Article Sidebar

Submitted
April 19, 2025
Accepted
November 22, 2025
Published
June 30, 2025
Download
PDF
Statistic
Read Counter : 671

Main Article Content

Abstract

Background :The thalassemia syndromes are a group of inherent hemolytic anemias characterized by the decrease or absence of the synthesis of one or more globin chains of hemoglobin. Elevated levels of NOD-like receptor protein 3 (NLRP3) and ferritin, along with oxidative stress markers such as malondialdehyde (MDA) and catalase activity, have been linked to thalassemia disease progression and prognosis.


Aim :This study aims to investigate the relationship between serum levels of NLRP3, ferritin, MDA, and catalase activity in thalassemia patients compared to healthy controls, providing insights into potential diagnostic and prognostic biomarkers.


Materials and Methods :Seventy-five patients with beta-thalassemia major aged 6-18 years along with forty-five normal people of the same age without any history of hematological diseases, chronic diseases, acute illness, or infection. Patients who met the selection criteria were included in the study. Serum levels of NLRP3, ferritin, MDA, and catalase were analyzed using enzyme-linked immunosorbent assay (ELISA) and spectrophotometric methods.


Results: The study found elevated levels of NLRP3 in thalassemia patients (7.006 ± 1.014) compared to the healthy group (1.35 ± 0.2868), with a P value of 0.0003. Ferritin levels were also higher in patients (1576 ± 85.09) (ng/ml) compared to the healthy group (73.1 ± 13.67) (ng/ml), with a P value of <0.0001. MDA levels increased in patients (0.157 ± 0.01964) compared to the healthy group (0.06813 ± 0.0149), with a highly significant P value of 0.0007. In contrast, catalase activity was significantly lower in the patient group (0.5321 ± 0.07339) than in the healthy group (0.8746 ± 0.1104), with a P value of 0.0129. These findings suggest that an increase in NLRP3, ferritin, and MDA levels and a decrease in catalase activity are associated with an increased risk of thalassemia disease.


Conclusion: Elevated NLRP3, ferritin, and MDA levels, alongside reduced catalase activity, are associated with thalassemia disease progression. These biomarkers could serve as valuable tools for early detection and monitoring therapeutic responses in thalassemia patients.

Keywords

Irritable bowel syndrome (IBS) Lifestyle factors Dietary habits

Article Details

License

Copyright (c) 2025 Ali Abd Al-Bari Al-Dhalimi, Zainab N. Al-Abady (Author)

Creative Commons License

This work is licensed under a Creative Commons Attribution 4.0 International License.

How to Cite
Al-Dhalimi, A.A.A.-B. and Al-Abady, Z.N. (2025) “Analysis of the Relationship between NLRP3, Ferritin, MDA, and Catalase Enzyme in Patients with Beta-Thalassemia Major: A Clinical Study”, Journal of Biomedicine and Biochemistry, 4(2), pp. 1–20. doi:10.57238/jbb.2025.7432.1137.
Download Citation
Endnote/Zotero/Mendeley (RIS)
BibTeX

How to Cite

Al-Dhalimi, A.A.A.-B. and Al-Abady, Z.N. (2025) “Analysis of the Relationship between NLRP3, Ferritin, MDA, and Catalase Enzyme in Patients with Beta-Thalassemia Major: A Clinical Study”, Journal of Biomedicine and Biochemistry, 4(2), pp. 1–20. doi:10.57238/jbb.2025.7432.1137.
Crossref
Scopus
Google Scholar
Europe PMC

