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Evaluation of the relationship between hepatic and cardiac iron overload with MRI T2* and carotid intima media thickness with Doppler ultrasound in beta thalassemia major patients

Publikace na Přírodovědecká fakulta |
2021

Tento text není v aktuálním jazyce dostupný. Zobrazuje se verze "en".Abstrakt

Background: Iron overload is caused early progression of atherosclerosis in beta thalassemia patients due to regular repeated blood transfusion. MRI T2* is a gold standard non-invasive method for detecting hepatic and cardiac iron overload.

The aim of this study was the comparison of carotid intima media thickness (CIMT) in the patients and healthy control groups with Doppler ultrasound for early diagnosis of atherogenesis. Another purpose was to assess the relationship between CIMT and iron overload among patients.

Materials and methods: This cross-sectional study was performed on twenty patients referred to the Sarvar clinic and twenty age- and sex-matched control group. The CIMT was measured with Color Doppler ultrasound in both groups.

Then, MRI T2* results, demographic, and therapeutic information were extracted from their documents. Results: CIMT was insignificantly higher in the patients compared to the control group.

For example, it was 0.49 +/- 0.05 vs. 0.45 +/- 0.03 (p = 0.009) for the right common carotid artery (RCCA) and 0.48 +/- 0.06 vs. 0.46 +/- 0.04 (p = 0.17) for the left common carotid artery (LCCA). There was no strong relationship between CIMT and age (p = 0.09 for RCCA, p = 0.00 for LCCA), sex, chelation type (for example, p = 0.51 for RCCA with Desferal and p = 0.91 for LCCA with Desferal), age at diagnosis, age at the beginning on transfusion (p = 0.49 for RCCA, p = 0.20 for LCCA), age at the start of chelator (p = 0.74 for RCCA, p = 0.78 for LCCA), and hepatic and cardiac iron overload.

Conclusion: Preventive and curative methods should be planned to cease its progression. Furthermore, early initiation of chelator drugs with better efficacy and compliance may reverse the hepatotoxic and adverse myocardial effects of excessive iron.