Table 2.
Association between statin use and prevalence of OA phenotypes in the GOAL study
Adjusted for age, sex, BMI | Adjusted for additional covariates | |||||
---|---|---|---|---|---|---|
OR* | 95% CI | p Value | OR† | 95% CI | p Value | |
Nodal OA | 1.11 | (0.59 to 2.09) | 0.74 | 1.04 | (0.53 to 2.05) | 0.91 |
Hip OA | 0.98 | (0.70 to 1.38) | 0.93 | 1.00 | (0.68 to 1.48) | 0.99 |
Knee OA | 1.32 | (0.99 to 1.75) | 0.06 | 1.27 | (0.91 to 1.77) | 0.15 |
Knee and hip OA | 1.04 | (0.75 to 1.43) | 0.83 | 0.92 | (0.63 to 1.34) | 0.66 |
Generalised hip OA | 0.85 | (0.52 to 1.38) | 0.51 | 0.80 | (0.47 to 1.35) | 0.40 |
Generalised knee OA | 0.91 | (0.59 to 1.41) | 0.67 | 0.79 | (0.46 to 1.35) | 0.40 |
Generalised knee and hip OA | 0.66 | (0.42 to 1.01) | 0.06 | 0.63 | (0.38 to 1.04) | 0.07 |
All generalised OA | 0.75 | (0.59 to 0.94) | 0.012 | 0.76‡ | (0.59 to 0.97) | 0.028 |
*OR=OR for association between statin use and OA. Association was assessed by logistic regression, with hip OA, knee OA or generalised OA being the outcome variables, statin use (yes/no) the independent variable, and including age, sex and Body Mass Index (BMI), as covariates.
†Further adjustment for a diagnosis of hypertenstion or any form of cardiovascular comorbidity, smoking (never smoked=0, ex-smoker=1, current smoker=2) and use of pain medication was also performed.
‡Additional adjustment for stroke, kidney disease, type 2 diabetes, and years with pain at the target joint OR=0.77 (0.60 to 0.99) p<0.048.
GOAL, genetics of OA and lifestyle; OA, osteoarthritis.
Bold font indicates a statistically significant (p<0.05) result.