References

  1. Musallam KM, Lombard L, Kistler KD, Arregui M, Gilroy KS, Chamberlain C, et al. Epidemiology of clinically significant forms of alpha‐and beta‐thalassemia: a global map of evidence and gaps. American journal of hematology. 2023;98(9):1436-51. https://doi.org/10.1002/ajh.27006
  2. Galanello R, Origa R. Beta-thalassemia. Orphanet journal of rare diseases. 2010;5:1-15. https://doi.org/10.1186/1750-1172-5-11
  3. Karimi M, Cohan N, De Sanctis V, Mallat NS, Taher A. Guidelines for diagnosis and management of Beta-thalassemia intermedia. Pediatric hematology and oncology. 2014;31(7):583-96. https://doi.org/10.3109/08880018.2014.937884
  4. Nemtsas P, Arnaoutoglou M, Perifanis V, Koutsouraki E, Orologas A. Neurological complications of beta-thalassemia. Annals of hematology. 2015;94:1261-5. https://doi.org/10.1007/s00277-015-2378-z
  5. Shamshirsaz AA, Bekheirnia MR, Kamgar M, Pourzahedgilani N, Bouzari N, Habibzadeh M, et al. Metabolic and endocrinologic complications in beta-thalassemia major: a multicenter study in Tehran. BMC endocrine disorders. 2003;3:1-6. https://doi.org/10.1186/1472-6823-3-4
  6. Shawkat AJ, Jwaid AH. Clinical complications of beta-thalassemia major. Iraqi Journal of Pharmaceutical Sciences (P-ISSN 1683-3597 E-ISSN 2521-3512). 2019;28(2):1-8. https://doi.org/10.31351/vol28iss2pp1-8
  7. Mishra AK, Tiwari A. Iron overload in Beta thalassaemia major and intermedia patients. Maedica. 2013;8(4):328. PMID: 24790662
  8. Saad BH, Abdul-AM A-HH, Hussein A-MB, Mazin J. The study of serum ferritin level as a predictor of growth retardation in Thalassemia-major. Archivos Venezolanos de Farmacologia y Terapeutica. 2021;40(5):492-501.
  9. Gunarsih A, Amalia P, Boediman I. Variables associated with malondialdehyde level in thalassemia major patients. Paediatrica Indonesiana. 2012;52(3):125-31.
  10. Pavlova L, Savov V, Petkov H, Charova I. Oxidative stress in patients with beta-thalassemia major. Prilozi. 2007;28(1):145-54.
  11. Fibach E, Rachmilewitz EA. The role of antioxidants and iron chelators in the treatment of oxidative stress in thalassemia. Annals of the New York Academy of Sciences. 2010;1202(1):10-6. https://doi.org/10.1111/j.1749-6632.2010.05577.x
  12. Shazia Q, Mohammad Z, Rahman T, Shekhar HU. Correlation of oxidative stress with serum trace element levels and antioxidant enzyme status in Beta thalassemia major patients: a review of the literature. Anemia. 2012;2012(1):270923. https://doi.org/10.1155/2012/270923
  13. Xu X, Wu X, Yue G, An Q, Lou J, Yang X, et al. The role of Nod-like receptor protein 3 inflammasome activated by ion channels in multiple diseases. Mol Cell Biochem. 2023;478(6):1397-410. https://doi.org/10.1007/s11010-022-04602-1
  14. Almeida-da-Silva CLC, Savio LEB, Coutinho-Silva R, Ojcius DM. The role of NOD-like receptors in innate immunity. Frontiers in Immunology. 2023;14:1122586. https://doi.org/10.3389/fimmu.2023.1122586
  15. Şimşek F, Öztürk G, Kemahlı S, Erbaş D, Hasanoğlu A. Oxidant and antioxidant status in beta thalassemia major patients. Journal of Ankara University Faculty of Medicine. 2005;58(1):34-8.
  16. Bou-Fakhredin R, De Franceschi L, Motta I, Eid AA, Taher AT, Cappellini MD. Redox Balance in β-Thalassemia and sickle cell disease: a love and hate relationship. Antioxidants. 2022;11(5):967. https://doi.org/10.3390/antiox11050967
