What Did ‘Safe’ Mean To Prescribes Of Selective Cox-2 Inhibitors?

Patricia McGettigan, Roseanne Peel, Barrie J. Stokes, Kim M. Henderson, Diana Whitaker, David A Henry

Research output: Contribution to journalMeeting AbstractResearchpeer-review

Abstract

Introduction: Among vulnerable individuals, cyclo-oxygenase-2
(COX-2) inhibition increases the risk of cardiovascular thrombotic
events. Promotional safety messages led to ‘channeling’ of selective
COX-2 inhibitors to individuals with gastrointestinal risks.
Aims: We investigated whether this was associated with inappropriate
channeling of COX-2 inhibitors to patients at risk of cardiovascular events.
Methods: Case–control study, August 2003–October 2006. Cases:
patients admitted to hospital with acute coronary syndrome (ACS, myocardial infarction/unstable angina) (n = 814). Controls:
Patients admitted for reasons other than acute vascular ischaemia, heart
failure, renal failure, or upper gastro-intestinal ulceration/bleeding
(n = 1500). Structured interviews gathered information on cardiovascular
events, risk factors, and ingested drugs, including selective COX-2 inhibitors and non-selective non-steroidal anti-inflammatory drugs (NSAIDs).
Controls were frequency matched to cases by age and sex. Relative risks
were estimated from exposure odds ratios (ORs), adjusted for multiple
potential confounders.
Results: Among cases, 386 (47.6%) had experienced prior vascular
events; 425 reported no vascular history. In multivariate modeling, the
strongest association with ACS was a vascular history (adjusted OR 4.47
(95% Confidence Interval 3.33, 6.00). However, cases with a vascular
history were significantly less likely than those without to have used
anti-inflammatory drugs in the preceding week: OR 0.65 (0.47, 0.89).
This effect was seen with non-selective NSAIDs, 0.51 (0.33, 0.79), but
not with selective COX-2 inhibitors (rofecoxib/celecoxib/diclofenac/meloxicam), 0.90 (0.60, 1.35).
Conclusions: Prescribers avoided non-selective NSAIDs but not selective COX-2 inhibitors in some patients. This sidestepped gastrointestinal
risk but caused inappropriate channeling of selective COX-2 inhibitors to
patients with vascular risks.
Original languageEnglish
Article numberTP23
Pages (from-to)90
JournalBasic and Clinical Pharmacology and Toxicology
Volume105
Issue numbers1
DOIs
Publication statusPublished - 2009
Externally publishedYes

Fingerprint

Cyclooxygenase Inhibitors
Prostaglandin-Endoperoxide Synthases
Blood Vessels
Anti-Inflammatory Agents
Pharmaceutical Preparations
meloxicam
Celecoxib
Odds Ratio
History
Diclofenac
Unstable Angina
Acute Coronary Syndrome
Renal Insufficiency
Ischemia
Myocardial Infarction
Confidence Intervals
Interviews
Hemorrhage
Safety

Cite this

McGettigan, Patricia ; Peel, Roseanne ; Stokes, Barrie J. ; Henderson, Kim M. ; Whitaker, Diana ; Henry, David A. / What Did ‘Safe’ Mean To Prescribes Of Selective Cox-2 Inhibitors?. In: Basic and Clinical Pharmacology and Toxicology. 2009 ; Vol. 105, No. s1. pp. 90.
@article{67b94a91e19344a1812748b3a1f52e01,
title = "What Did ‘Safe’ Mean To Prescribes Of Selective Cox-2 Inhibitors?",
abstract = "Introduction: Among vulnerable individuals, cyclo-oxygenase-2(COX-2) inhibition increases the risk of cardiovascular thromboticevents. Promotional safety messages led to ‘channeling’ of selectiveCOX-2 inhibitors to individuals with gastrointestinal risks.Aims: We investigated whether this was associated with inappropriatechanneling of COX-2 inhibitors to patients at risk of cardiovascular events.Methods: Case–control study, August 2003–October 2006. Cases:patients admitted to hospital with acute coronary syndrome (ACS, myocardial infarction/unstable angina) (n = 814). Controls:Patients admitted for reasons other than acute vascular ischaemia, heartfailure, renal failure, or upper gastro-intestinal ulceration/bleeding(n = 1500). Structured interviews gathered information on cardiovascularevents, risk factors, and ingested drugs, including selective COX-2 inhibitors and non-selective non-steroidal anti-inflammatory drugs (NSAIDs).Controls were frequency matched to cases by age and sex. Relative riskswere estimated from exposure odds ratios (ORs), adjusted for multiplepotential confounders.Results: Among cases, 386 (47.6{\%}) had experienced prior vascularevents; 425 reported no vascular history. In multivariate modeling, thestrongest association with ACS was a vascular history (adjusted OR 4.47(95{\%} Confidence Interval 3.33, 6.00). However, cases with a vascularhistory were significantly less likely than those without to have usedanti-inflammatory drugs in the preceding week: OR 0.65 (0.47, 0.89).This effect was seen with non-selective NSAIDs, 0.51 (0.33, 0.79), butnot with selective COX-2 inhibitors (rofecoxib/celecoxib/diclofenac/meloxicam), 0.90 (0.60, 1.35).Conclusions: Prescribers avoided non-selective NSAIDs but not selective COX-2 inhibitors in some patients. This sidestepped gastrointestinalrisk but caused inappropriate channeling of selective COX-2 inhibitors topatients with vascular risks.",
author = "Patricia McGettigan and Roseanne Peel and Stokes, {Barrie J.} and Henderson, {Kim M.} and Diana Whitaker and Henry, {David A}",
year = "2009",
doi = "10.1111/j.1742-7843.2009.00437.x",
language = "English",
volume = "105",
pages = "90",
journal = "Pharmacology and Toxicology",
issn = "0901-9928",
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What Did ‘Safe’ Mean To Prescribes Of Selective Cox-2 Inhibitors? / McGettigan, Patricia; Peel, Roseanne; Stokes, Barrie J.; Henderson, Kim M.; Whitaker, Diana; Henry, David A.

