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      Dexamethasone and diclofenac intramuscular mixture injection and risk of death: A case series study

      case-report

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          Abstract

          Diclofenac and dexamethasone injection mixture could be associated with fatal cardiovascular events, further studies are warrantied to explore the safety of this injection mixture and explore the genetic role of it.

          Abstract

          Dexamethasone and diclofenac are commonly used medications for multiple anti inflammatory and analgesic purposes. Despite the multiple evidences on the synergistic anti inflammatory actions of them, there are no studies on the safety of mixing them in the same syringe for injection. Three patients have died due to cardiovascular events within 24 hours of receiving dexamethasone and diclofenac injection mixture, which we hypothesis that it could be the main reason for their death due to potential drug‐drug interaction.

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          Most cited references27

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          Diclofenac: an update on its mechanism of action and safety profile.

          Tong Gan (2010)
          Diclofenac is a proven, commonly prescribed nonsteroidal anti-inflammatory drug (NSAID) that has analgesic, anti-inflammatory, and antipyretic properties, and has been shown to be effective in treating a variety of acute and chronic pain and inflammatory conditions. As with all NSAIDs, diclofenac exerts its action via inhibition of prostaglandin synthesis by inhibiting cyclooxygenase-1 (COX-1) and cyclooxygenase-2 (COX-2) with relative equipotency. However, extensive research shows the pharmacologic activity of diclofenac goes beyond COX inhibition, and includes multimodal and, in some instances, novel mechanisms of action (MOA). Literature retrieval was performed through PubMed/MEDLINE (through May 2009) using combinations of the terms diclofenac, NSAID, mechanism of action, COX-1, COX-2, and pharmacology. Reference citations resulting from publications identified in the literature search were reviewed when appropriate. This article reviews the established, putative, and emerging MOAs of diclofenac; compares the drug's pharmacologic and pharmacodynamic properties with other NSAIDs to delineate its potentially unique qualities; hypothesizes why it has been chosen for further recent formulation enhancement; and evaluates the potential effect of its MOA characteristics on safety. Research suggests diclofenac can inhibit the thromboxane-prostanoid receptor, affect arachidonic acid release and uptake, inhibit lipoxygenase enzymes, and activate the nitric oxide-cGMP antinociceptive pathway. Other novel MOAs may include the inhibition of substrate P, inhibition of peroxisome proliferator activated receptor gamma (PPARgamma), blockage of acid-sensing ion channels, alteration of interleukin-6 production, and inhibition of N-methyl-D-aspartate (NMDA) receptor hyperalgesia. The review was not designed to compare MOAs of diclofenac with other NSAIDs. Additionally, as the highlighted putative and emerging MOAs do not have clinical data to demonstrate that these models are correct, further research is necessary to ascertain if the proposed pathways will translate into clinical benefits. The diversity in diclofenac's MOA may suggest the potential for a relatively more favorable profile compared with other NSAIDs.
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            Mechanism of action of nonsteroidal anti-inflammatory drugs.

            John R. Vane, Regina Botting (1998)
            Salicylic acid and salicylates, obtained from natural sources, have long been used as medicaments. Salicylic acid was chemically synthesized in 1860 and was used as an antiseptic, an antipyretic, and an antirheumatic. Almost 40 years later, aspirin was developed as a more palatable form of salicylate. Soon after, other drugs having similar actions to aspirin were discovered, and the group was termed the "aspirin-like drugs" (also now termed the nonsteroidal anti-inflammatory drugs [NSAIDs]). Twenty-five years ago, it was proposed that the mechanism of action of NSAIDs was through their inhibition of prostaglandin biosynthesis. Since then, there has been general acceptance of the concept that these drugs work by inhibition of the enzyme cyclo-oxygenase (COX), which we now know to have at least two distinct isoforms: the constitutive isoform, COX-1, and the inducible isoform, COX-2. COX-1 has clear physiologic functions. Its activation leads, for instance, to the production of prostacyclin, which when released by the endothelium is antithrombogenic and when released by the gastric mucosa is cytoprotective. COX-2, discovered 6 years ago, is induced by inflammatory stimuli and cytokines in migratory and other cells. It is therefore attractive to suggest that the anti-inflammatory actions of NSAIDs are due to inhibition of COX-2, whereas the unwanted side-effects, such as irritation of the stomach lining, are due to inhibition of COX-1. Drugs that have the highest COX-2 activity and a more favorable COX-2: COX-1 activity ratio will have a potent anti-inflammatory activity with fewer side-effects than drugs with a less favorable COX-2: COX-1 activity ratio. The identification of selective inhibitors of COX-2 will therefore lead to advances in therapy.
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              Differential inhibition of prostaglandin endoperoxide synthase (cyclooxygenase) isozymes by aspirin and other non-steroidal anti-inflammatory drugs.

