Abstract

In response to the article titled “Duration of Bare Sclera Pterygium Surgery Combined with Mitomycin C with and Without Tranexamic Acid: A Randomized Double-Blind Controlled Trial” published in your esteemed journal, which is a well thought off and written article, I would like to raise few points regarding this study.
The study concludes that subconjunctival injection of tranexamic acid (TXA) did not significantly reduce intraoperative bleeding, shorten the duration of surgery, or improve postoperative outcomes in pterygium surgery. 1 This finding contrasts with the broader application of TXA as a widely used antifibrinolytic agent in various surgical fields to control bleeding. It has been shown to reduce blood loss and improve visibility during surgery, as well as to aid in wound healing and postoperative inflammation control.
Tranexamic acid (TXA) is a well-known fibrinolysis inhibitor that significantly reduces blood loss in a variety of surgical procedures and improves survival rates in patients with severe bleeding, particularly in obstetric and trauma contexts. In addition to its antifibrinolytic activity, TXA exhibits anti-inflammatory effects and may help attenuate the systemic inflammatory response syndrome observed in certain cardiac surgeries. 2
Emerging research suggests that a mutation in the p53 gene, located on chromosome 17, may be associated with the development of pterygium and its recurrence after surgical removal. This condition appears to be linked to altered expression of several growth factors, including basic fibroblast growth factor (bFGF), transforming growth factor β (TGF-β), vascular endothelial growth factor (VEGF), and platelet-derived growth factor (PDGF). These factors are found in various cellular components of the pterygium, such as epithelial cells, vascular endothelial cells, the basement membrane of vessels, fibroblasts, and inflammatory cells. As a result, pterygium is increasingly regarded as a condition driven by uncontrolled inflammation and abnormal cellular proliferation, rather than simply a degenerative disorder.3,4
Given these findings, it would be worthwhile to investigate whether the antifibrinolytic action of tranexamic acid (TXA) could have an impact on any of the aforementioned factors associated with the pathophysiology of pterygium. Further studies could explore TXA’s potential role in modulating these growth factors, especially those related to cellular proliferation and inflammation, such as TGF-β, VEGF, and PDGF. This line of research could provide new perspectives on the treatment and prevention of pterygium recurrence.
Footnotes
Author Disclosure Statement
The author has completed and submitted the ICMJE Form for Disclosure of Potential Conflicts of Interest, and none were reported.
Funding Information
No funding was received for this article.
