Adverse drug reaction processing in the United States and its dependence on physician reporting: Zomepirac (Zomax®) as a case in point

Corre, Kenneth A; Spielberg, Theodore E.

doi:10.1016/s0196-0644(88)80300-7

Cited by 13 publications

(5 citation statements)

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“…A small but significant number of fatalities occur due to a drug administration error, that is, the patient was already known to be allergic to the relevant drug, or a closely related drug. 45 This was most clearly reported in Australia, where 9 of 27 cases of fatal penicillin or cephalosporin anaphylaxis were known to be penicillin-allergic. 11 …”

Section: Fatal Drug Anaphylaxismentioning

confidence: 98%

Fatal Anaphylaxis: Mortality Rate and Risk Factors

Turner

Jerschow

Umasunthar

et al. 2017

The Journal of Allergy and Clinical Immunology: In Practice

417

269

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Up to 5% of the US population has suffered anaphylaxis. Fatal outcome is rare, such that even for people with known venom or food allergy, fatal anaphylaxis constitutes less than 1% of total mortality risk. The incidence of fatal anaphylaxis has not increased in line with hospital admissions for anaphylaxis. Fatal drug anaphylaxis may be increasing, but rates of fatal anaphylaxis to venom and food are stable. Risk factors for fatal anaphylaxis vary according to cause. For fatal drug anaphylaxis, previous cardiovascular morbidity and older age are risk factors, with beta-lactam antibiotics, general anesthetic agents, and radiocontrast injections the commonest triggers. Fatal food anaphylaxis most commonly occurs during the second and third decades. Delayed epinephrine administration is a risk factor; common triggers are nuts, seafood, and in children, milk. For fatal venom anaphylaxis, risk factors include middle age, male sex, white race, cardiovascular disease, and possibly mastocytosis; insect triggers vary by region. Upright posture is a feature of fatal anaphylaxis to both food and venom. The rarity of fatal anaphylaxis and the significant quality of life impact of allergic conditions suggest that quality of life impairment should be a key consideration when making treatment decisions in patients at risk for anaphylaxis.

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Section: Fatal Drug Anaphylaxismentioning

confidence: 98%

Fatal Anaphylaxis: Mortality Rate and Risk Factors

Turner

Jerschow

Umasunthar

et al. 2017

The Journal of Allergy and Clinical Immunology: In Practice

417

269

View full text Add to dashboard Cite

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“…14,20 Thus, the main objective of this study was to examine the TNP-OVA PLNA as a pre-clinical predictive assay for use in identifying the immunostimulating potential of LMWCs associated with anaphylaxis in humans and to determine if the immunostimulation results in IgE antibody production. This study used the NSAID zomepirac and the analgesic glafenine, because both were pulled from the market due to a high association with anaphylaxis, 17,18 and it used the NSAID diclofenac, which is frequently associated with anaphylaxis but remains on the market. 19 In the TNP-OVA PLNA, all three drugs increased PLN diameter, weight and cellularity.…”

Section: Discussionmentioning

confidence: 99%

Investigating the TNP‐OVA and direct popliteal lymph node assays for the detection of immunostimulation by drugs associated with anaphylaxis in humans

