleeding.
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 cardiovascular-relatedrisks(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 with an iron overloadcondition(10). The decreased MPV showed in a highdose
iron treatment group of this study impliesthe eventual toxic effect of iron accumulation
toplatelet function. Still, specific platelet functionmarker analysis i.e. P-selectin,
fibrinogen receptor,and the CD40 ligand is imperative to be exploredto understand the
fundamental notion of how IOaffects the platelet functionality.
Platelets were affected by iron overloadindicated by differential platelet indices
i.e.platelet count, mean platelet volume, plateletcrit,and platelet distribution width
(figure1). Asignificant effect of iron treatment was showedin mean platelet volume among
groups, applyingANOVA, [F (2, 17) = 4.263, P = 0.031]. Post hoccomparisons using the Tukey's
test indicated thatthe mean platelet volume for the high dose irontreatment (2.5+0.5) was
significantly lower (P =0.02) than the low dose iron treatment group (3.7+0.7). However, the
mean platelet volume of thecontrolgroup (3.1 +0.9) did not significantly differfrom the low
and the high iron treatment groups.
low mean platelet volume following acquired platelet function attenuation was evidenced by
iron overload directing that platelet was also affected blood component.
In study ,theexpiremental mice model was established by a law and high dose of iron dextran
intraperitoneally. High dose iron treatment showed asignificantly lower mean platelet volume
(MPV) The result showed that the IO decrease the MPV.
