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Evaluation of Hepcidine

in Betathalasemic Iraqi
Patients

By
Ban Salman
Aya Saad
Supervised By
Assit. Proof. Dr. Raghad
Abdulmuhdi
Introduction
 Hepcidin is a vital peptide hormone secreted by hepatocytes that regulates iron
homeostasis by controlling the concentration and distribution of iron in the body. It
circulates in the blood plasma and is excreted in urine. Dysregulation of hepcidin
production is associated with various iron disorders: excessive hepcidin causes
iron-restricted anemia, while hepcidin deficiency leads to iron overload in tissues,
particularly the liver.
 Hepcidin exerts its effects by modulating the cellular concentration of ferroportin,
the sole known cellular iron exporter. Binding of hepcidin to ferroportin triggers its
internalization and degradation, reducing cellular iron export and decreasing iron
supply into the plasma. Conversely, low hepcidin levels result in increased
ferroportin on cell surfaces, promoting iron absorption and export from
macrophages. This unregulated iron absorption can lead to iron overload over time.
Aims of study
The aim of this study is to assess the levels and regulatory role of
hepcidin in Iraqi patients with beta-thalassemia. Through
comprehensive evaluation, we seek to understand the implications
of hepcidin dysregulation in the context of beta-thalassemia,
shedding light on its potential impact on iron homeostasis and
associated complications in this specific population. This
investigation aims to contribute valuable insights into the interplay
between hepcidin and beta-thalassemia, with the ultimate goal of
informing targeted interventions and improving the management of
iron-related disorders in betathalasemic patients in Iraq.
Materials and Methods
1. Microplate reader capable of measuring absorbance at 450 ± 10 nm.
2. High-speed centrifuge for sample preparation.
3. Electro-heating standing-temperature cultivator for maintaining incubation
temperatures.
4. Absorbent paper for drying the microplate during washing steps.
5. Double distilled water or deionized water used in various steps of the
assay.
6. Single or multi-channel pipettes with high precision and disposable tips for
accurate sample and reagent measurement.
7. Precision pipettes to deliver volumes ranging from 2 μL to 1 mL.
8. Plate shaker for mixing and agitation during certain steps. 13
9. Plate covers to prevent evaporation during incubation.
10. Sterile containers for sample collection and storage.
Results
TSB(mean±SD) ALT(mean±SD) AST(mean±SD) Hibsidine(mean±SD) TEST

47.5±7.79 42.8±8.31 44.7±12.2 7.98±1.9 patients

0.34 32.1±9.1 16.5±1.2 6.2 control

0.001** 0.027* **0.001 0.001** p-value

Table 1 showing the comparison of hibcidine between patients and control


group
Results
hibsdine

hibsidine level
7.98
6.2

1 2
patients control

Figure 2 shows a comparison between the number pf patients that have high
hibsdine and control group
Results
AST

AST LEVEL

44.7

16.5

1 2
PATIENTS CONTROL

Figure 3 shows comparison of patient with high AST levels and control
group
Results
ALT

ALT LEVEL 42.8

32.1

1 2
PATIENTS CONTROL

Figure 4 shows comparison of patient with high ALT levels and control group
Results
TSB

TSB LEVEL
47.5

0.34
1 2
PATIENTS CONTROL

Figure 5 shows comparison of patient with high TSB levels and control
group
Conclusion
Based on these findings, it is evident that there are notable
differences in the mean values of TSB, ALT, AST, and
Hibsidine between patients and controls. These
differences likely reflect underlying pathological
conditions affecting liver function and metabolism in the
patient group. Further investigations and clinical
assessments are warranted to elucidate the implications of
these biochemical alterations and their relevance in
disease diagnosis and management.
Recommendation

Expand Sample Size and Diversity


Longitudinal Investigations
Explore Mechanistic Insights
Examine Biomarker Correlation
Evaluate Therapeutic Interventions
Validate hs-Hepc25 Assay Performance
Consider Comorbidities and Interactions
Clinical Translation and Impact
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