Responsible Prompt Engineering: An Embedding Based Approach to Secure LLM Interactions

Abstract

Non-steroidal anti-inflammatory medications are commonly used to treat fever, inflammation, and pain. Among them, the most commonly recommended medications are Indomethacin, Diclofenac Sodium, and Ibuprofen. The purpose of this review is to evaluate and contrast these three NSAIDs according to their safety, effectiveness, clinical applications, and pharmacological characteristics. It mainly works by preventing the creation of prostaglandins by blocking cyclooxygenase enzymes. Their therapeutic and side effect profiles are influenced by differences in these selectivities, though. Ibuprofen is widely accessible over-the-counter, has a good safety margin, and is frequently used for mild to severe discomfort. For inflammatory diseases like arthritis, diclofenac is commonly used since it is thought to be more effective. Because of its increased potential of adverse effects, the powerful NSAID indomethacin is primarily used to treat certain illnesses like gout and ankylosing spondylitis. The chemical classification, mode of action, pharmacokinetics, pharmacodynamics, clinical indications, and therapeutic comparisons of these medications are all examined in this article. Recent research and meta-analyses that shed light on the relative efficacy and tolerability of these medications are also examined in the review. In order to choose the best NSAID for each patient, taking into account comorbid diseases, side effects, and efficacy, it is essential to comprehend these variations. The development of NSAIDs in the future is also covered, with an emphasis on increasing effectiveness while lowering dangers to the heart, kidneys, and gastrointestinal tract.

Introduction

Non-steroidal anti-inflammatory drugs (NSAIDs) such as ibuprofen, diclofenac sodium, and indomethacin are widely used for their analgesic, antipyretic, and anti-inflammatory effects. These drugs inhibit cyclooxygenase (COX) enzymes to reduce pain and inflammation but differ in pharmacokinetics, potency, selectivity, and side-effect profiles.

• Ibuprofen is a propionic acid derivative with balanced COX inhibition and a short half-life, making it suitable for mild to moderate pain, fever, and common inflammatory conditions. It generally has a safer gastrointestinal (GI) profile.

• Diclofenac sodium, an acetic acid derivative with greater COX-2 selectivity, offers stronger anti-inflammatory effects but carries higher cardiovascular risks.

• Indomethacin, another acetic acid derivative, is very potent but associated with more GI and central nervous system side effects. It is used for severe inflammatory diseases and specific conditions like acute gout and neonatal patent ductus arteriosus.

NSAID-induced gastropathy remains a significant adverse effect, emphasizing the need for personalized medicine based on patient comorbidities and co-administration with gastroprotective agents. Pharmacokinetic and pharmacodynamic differences influence dosing and clinical use.

The chemical classification of NSAIDs includes salicylates, propionic acid derivatives, acetic acid derivatives, enolic acid derivatives, fenamates, and selective COX-2 inhibitors. Understanding these differences supports evidence-based, patient-tailored therapy.

Future NSAID research is focused on safer drugs with fewer side effects, precision medicine through pharmacogenomics, novel drug delivery methods like nanotechnology, and integrative approaches combining synthetic and herbal agents. Enhanced regulatory monitoring and sustainable drug production are also priorities.

Conclusion

In conclusion, the comparative evaluation of ibuprofen, diclofenac sodium, and indomethacin provides valuable insights into their pharmacological profiles, therapeutic uses, and safety considerations. Ibuprofen remains a widely accepted over-the-counter NSAID for mild to moderate pain and fever due to its favorable safety profile and minimal gastrointestinal and cardiovascular side effects. Diclofenac sodium, although more potent in its anti-inflammatory effects, requires cautious use owing to its associated cardiovascular risks, especially with long-term therapy. Indomethacin stands out for its strong anti-inflammatory and analgesic properties, making it particularly effective in conditions like gout and rheumatoid arthritis; however, its higher incidence of gastrointestinal and central nervous system side effects limits its broader applicability. The pharmacokinetic and pharmacodynamic differences among these NSAIDs dictate their clinical applications, dosing frequencies, and side effect profiles. While non-selective COX inhibition offers broad anti-inflammatory benefits, selective COX-2 inhibition, as seen in diclofenac to some extent, underscores the need to balance efficacy with cardiovascular safety. As research advances, personalized NSAID therapy guided by pharmacogenomics may become integral to clinical practice, optimizing efficacy and minimizing adverse outcomes. In light of ongoing drug development and formulation innovations, these NSAIDs continue to hold clinical significance. However, there is a growing need to explore safer derivatives, alternative delivery systems, and combination therapies to enhance therapeutic outcomes. Thus, continued research and post-market surveillance are essential to ensure patient safety, therapeutic success, and the evolution of evidence-based clinical guidelines.

