Objective To determine the independent associations of antihypertensive drugs with the risk of incident gout among people with hypertension.Design Nested case-control study.Setting UK general practice database, 2000-7.Participants All incident cases of gout (n=24 768) among adults aged 20-79 and a random sample of 50 000 matched controls.Main outcome measure Relative risk of incident gout associated with use of antihypertensive drugs.Results After adjusting for age, sex, body mass index, visits to the general practitioner, alcohol intake, and pertinent drugs and comorbidities, the multivariate relative risks of incident gout associated with current use of antihypertensive drugs among those with hypertension (n=29 138) were 0.87 (95% confidence interval 0.82 to 0.93) for calcium channel blockers, 0.81 (0.70 to 0.94) for losartan, 2.36 (2.21 to 2.52) for diuretics, 1.48 (1.40 to 1.57) for β blockers, 1.24 (1.17 to 1.32) for angiotensin converting enzyme inhibitors, and 1.29 (1.16 to 1.43) for non-losartan angiotensin II receptor blockers. Similar results were obtained among those without hypertension. The multivariate relative risks for the duration of use of calcium channel blockers among those with hypertension were 1.02 for less than one year, 0.88 for 1-1.9 years, and 0.75 for two or more years and for use of losartan they were 0.98, 0.87, and 0.71, respectively (both P<0.05 for trend).Conclusions Compatible with their urate lowering properties, calcium channel blockers and losartan are associated with a lower risk of incident gout among people with hypertension. By contrast, diuretics, β blockers, angiotensin converting enzyme inhibitors, and non-losartan angiotensin II receptor blockers are associated with an increased risk of gout.

Objectives To evaluate the risk of myocardial infarction and death from coronary heart disease after discontinuation of low dose aspirin in primary care patients with a history of cardiovascular events. Design Nested case-control study. Setting The Health Improvement Network (THIN) database in the United Kingdom. Participants Individuals aged 50-84 with a first prescription for aspirin (75-300 mg/day) for secondary prevention of cardiovascular outcomes in 2000-7 (n=39 513). Main outcome measures Individuals were followed up for a mean of 3.2 years to identify cases of non-fatal myocardial infarction or death from coronary heart disease. A nested case-control analysis assessed the risk of these events in those who had stopped taking low dose aspirin compared with those who had continued treatment. Results There were 876 non-fatal myocardial infarctions and 346 deaths from coronary heart disease. Compared with current users, people who had recently stopped taking aspirin had a significantly increased risk of non-fatal myocardial infarction or death from coronary heart disease combined (rate ratio 1.43, 95% confidence interval 1.12 to 1.84) and non-fatal myocardial infarction alone (1.63, 1.23 to 2.14). There was no significant association between recently stopping low dose aspirin and the risk of death from coronary heart disease (1.07, 0.67 to 1.69). For every 1000 patients, over a period of one year there were about four more cases of non-fatal myocardial infarction among patients who discontinued treatment with low dose aspirin (recent discontinuers) compared with patients who continued treatment. Conclusions Individuals with a history of cardiovascular events who stop taking low dose aspirin are at increased risk of non-fatal myocardial infarction compared with those who continue treatment.

Background Recent hospital-based studies have suggested a sixfold increased risk of pulmonary embolism (PE) in rheumatoid arthritis (RA) in the year following admission. We evaluated the risk of PE and deep vein thrombosis (DVT) and associated time trend among RA patients (84.5% without a history of hospitalisation during the past year) derived from the general population. Methods We conducted a cohort study using an electronic medical records database representative of the UK general population, collected from 1986 to 2010. Primary definitions of the RA cohort (exposure) and PE/DVT outcomes required physician diagnoses followed by corresponding treatments. We estimated relative risks (RRs) of PE and DVT compared with a matched non-RA comparison cohort, adjusting for age, sex, smoking, body mass index, comorbidities and hospitalisations. Results Among 9589 individuals with RA (69% female, mean age of 58 years), 82 developed PE and 110 developed DVT (incidence rates, 1.5 and 2.1 per 1000 person-years). Compared with non-RA individuals (N=95 776), the age-, sex- and entry-time-matched RRs were 2.23 (95% CI 1.75 to 2.86) for PE and 2.20 (CI 1.78 to 2.71) for DVT. Adjusting for other covariates, the corresponding RRs were 2.16 (CI 1.68 to 2.79) and 2.16 (CI 1.74 to 2.69). The time-specific RRs for PE were 3.27, 1.88 and 2.35 for follow-up times of <1 year, 1–4.9 years, and ≥5 years, and corresponding RRs for DVT were 3.16, 1.82 and 2.32. Conclusions This population-based study indicates an increased risk of PE and DVT in RA, supporting increased monitoring of venous-thromboembolic complications and risk factors in RA, regardless of hospitalisation.

