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Review Article

Serratiopeptidase as an adjunct in burn care: a critical review and testable hypothesis for reducing NSAID exposure

  • Paper ID 10
  • Volume 1, Issue 3
  • Pages: 01-11
  • Published Online: September-December 2026
  • 290 Views
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Authors

  • Dr. Madhav Vasudeo Deshpande1
  • Manik Chaudhuri2
  • Girisha Maheshwari3

1 Director and Medical Advisor, Eutherva Medicament Pvt. Ltd., Mumbai, India. 2 Senior Consultant Projects and Operations, Xplora Clinical Research Services Pvt. Ltd., Bangalore, Karnataka, India. 3 PhD Scholar, Chitkara University, Punjab, India.

Article Information

DOI
No Doi
Published Online
September-December 2026
Pages
01-11
Article Type
Review Article
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Abstract

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Burn care requires effective pain relief while maintaining the biological processes involved in tissue repair. Nonsteroidal anti inflammatory drugs (NSAIDs) reduce pain through cyclooxygenase inhibition, but this action also modifies lipid mediators involved in vascular regulation, epithelial migration and immune function. Whether short courses of NSAIDs meaningfully delay human burn healing remains uncertain. Serratiopeptidase is a proteolytic enzyme investigated for swelling and inflammatory symptoms in several clinical settings. Its potential use in burns requires careful evaluation because evidence from dental and other inflammatory conditions does not establish efficacy in thermal injury. This critical narrative review examines burn biology, cyclooxygenase dependent repair pathways, serratiopeptidase pharmacology and the evidence supporting an NSAID sparing hypothesis. Clinical studies provide inconsistent evidence of analgesic benefit, while human systemic exposure, optimal burn dosing and safety remain insufficiently characterized. We therefore propose that a standardized oral serratiopeptidase preparation could be investigated for reducing edema and NSAID consumption in adults with uncomplicated superficial partial thickness burns, provided that pain control and epithelialization are not compromised. Preservation of local prostaglandin signaling is a separate mechanistic hypothesis requiring direct measurement, rather than an assumed consequence of lower NSAID intake. A staged research pathway should establish formulation quality and exposure before a blinded feasibility trial using identical background care and rescue analgesia in both groups. The concept is biologically plausible but remains clinically unproven. Its value will depend on demonstrating a patient relevant reduction in medication burden without impaired comfort, wound closure or safety.

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