  17. Kósa Z, Nagy T, Nagy E, Fazakas F, Góth L. Decreased blood catalase activity is not related to specific beta‐thalassemia mutations in Hungary. International Journal of Laboratory Hematology. 2012;34(2):172-8. https://doi.org/10.1111/j.1751-553X.2011.01377.x
  18. Gerli G, Beretta L, Bianchi M, Pellegatta A, Agostoni A. Erythrocyte superoxide dismutase, Catalase and glutathione peroxidase activities in β‐thalassaemia (major and minor). Scandinavian Journal of Haematology. 1981;25(1):87-92. https://doi.org/10.1111/j.1600-0609.1981.tb01370.x
  19. Tantiworawit A, Khemakapasiddhi S, Rattanathammethee T, Hantrakool S, Chai-Adisaksopha C, Rattarittamrong E, et al. Correlation of hepcidin and serum ferritin levels in thalassemia patients at Chiang Mai University Hospital. Bioscience Reports. 2021;41(2):BSR20203352. https://doi.org/10.1042/BSR20203352
  20. Saraya AK, Kumar R, Choudhry VP, Kailash S, Sehgal AK. A study of serum ferritin in beta thalassemia: iron deficiency and overload. American journal of clinical pathology. 1985;84(1):103-7. https://doi.org/10.1093/ajcp/84.1.103
  21. Wood JC, Tyszka JM, Carson S, Nelson MD, Coates TD. Myocardial iron loading in transfusion-dependent thalassemia and sickle cell disease. Blood. 2004;103(5):1934-6. https://doi.org/10.1182/blood-2003-06-1919
  22. Trinder D, Fox C, Vautier G, Olynyk J. Molecular pathogenesis of iron overload. Gut. 2002;51(2):290-5. https://doi.org/10.1136/gut.51.2.290
  23. Zhou R, Yazdi AS, Menu P, Tschopp J. A role for mitochondria in NLRP3 inflammasome activation. Nature. 2011;469(7329):221-5. https://doi.org/10.1038/nature09663
  24. Martinon F. Signaling by ROS drives inflammasome activation. European journal of immunology. 2010;40(3):616-9. https://doi.org/10.1002/eji.200940168Esposito BP, Breuer W, Sirankapracha P, Pootrakul P, Hershko C, Cabantchik ZI. Labile plasma iron in iron overload: redox activity and susceptibility to chelation. Blood. 2003;102(7):2670-7. https://doi.org/10.1182/blood-2003-03-0807
  25. Gieling RG, Wallace K, Han Y-P. Interleukin-1 participates in the progression from liver injury to fibrosis. American Journal of Physiology-Gastrointestinal and Liver Physiology. 2009;296(6):G1324-G31.
  26. Artlett CM. The role of the NLRP3 inflammasome in fibrosis. The open rheumatology journal. 2012;6:80. https://doi.org/10.2174/1874312901206010080
  27. Rajamaki K, Lappalainen J. Oö rni K, Vä limä ki E, Matikainen S, Kovanen PT, et al. Cholesterol crystals activate the NLRP3 inflammasome in human macrophages: a novel link between cholesterol metabolism and inflammation. PLoS One. 2010;5:e11765. https://doi.org/10.1371/journal.pone.0011765
  28. Nakamura K, Kawakami T, Yamamoto N, Tomizawa M, Fujiwara T, Ishii T, et al. Activation of the NLRP3 inflammasome by cellular labile iron. Experimental hematology. 2016;44(2):116-24.
  29. Rund D, Rachmilewitz E. β-Thalassemia. New England Journal of Medicine. 2005;353(11):1135-46. https://doi.org/10.1016/j.exphem.2015.11.002
  30. Basu D, Adhya DG, Sinha R, Chakravorty N. Role of malonaldehyde as a surrogate biomarker for iron overload in the β-thalassemia patient: A systematic meta-analysis. Advances in Redox Research. 2021;3:100017. https://doi.org/10.1016/j.arres.2021.100017