Introduction: The objective of this study was to investigate the contemporary incidence of gout, examine potential risk factors, and evaluate specific gout treatment patterns in the general population. Methods: Using the health improvement network (THIN) UK primary care database, we estimated the incidence of gout based on 24,768 newly diagnosed gout patients among a cohort of 1,775,505 individuals aged 20 to 89 years between 2000 and 2007. We evaluated potential risk factors for incident gout in a nested case-control study with 50,000 controls frequency-matched by age, sex and calendar time. We calculated odds ratios (OR) by means of unconditional logistic regression adjusting for demographic variables, lifestyle variables, relevant medical conditions and drug exposures. Results: The incidence of gout per 1,000 person-years was 2.68 (4.42 in men and 1.32 in women) and increased with age. Conventional risk factors were significantly and strongly associated with the risk of gout, with multivariate ORs of 3.00 (95% confidence interval (CI)) for excessive alcohol intake (that is, more than 42 units per week), 2.34 (95% CI 2.22 to 2.47) for obesity (body mass index > = 30 kg/m²), 2.48 (95% CI 2.19 to 2.81) for chronic renal impairment, and 3.00 (95% CI 2.85 to 3.15) for current diuretic use. For other medical conditions the multivariate OR were 1.84 (95% CI 1.70 to 2.00) for heart failure, 1.45 (95% CI 1.18 to 1.79) for hypertriglyceridemia and 1.12 (95% CI 1.04 to 1.22) for psoriasis. Use of cyclosporine was associated with an OR of 3.72 (95% CI, 2.17 to 6.40). Among gout-specific therapies, allopurinol was the most frequently used with a one-year cumulative incidence of 28% in a cohort of incident gout diagnosed from 2000 to 2001. Use of gout-specific treatment has not changed over recent years except for an increase of colchicine. Conclusions: The contemporary incidence of gout in UK remains substantial. In this general population cohort, associations with previously purported risk factors were evident including psoriasis, heart failure, hypertriglyceridemia, and cyclosporine therapy. Use of gout-specific treatment has remained relatively constant in recent years except for an increase of colchicine.

Objective. So far, few data are available to characterize the flare history of patients with gout. The objective of this study was to describe the frequency and risk factors of gout flares with special consideration of the comorbidity. Methods. A cohort study was conducted in a UK general practice database (The Health Improvement Network) including all patients aged 20–89 years diagnosed with incident gout between the years 2000 and 2007. Results. In this study, 23 857 incident gout patients (mean age 61.9 years) were included, overall incidence rate was 2.68 (95% CI 2.65, 2.72) per 1000 person-years. The proportion of patients with at least one flare during the follow-up period (mean 3.8 years) was 36.9% (n = 8806). A history of ischaemic heart disease [hazard ratio (HR) 1.12 (95% CI 1.06, 1.19)], hypertension [HR 1.15 (95% CI 1.10, 1.20)] and renal failure [HR 1.33 (95% CI 1.20, 1.48)] were independently associated with a higher risk of a first gout flare. Use of allopurinol at initial gout diagnosis was associated with a lower risk [HR 0.80 (95% CI 0.75, 0.85)]. Conclusions. Gout flares are relatively common among patients with gout. Some of the underlying cardiometabolic comorbid conditions are themselves independent risk factors for flares, which further contribute to the complexity of treatment of gout flares.