References

[1] Brune, K., & Patrignani, P. (2015). New insights into the use of currently available non-steroidal anti-inflammatory drugs. Journal of Pain Research, 8, 105–118. [2] Davies, N. M. (1998). Clinical pharmacokinetics of ibuprofen: The first 30 years. Clinical Pharmacokinetics, 34(2), 101–154. [3] Hinz, B., & Brune, K. (2002). Cyclooxygenase-2–10 years later. Journal of Pharmacology and Experimental Therapeutics, 300(2), 367–375. [4] Hawkey, C. J. (2001). COX-2 inhibitors. The Lancet, 353(9149), 307–314. [5] McGettigan, P., & Henry, D. (2011). Cardiovascular risk with non-steroidal anti-inflammatory drugs: Systematic review of population-based controlled observational studies. PLoS Medicine, 8(9), e1001098. [6] Wallace, J. L. (2008). Prostaglandins, NSAIDs, and gastric mucosal protection: Why doesn\\\'t the stomach digest itself? Physiological Reviews, 88(4), 1547–1565. [7] Rainsford, K. D. (2009). Ibuprofen: Pharmacology, efficacy and safety. Inflammopharmacology, 17(6), 275–342. [8] Bindu, S., Mazumder, S., & Bandyopadhyay, U. (2020). Non-steroidal anti-inflammatory drugs (NSAIDs) and organ damage: A current perspective. Biochemical Pharmacology, 180, 114147. [9] Moore, N., Pollack, C., & Butkerait, P. (2015). Adverse drug reactions and drug–drug interactions with over-the-counter NSAIDs. Therapeutics and Clinical Risk Management, 11, 1061–1075. [10] Patrono, C., & Baigent, C. (2014). Nonsteroidal anti-inflammatory drugs and the heart. Circulation, 129(8), 907–916. [11] Crofford, L. J. (2013). Use of NSAIDs in treating patients with arthritis. Arthritis Research & Therapy, 15(S3), S2. [12] Bjarnason, I., Scarpignato, C., Takeuchi, K., & Rainsford, K. D. (2007). Determinants of the short-term gastric damage caused by NSAIDs in man. Alimentary Pharmacology & Therapeutics, 26(1), 95–106. [13] Farkouh, M. E., Greenberg, J. D., & Jeger, R. V. (2017). Cardiovascular safety of nonsteroidal anti-inflammatory drugs: Current state of evidence. Current Cardiology Reports, 19(5), 20. [14] Simon, L. S. (1999). Role and regulation of cyclooxygenase-2 during inflammation. American Journal of Medicine, 106(5), 37S–42S. [15] Zidar, N., & Bonaca, M. P. (2018). NSAIDs and cardiovascular risk: Current perspectives. Current Cardiology Reports, 20(10), 85. [16] Derry, S., Moore, R. A., & McQuay, H. J. (2015). Single dose oral ibuprofen for acute postoperative pain in adults. Cochrane Database of Systematic Reviews, 2015(7), CD001548. [17] Scharf, J. Y., & Uhl, K. (2003). Risk assessment of NSAIDs in the elderly. Drugs & Aging, 20(7), 529–543. [18] Motsko, S. P., Rascati, K. L., Busti, A. J., & Cziraky, M. J. (2006). Temporal patterns of NSAID use and risk of gastrointestinal complications. Pharmacotherapy, 26(10), 1427–1436. [19] Wehling, M. (2014). Non-steroidal anti-inflammatory drug use in chronic pain conditions. Drugs & Aging, 31(6), 469–472. [20] Levesque, L. E., Brophy, J. M., & Zhang, B. (2005). The risk for myocardial infarction with cyclooxygenase-2 inhibitors. The Lancet, 365(9454), 475–481. [21] Roelofs, M. M., Deyo, R. A., Koes, B. W., Scholten, R. J., & van Tulder, M. W. (2008). Non-steroidal anti-inflammatory drugs for low back pain. Cochrane Database of Systematic Reviews, 2008(1), CD000396. [22] Derry, S., Rabbie, R., & Moore, R. A. (2013). Diclofenac for acute postoperative pain in adults. Cochrane Database of Systematic Reviews, 2013(2), CD004768. [23] Whelton, A. (1999). Nephrotoxicity of nonsteroidal anti-inflammatory drugs: Physiologic foundations and clinical implications. American Journal of Medicine, 106(5), 13S–24S. [24] Laine, L. (2001). Approaches to nonsteroidal anti-inflammatory drug use in the high-risk patient. Gastroenterology, 120(3), 594–606. [25] Bombardier, C., Laine, L., Reicin, A., et al. (2000). Comparison of upper gastrointestinal toxicity of rofecoxib and naproxen in patients with rheumatoid arthritis. New England Journal of Medicine, 343(21), 1520–1528. [26] Griffin, M. R. (1998). Epidemiology of nonsteroidal anti-inflammatory drug–associated gastrointestinal injury. American Journal of Medicine, 104(3), 23S–29S. [27] Mukherjee, D., Nissen, S. E., & Topol, E. J. (2001). Risk of cardiovascular events associated with selective COX-2 inhibitors. JAMA, 286(8), 954–959. [28] Cheng, Y., Austin, S. C., Rocca, B., et al. (2002). Role of prostacyclin in the cardiovascular response to thromboxane A2. Science, 296(5567), 539–541. [29] Bjarnason, I., & Takeuchi, K. (2009). Intestinal permeability and NSAIDs. Gut, 58(10), 1334–1336. [30] Silverstein, F. E., Faich, G., Goldstein, J. L., et al. (2000). Gastrointestinal toxicity with celecoxib vs. nonsteroidal anti-inflammatory drugs for osteoarthritis and rheumatoid arthritis. JAMA, 284(10), 1247–1255.

Copyright

Copyright © 2025 Kanika ., Prof. Sanjay Kumar Sharma. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.