Gutting

Updyke

Amacher

2002

J of Applied Toxicology

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Using current animal models, it is not possible to identify low-molecular-weight compounds (LMWCs) that are likely to be associated with anaphylaxis. It is generally accepted that the ultimate effector mechanism involves drug-induced IgE antibody. The objective of the present study was to determine if diclofenac, zomepirac and glafenine, which are associated with anaphylaxis in humans, have immunostimulating potential in the murine TNP-OVA (trinitrophenyl-ovalbumin) popliteal lymph node assay (PLNA), and more specifically to determine if the immunostimulation caused by these LMWCs results in IgE antibody production. These LMWCs were chosen because both zomepirac and glafenine were removed from the market due to high association with anaphylaxis, and diclofenac, which remains on the market, is frequently associated with anaphylaxis. In addition to conducting a TNP-OVA PLNA, the immunostimulating potential of these compounds was examined in the direct PLNA. When co-administered with TNP-OVA, all three LMWCs caused dose-dependent (0.25, 0.50, 1.00 and 1.25 mg) increases in popliteal lymph node (PLN) weight and cellularity that were observed beginning with the 0.25-mg dose. In addition, beginning with the 0.25-mg dose, all three compounds caused dose-dependent increases in TNP-OVA specific IgM and IgG(1) antibody-forming cells (AFCs). Diclofenac induced an isotype switch and caused a dose-dependent increase in the number of IgE AFCs with no detectable IgG(2a) AFCs and minimal high-dose-only IgG(2b) AFCs. Zomepirac induced IgE, IgG(2a) and IgG(2b) AFCs following the injection of 0.50 mg only, and glafenine induced IgE, IgG(2a) and IgG(2b) AFCs following the injection of 0.50-1.00 mg. In the direct PLNA, diclofenac caused dose-dependent increases in PLN weight and cellularity that were observed beginning with dose of 0.50 mg, whereas zomepirac failed to increase any PLN parameter and glafenine only increased the PLN weight. These results suggest that diclofenac, zomepirac and glafenine are immunostimulating LMWCs in the TNP-OVA PLNA with the potential to induce IgE antibody against a co-administered hapten-conjugate. Furthermore, these results suggest that the TNP-OVA PLNA offered significant advantages over the direct PLNA. Although it is not realistic to suggest that a single assay, based on a low number of test compounds, can identify all LMWCs with the potential to cause anaphylaxis in humans, these observations do demonstrate the potential utility of the PLNAs in examining LMWC-induced immunomodulation and support further development and investigation of the assays.

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“…The SRS was meant to serve as a type of early warning system for adverse drug reactions that were not noticed in clinical trials. 17,18 Because it is mandatory for manufacturers to report any serious adverse drug reactions that are reported to them, approximately 80% of the reports submitted to the SRS are from manufacturers' reports. The other 20% come directly from healthcare professionals and individual consumers.…”

Section: Methodsmentioning

confidence: 99%

“…The other 20% come directly from healthcare professionals and individual consumers. 17 Although the SRS was developed in the early 1960s, computerized reports are only available starting January 1969. 17,18 In an effort to standardize and globalize the US reporting database, the FDA implemented a new reporting system, the AERS, in November 1997.…”

Section: Methodsmentioning

confidence: 99%

“…17 Although the SRS was developed in the early 1960s, computerized reports are only available starting January 1969. 17,18 In an effort to standardize and globalize the US reporting database, the FDA implemented a new reporting system, the AERS, in November 1997. 16,19 Adverse event reports that were submitted to the FDA after October 31, 1997, were designed to be entered into the AERS.…”

Section: Methodsmentioning

confidence: 99%

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Adverse Event Reporting with Selective Serotonin-Reuptake Inhibitors

et al. 2003

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Within 1 class of medications, it is possible for a few agents to exhibit the Weber effect, while there is no definite pattern with others. A new observation in adverse event reporting is introduced and suggests that a peak in adverse event reporting occurs 1-2 years after a medication receives approval for a new indication. Future research is necessary to validate this effect and examine the generalizability to other medications.

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Adverse drug reaction processing in the United States and its dependence on physician reporting: Zomepirac (Zomax®) as a case in point

Cited by 13 publications

References 0 publications

Fatal Anaphylaxis: Mortality Rate and Risk Factors

Fatal Anaphylaxis: Mortality Rate and Risk Factors

Investigating the TNP‐OVA and direct popliteal lymph node assays for the detection of immunostimulation by drugs associated with anaphylaxis in humans

Adverse Event Reporting with Selective Serotonin-Reuptake Inhibitors

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