Session Title: Metabolic and Crystal Arthropathies I
Session Type: Abstract Submissions (ACR)
Background/Purpose: Gout patients are at increased cardiovascular (CV) risk. Since atherosclerosis is an inflammatory process, anti-inflammatory strategies to reduce CV risk are currently being investigated. The anti-inflammatory colchicine is commonly used in gout, and inhibits cell types implicated in atherosclerosis. Our preliminary data suggest that colchicine may reduce myocardial infarction (MI) among gout patients (Crittenden et al, J Rheum 2012). To further assess colchicine’s possible effect on MI risk, we initiated a retrospective cohort study in a Veterans Affairs population and here present an interim analysis.
Methods: We identified all active NY Harbor VA patients with an ICD-9 code for gout or hyperuricemia from 2000-09. Charts were manually screened to confirm gout diagnosis (ACR criteria) and pharmacy records were used to identify subjects on daily colchicine for ≥ 30 days (colchicine group). Subjects receiving no colchicine formed the control group. We excluded patients who did not meet gout criteria, or who received PRN colchicine only. We defined colchicine lapse as any period of non-colchicine use ≥ 2 weeks after medication cessation (to account for colchicine elimination time). Primary outcome was MI (adjudicated by universal criteria) during the study period.
Results: 7819 subjects had requisite ICD-9 codes. 4486 charts have been reviewed to date; 844 patients met ACR gout criteria and 644 were enrolled. 410 subjects (64%) used colchicine (1184 person-years of active use and 682 person-years of lapse); 234 (36%) used no colchicine (1041 person-years of follow-up). Colchicine and control groups did not differ in baseline characteristics including gender (99.3 vs 97.4% male, p=0.08); age (66 vs 67 years, p=0.3); BMI (30.5 vs 30.2, p=0.7); uric acid level (8.4 vs 8.0 mg/dL, p=0.1); hypertension (80 vs 81%, p=0.9); diabetes (30 vs 30% p=1.0); hyperlipidemia (51 vs 43%, p=0.06); coronary artery disease (24 vs 26%, p= 0.6); and medication use including allopurinol (22 vs 20%, p=0.1); aspirin (30 vs 32%, p=0.7); statins (41 vs 39%, p=0.5); ACE-inhibitors (48 vs 42%, p=0.1); and beta-blockers (41 vs 34%, p=0.1). Colchicine users experienced 11 total MIs—8 occurring during lapse time (2%) and 3 during active use (0.7%). Control patients had 7 MIs (3%; active colchicine vs control p=0.04). The shortest time from last colchicine use to MI was 2 months (mean 4 months). We also compared rates of MI per person-year exposure to colchicine (0.003), control (0.007), lapse (0.012), and pooled control+lapse (0.009) periods, and observed significant differences between colchicine active use vs lapse (p=0.02), and vs lapse+control (p=0.04). Active colchicine use vs control was not statistically different (p=0.16), but is expected to reach significance if the current rates persist through the remaining data collection.
Conclusion: In this interim analysis, gout patients actively taking colchicine had a significantly reduced incidence of MI vs never-users, and significantly reduced person-year incidence rates vs lapse patients and vs a pooled group of patients not on colchicine. These data suggest that colchicine protects against MI, though probably only during active use. Evaluation of the remaining 3333 patients is ongoing.
D. B. Crittenden,
J. N. Kimmel,
V. C. Pike,
C. J. White,
C. J. Swearingen,
J. D. Greenberg,
S. P. Sedlis,
C. T. Tenner,
B. N. Cronstein,
NIH, Gilead, Takeda, AstraZeneca,
NYU School of Medicine,
Merck-SeronoBristol-Myers Squibb, Novartis, CanFite Biopharmaceuticals, Cypress Laboratories, Regeneron (Westat, DSMB), Endocyte, Protalex, Allos, Inc., Savient, Gismo Therapeutics, Antares Pharmaceutical, Medivector,
Multiple patents on adenosine receptors and bone metabolism, pharmacology,
M. H. Pillinger,
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ACR Meeting Abstracts - https://acrabstracts.org/abstract/colchicine-use-and-the-risk-of-myocardial-infarction-among-gout-patients-interim-results-from-a-va-retrospective-cohort-study/