In: Basic and Clinical Pharmacology and Toxicology, Vol. 105, No. s1, TP23, 2009, p. 90.

Research output: Contribution to journalMeeting AbstractResearchpeer-review

TY - JOUR

T1 - What Did ‘Safe’ Mean To Prescribes Of Selective Cox-2 Inhibitors?

AU - McGettigan, Patricia

AU - Peel, Roseanne

AU - Stokes, Barrie J.

AU - Henderson, Kim M.

AU - Whitaker, Diana

AU - Henry, David A

PY - 2009

Y1 - 2009

N2 - Introduction: Among vulnerable individuals, cyclo-oxygenase-2(COX-2) inhibition increases the risk of cardiovascular thromboticevents. Promotional safety messages led to ‘channeling’ of selectiveCOX-2 inhibitors to individuals with gastrointestinal risks.Aims: We investigated whether this was associated with inappropriatechanneling of COX-2 inhibitors to patients at risk of cardiovascular events.Methods: Case–control study, August 2003–October 2006. Cases:patients admitted to hospital with acute coronary syndrome (ACS, myocardial infarction/unstable angina) (n = 814). Controls:Patients admitted for reasons other than acute vascular ischaemia, heartfailure, renal failure, or upper gastro-intestinal ulceration/bleeding(n = 1500). Structured interviews gathered information on cardiovascularevents, risk factors, and ingested drugs, including selective COX-2 inhibitors and non-selective non-steroidal anti-inflammatory drugs (NSAIDs).Controls were frequency matched to cases by age and sex. Relative riskswere estimated from exposure odds ratios (ORs), adjusted for multiplepotential confounders.Results: Among cases, 386 (47.6%) had experienced prior vascularevents; 425 reported no vascular history. In multivariate modeling, thestrongest association with ACS was a vascular history (adjusted OR 4.47(95% Confidence Interval 3.33, 6.00). However, cases with a vascularhistory were significantly less likely than those without to have usedanti-inflammatory drugs in the preceding week: OR 0.65 (0.47, 0.89).This effect was seen with non-selective NSAIDs, 0.51 (0.33, 0.79), butnot with selective COX-2 inhibitors (rofecoxib/celecoxib/diclofenac/meloxicam), 0.90 (0.60, 1.35).Conclusions: Prescribers avoided non-selective NSAIDs but not selective COX-2 inhibitors in some patients. This sidestepped gastrointestinalrisk but caused inappropriate channeling of selective COX-2 inhibitors topatients with vascular risks.

AB - Introduction: Among vulnerable individuals, cyclo-oxygenase-2(COX-2) inhibition increases the risk of cardiovascular thromboticevents. Promotional safety messages led to ‘channeling’ of selectiveCOX-2 inhibitors to individuals with gastrointestinal risks.Aims: We investigated whether this was associated with inappropriatechanneling of COX-2 inhibitors to patients at risk of cardiovascular events.Methods: Case–control study, August 2003–October 2006. Cases:patients admitted to hospital with acute coronary syndrome (ACS, myocardial infarction/unstable angina) (n = 814). Controls:Patients admitted for reasons other than acute vascular ischaemia, heartfailure, renal failure, or upper gastro-intestinal ulceration/bleeding(n = 1500). Structured interviews gathered information on cardiovascularevents, risk factors, and ingested drugs, including selective COX-2 inhibitors and non-selective non-steroidal anti-inflammatory drugs (NSAIDs).Controls were frequency matched to cases by age and sex. Relative riskswere estimated from exposure odds ratios (ORs), adjusted for multiplepotential confounders.Results: Among cases, 386 (47.6%) had experienced prior vascularevents; 425 reported no vascular history. In multivariate modeling, thestrongest association with ACS was a vascular history (adjusted OR 4.47(95% Confidence Interval 3.33, 6.00). However, cases with a vascularhistory were significantly less likely than those without to have usedanti-inflammatory drugs in the preceding week: OR 0.65 (0.47, 0.89).This effect was seen with non-selective NSAIDs, 0.51 (0.33, 0.79), butnot with selective COX-2 inhibitors (rofecoxib/celecoxib/diclofenac/meloxicam), 0.90 (0.60, 1.35).Conclusions: Prescribers avoided non-selective NSAIDs but not selective COX-2 inhibitors in some patients. This sidestepped gastrointestinalrisk but caused inappropriate channeling of selective COX-2 inhibitors topatients with vascular risks.

U2 - 10.1111/j.1742-7843.2009.00437.x

DO - 10.1111/j.1742-7843.2009.00437.x

M3 - Meeting Abstract

VL - 105

SP - 90

JO - Pharmacology and Toxicology

JF - Pharmacology and Toxicology

SN - 0901-9928

IS - s1

M1 - TP23

ER -