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Abstract Number: 1986

Colchicine Use and The Risk Of Myocardial Infarction Among Gout Patients: Results From a Community-Based, Informatics-Driven Retrospective Cohort Study

Daria B. Crittenden1, Binita Shah2, Steven P. Sedlis2, Christopher J. Swearingen3, Eric S. Wagner4, Yvette M. Henry4, Peter B. Berger4, Bruce N. Cronstein1 and Michael H. Pillinger5, 1Internal Medicine, NYU School of Medicine, Division of Rheumatology, New York, NY, 2NYU School of Medicine, Division of Cardiology, New York, NY, 3Pediatric Biostatistics, University of Arkansas for Medical Sciences, Little Rock, AR, 4Geisinger Health System, Cardiovascular Center for Clinical Research, Danville, PA, 5NYU School of Medicine, Division of Rheumatology, New York, NY

Meeting: 2013 ACR/ARHP Annual Meeting

Keywords: Cardiovascular disease, Co-morbidities, Colchicine, Gout and inflammation

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Session Information

Title: Metabolic and Crystal Arthropathies II

Session Type: Abstract Submissions (ACR)

Background/Purpose: Gout patients have an increased risk of myocardial infarction (MI). Since atherosclerosis and plaque rupture are inflammatory processes, anti-inflammatory gout medications might also reduce MI. Colchicine inhibits inflammatory cells implicated in gout and MI; our prior study suggests that colchicine might reduce MI in gout patients (Crittenden, J Rheum 2012). To further assess the effect of colchicine on risk of MI, we performed a retrospective cohort study of patients in the Geisinger Health System, a large community-based health care system.

Methods: We analyzed Geisinger’s electronic records and identified all patients in the Geisinger Health Plan with ICD-9 codes for gout on at least two different encounters between 2001-12. Patients were separated into 2 groups: chronic (> 30 days; n=628) and no colchicine (controls; n=2436) use. Patients with > 0 but ≤ 30 days of use were excluded from analysis. For patients in each cohort, we set the index date as 1st colchicine use or 1st gout diagnosis date (colchicine and controls, respectively). For colchicine users, we defined a colchicine lapse as any period of non-use ≥ 2 weeks after medication cessation, to account for the kinetics of colchicine elimination. The primary outcome was MI during the study period. Demographic and baseline clinical features were compared between the 2 groups using equivalence tests (20% margin). Difference in frequency of MI between groups was estimated using Chi-square test and logistic regression adjusting for age, diabetes, heart failure, prior MI, and length of follow-up. 

Results: Of the 3064 patients who met the inclusion criteria, 2316 (76%) were male and 3010 (98%) were white. The 2 groups were equivalent with regard to age, sex, hypertension, hyperlipidemia, allopurinol use (45 vs 43%), and mean serum urate (7.8 vs 8.0 mg/dL). Forty-eight MIs were reported during the study period; 35 (1.4%) in the control group vs 5 (0.8%) among active colchicine users (OR=1.78, P=0.22), and 8 (1.3%) during colchicine lapse or after its final discontinuation. The odds of MI were larger in the control vs colchicine group using logistic regression, though the effect lessened over time (OR at 6 months = 2.29 [P=0.263] at 2 years = 1.35 [P=0.609]). In contrast, the MI incident rate/1000 person-years of exposure was higher in the colchicine group (6.3 vs 2.3, P=0.064), probably relating to a much longer follow-up (i.e. denominator) for the control group (14,996 vs 796 person-years). Among colchicine users overall, the incidence rate of MI during periods of active use was lower than during lapse periods (6.3 vs 11.2/1000 person-years [P=0.324]).  

Conclusion: Active colchicine users demonstrated trends toward a reduced incidence of MI and reduced odds of MI in the first 2 years of observation vs controls. Colchicine users also had a reduced risk of MI during periods of active use vs lapse. In contrast, MI person-year incidence rate was higher among the colchicine users vs controls, possibly a consequence of the much longer observation period in the control group. Overall, the number of MI events was unexpectedly low, limiting our ability to draw conclusions; additional studies are needed to clarify the potential cardioprotective effect of colchicine.


Disclosure:

D. B. Crittenden,
None;

B. Shah,

Takeda Pharmaceuticals,

2,

Guerbet,

2;

S. P. Sedlis,
None;

C. J. Swearingen,
None;

E. S. Wagner,
None;

Y. M. Henry,
None;

P. B. Berger,
None;

B. N. Cronstein,

Canfite Pharma,

1,

NIH, Gilead, Takeda, AstraZeneca,

2,

NYU School of Medicine,

3,

Merck-SeronoBristol-Myers Squibb, Novartis, CanFite Biopharmaceuticals, Cypress Laboratories, Regeneron (Westat, DSMB), Endocyte, Protalex, Allos, Inc., Savient, Gismo Therapeutics, Antares Pharmaceutical, Medivector,

5,

Multiple patents on adenosine receptors and bone metabolism, pharmacology,

9;

M. H. Pillinger,

Takeda Pharmaceuticals,

2,

Savient Pharmaceuticals,

2.

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