Can galectin-3 be used to predict the severity of vasoocclusive crisis in patients with sickle cell anaemia?

Main Article Content

Mahmut Bakir Koyuncu
Hakan Basir
Berkan Karadurmus
Selma Unal
Anil Tombak
Eyup Naci Tiftik

Abstract

Objective: The number of markers showing the severity of the disease and the number of drugs that can be used in the treatment is very low in vasooclusive crises seen in patients with sickle cell anemia. This study aims to evaluate the levels and changes of serum galectin-3 levels, which are known to have many roles in the body, during a painful crisis.


Material and Methods: In addition to the 0th and 48th hour galectin-3 levels in patients hospitalized for a painful crisis, galectin-3 measurements were also performed in stable patients with sickle cell anemia and healthy individuals.


Results: Galectin-3 levels were statistically significantly different in patient groups (p=0.001). It was observed that galectin-3 levels at the 48th hour were markedly higher than at the 0th hour in patients with painful crises. It was found that galectin-3 levels at both 0th and 48th hours were correlated with the duration of hospitalization due to painful crisis and the period of intravenous opioid use.


Conclusion: Galectin-3 levels, which are elevated during the painful crisis in patients with sickle cell anemia, are associated with the severity of the painful crisis

Downloads

Download data is not yet available.

Article Details

How to Cite
Koyuncu, M. B., Basir, H., Karadurmus, B., Unal, S., Tombak, A., & Tiftik, E. N. (2022). Can galectin-3 be used to predict the severity of vasoocclusive crisis in patients with sickle cell anaemia?. Medical Science and Discovery, 9(2), 96–100. https://doi.org/10.36472/msd.v9i2.675
Section
Research Article
Received 2022-01-17
Accepted 2022-02-08
Published 2022-02-18

References

Ware RE, de Montalembert M, Tshilolo L, Abboud MR. Sickle cell disease. Lancet. 2017;390(10091):311-23. DOI: https://doi.org/10.1016/S0140-6736(17)30193-9

Zhang D, Xu C, Manwani D, Frenette PS. Neutrophils, platelets, and inflammatory pathways at the nexus of sickle cell disease pathophysiology. Blood. 2016;127(7):801-9. DOI: https://doi.org/10.1182/blood-2015-09-618538

Dong R, Zhang M, Hu Q, Zheng S, Soh A, Zheng Y, et al. Galectin-3 as a novel biomarker for disease diagnosis and a target for therapy (Review). Int J Mol Med. 2018;41(2):599-614. DOI: https://doi.org/10.3892/ijmm.2017.3311

Mburu J, Odame I. Sickle cell disease: Reducing the global disease burden. Int J Lab Hematol. 2019;41 Suppl 1:82-8. DOI: https://doi.org/10.1111/ijlh.13023

Yawn BP, Buchanan GR, Afenyi-Annan AN, Ballas SK, Hassell KL, James AH, et al. Management of sickle cell disease: summary of the 2014 evidence-based report by expert panel members. Jama. 2014;312(10):1033-48. DOI: https://doi.org/10.1001/jama.2014.10517

Biemond BJ, Tombak A, Kilinc Y, Al-Khabori M, Abboud M, Nafea M, et al. Sevuparin for the treatment of acute pain crisis in patients with sickle cell disease: a multicentre, randomised, double-blind, placebo-controlled, phase 2 trial. Lancet Haematol. 2021;8(5):e334-e43. DOI: https://doi.org/10.1016/S2352-3026(21)00053-3

Niihara Y, Miller ST, Kanter J, Lanzkron S, Smith WR, Hsu LL, et al. A Phase 3 Trial of l-Glutamine in Sickle Cell Disease. N Engl J Med. 2018;379(3):226-35. DOI: https://doi.org/10.1056/NEJMoa1715971

Ataga KI, Kutlar A, Kanter J, Liles D, Cancado R, Friedrisch J, et al. Crizanlizumab for the Prevention of Pain Crises in Sickle Cell Disease. N Engl J Med. 2017;376(5):429-39. DOI: https://doi.org/10.1056/NEJMoa1611770

Mendonça Belmont TF, do Ó KP, Soares da Silva A, de Melo Vilar K, Silva Medeiros F, Silva Vasconcelos LR, et al. Single Nucleotide Polymorphisms at +191 and +292 of Galectin-3 Gene (LGALS3) Related to Lower GAL-3 Serum Levels Are Associated with Frequent Respiratory Tract Infection and Vaso-Occlusive Crisis in Children with Sickle Cell Anemia. PLoS One. 2016;11(9):e0162297. DOI: https://doi.org/10.1371/journal.pone.0162297

Aksan G, Gedikli Ö, Keskin K, Nar G, İnci S, Yıldız SS, et al. Is galectin-3 a biomarker, a player-or both-in the presence of coronary atherosclerosis? J Investig Med. 2016;64(3):764-70. DOI: https://doi.org/10.1136/jim-2015-000041

Barman SA, Li X, Haigh S, Kondrikov D, Mahboubi K, Bordan Z, et al. Galectin-3 is expressed in vascular smooth muscle cells and promotes pulmonary hypertension through changes in proliferation, apoptosis, and fibrosis. Am J Physiol Lung Cell Mol Physiol. 2019;316(5):L784-l97. DOI: https://doi.org/10.1152/ajplung.00186.2018

Cheng D, Liang B, Li Y. Serum galectin-3 as a potential marker for gastric cancer. Med Sci Monit. 2015;21:755-60. DOI: https://doi.org/10.12659/MSM.892386

Fort-Gallifa I, Hernández-Aguilera A, García-Heredia A, Cabré N, Luciano-Mateo F, Simó JM, et al. Galectin-3 in Peripheral Artery Disease. Relationships with Markers of Oxidative Stress and Inflammation. Int J Mol Sci. 2017;18(5). DOI: https://doi.org/10.3390/ijms18050973

Jiang SS, Weng DS, Wang QJ, Pan K, Zhang YJ, Li YQ, et al. Galectin-3 is associated with a poor prognosis in primary hepatocellular carcinoma. J Transl Med. 2014;12:273. DOI: https://doi.org/10.1186/s12967-014-0273-3

Wu KL, Huang EY, Yeh WL, Hsiao CC, Kuo CM. Synergistic interaction between galectin-3 and carcinoembryonic antigen promotes colorectal cancer metastasis. Oncotarget. 2017;8(37):61935-43. DOI: https://doi.org/10.18632/oncotarget.18721

Lee I, Anea C, Kumar S, Falls G, Oseghale A, Brittain J. Galectin-3 Is a Mediator of Pulmonary Fibrosis in Sickle Cell Disease: Novel Roles for Hemolysis and Acute Chest Syndrome. Blood. 2016;128(22):2480-. DOI: https://doi.org/10.1182/blood.V128.22.2480.2480