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Subclinical myocardial injury during vaso-occlusive crisis in pediatric sickle cell disease

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Abstract

Acute painful crisis is the most frequent complication of sickle cell disease (SCD) in children. Recurrent vaso-occlusion may be associated with cardiac injury. The study aimed to assess silent myocardial injuries for sickle cell children during acute painful crisis by measuring serum level of troponin I and galectin-3. The study included 87 participates; study group (n = 44) sickle cell children presented at Jeddah hospitals in Saudi Arabia by painful crisis or acute illness as fever or cough (2017–2018). The controls were healthy children (n = 43). Demographic and history data were collected from the cases. Troponin I and galectin-3 were measured. Galectin-3 values were higher among cases with significant difference when compared to controls (7.5 ± 3.1 versus 3.2 ± 1.6, < 0.001). Galectin-3 at a cutoff > 5.1 ng/ml, the sensitivity was 88.64 and specificity was 88.37. Galectin-3 levels were higher for the pain crisis subgroup in comparison to acute illness group with significant difference (r 0.551*, p < 0.001*). Galectin-3 values were higher among troponin-positive cases with significant difference (p = 0.046) to troponin-negative cases.

Conclusion: Positive results of troponin I and high levels of galectin-3 in sickle cell children during acute painful crisis were potent indicators for subclinical myocardial injury.

What is Known:

The hallmark of sickle cell disease is recurrent episodes of vaso-occlusive crisis which had deleterious effects on many organs.

Cardiac changes in pediatric sickle cell disease whether structural or functional are mainly attributed to chronic anemia and or pulmonary hypertension.

What is New:

The observed positive results of cardiac troponin I and high values of galectin-3 in sickle cell children during vaso-occlusive crisis are strong indicator of myocardial ischemia and ongoing cardiac fibrosis respectively.

The observed correlation between biological markers (positive troponin and high galectin-3) could be an indication of subclinical cardiac injury.

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Abbreviations

CTnI:

Cardiac troponin I

EF:

Ejection fraction

FS:

Fraction shortening

Gal-3:

Galectin-3

SCD:

Sickle cell disease

VOCs:

Vaso-occlusive crisis

ng:

nanogram

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Acknowledgements

The authors would particularly like to thank the staff of El Mosaeddyiha and El Azizyha hospitals at Jeddah for their cooperation during data collection and analysis with special thanks to lab facilities staff: Mr. Essa Arar Hamoud and Mrs. Doaa Abdullah Al-Maymani.

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Authors and Affiliations

Authors

Contributions

Dr. Reham Wagdy has the idea, concept, and design, collecting data of echocardiography, data analysis, interpretation of the results, writing the arrticle, editing and supervising the work, revision and final approval before submission.

Dr. Howayda practical part of biological markers, interpreting the data, revising the article.

Bashayer Bamashmaouse selecting patients at hospitals, taking history data, sharing in writing.

Arunima Samonti data collection from patients and controls and laboratory findings.

Abrar Aidaroos data collection from patients and controls and laboratory findings.

Zuhour Haneef and Fatima Awn interpretation of results, sharing in statistical analysis, and editing.

Corresponding author

Correspondence to Reham Wagdy.

Ethics declarations

The study was approved by the ethical review committee of Batterjee Medical College and Board of Research of Ministry of Health, Jeddah, Saudi Arabia (S.N: RES-2018-0040), and the ethical review board of the Faculty of Medicine, Alexandria University, Alexandria, Egypt.

Informed consent

Informed consent was obtained from the parents and legal guardians respectively.

Conflict of interest

The authors declare that they have no conflict of interest.

Additional information

Communicated by Peter de Winter

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Wagdy, R., Suliman, H., Bamashmose, B. et al. Subclinical myocardial injury during vaso-occlusive crisis in pediatric sickle cell disease. Eur J Pediatr 177, 1745–1752 (2018). https://doi.org/10.1007/s00431-018-3231-x

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  • DOI: https://doi.org/10.1007/s00431-018-3231-x

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