              D DeWitt, Katherine L W Smith, A. Meade (1993)
              Murine prostaglandin endoperoxide (PGH) synthase-1 and PGH synthase-2 expressed in cos-1 cells were found to be differentially sensitive to inhibition by common nonsteroidal anti-inflammatory drugs (NSAIDs). Aspirin completely inhibited bis-oxygenation of arachidonate by PGH synthase-1; in contrast, aspirin-treated PGH synthase-2 metabolized arachidonate primarily to 15-hydroxyeicosatetraenoic acid (15-HETE) instead of PGH2. ID50 values were determined for a panel of common NSAIDs by measuring instantaneous inhibition of cyclooxygenase activity using an oxygen electrode. Among common NSAIDs tested, indomethacin, sulindac sulfide, and piroxicam preferentially inhibited PGH synthase-1; ibuprofen, flurbiprofen, and meclofenamate inhibited both enzymes with comparable potencies; and 6-methoxy-2-naphthylacetic acid preferentially inhibited PGH synthase-2. These results demonstrate that the two PGH synthases are pharmacologically distinct and indicate that it may be possible to develop isozyme-specific cyclooxygenase inhibitors useful both for anti-inflammatory therapy and for delineating between the biological roles of the PGH synthase isozymes.
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                Author and article information

                Contributors
                Abdallah Y. Naser:
                ORCID: https://orcid.org/0000-0001-8440-7446
                abdallah.naser@iu.edu.jo
                Journal
                Journal ID (nlm-ta): Clin Case Rep
                Journal ID (iso-abbrev): Clin Case Rep
                Journal ID (doi): 10.1002/(ISSN)2050-0904
                Journal ID (publisher-id): CCR3
                Title: Clinical Case Reports
                Publisher: John Wiley and Sons Inc. (Hoboken )
                ISSN (Electronic): 2050-0904
                Publication date (Electronic): 27 February 2021
                Publication date Collection: April 2021
                Volume: 9
                Issue: 4 ( doiID: 10.1002/ccr3.v9.4 )
                Pages: 2218-2221
                Affiliations
                [ 1 ] Department of Applied Pharmaceutical Sciences and Clinical Pharmacy Faculty of Pharmacy Isra University Amman Jordan
                [ 2 ] Faculty of Medicine Umm Alqura University Mecca Saudi Arabia
                [ 3 ] Baiji General Hospital Ministry of Health Salah ad Din Iraq
                Author notes
                [*] [* ] Correspondence

                Abdallah Y. Naser, Department of Applied Pharmaceutical Sciences and Clinical Pharmacy, Faculty of Pharmacy, Isra University, Amman, Jordan.

                Email: abdallah.naser@ 123456iu.edu.jo

                Author information
                https://orcid.org/0000-0001-8440-7446
                Article
                Publisher ID: CCR33988
                DOI: 10.1002/ccr3.3988
                PMC ID: 8077341
                SO-VID: bc5f37ca-ae7a-479f-8e3f-6f1ffb5bb4d8
                Copyright © © 2021 The Authors. Clinical Case Reports published by John Wiley & Sons Ltd.
                License:

                This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes.

                History
                Date revision received : 08 February 2021
                Date received : 01 February 2021
                Date accepted : 13 February 2021
                Page count
                Figures: 1, Tables: 1, Pages: 4, Words: 2543
                Categories
                Subject: Case Report
                Subject: Case Reports
                Custom metadata
                source-schema-version-number 2.0
                cover-date April 2021
                details-of-publishers-convertor Converter:WILEY_ML3GV2_TO_JATSPMC version:6.0.2 mode:remove_FC converted:27.04.2021

                Keywords: cardiovascular,dexamethasone,diclofenac,mixture,safety
                Data availability:
                Keywords: cardiovascular, dexamethasone, diclofenac, mixture, safety

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