The smoking prevalence in Europe varies from 14% in Sweden to nearly 38% in Greece.1 In the USA it is now approximately 20%, with large differences between states and according to social class and ethnic background.2 The proportions of men and women smoking is rather variable, but the relative risk of cardiovascular diseases seems to be higher in women.3 Smoking prevalence decreases with higher educational level and higher family income. Smoking is a major risk factor for lung, cardiovascular and other diseases.4 5 Smokers double their risk of having a heart attack compared with non-smokers4 and many people die from diseases related to smoking.

The effects of nicotine, like those of other drugs with the potential for abuse and dependence, are centrally mediated. The impact of nicotine on the central nervous system is neuroregulatory in nature, affecting biochemical and physiological functions in a manner that reinforces drug-taking behaviour. Dose-dependent neurotransmitter and neuroendocrine effects occur as plasma nicotine levels rise when a cigarette is smoked.6 Smokers have increased blood cholesterol levels. Smoking may also stimulate the blood clotting system in the blood, and the cardiovascular risk in smoking women using contraceptives is increased.

Cardiovascular diseases occur more frequently in people with elevated C-reactive protein.7 The link between cardiovascular and rheumatic diseases is well established, and the increased mortality of patients with rheumatoid arthritis (RA)8 is caused by cardiovascular deaths. It was shown that mortality is significantly reduced by continuous therapy with methotrexate,9 and that the risk of myocial infarction can be significantly reduced by successful anti-tumour necrosis factor therapy.10

Smoking also has an unfavourable influence on other outcomes of rheumatic diseases, and more intensive therapy is required for RA patients who smoke.11 The interaction between genetic and environmental factors is of pathogenic importance for RA.12 The presence of anticitrullinated protein antibodies is a risk factor for developing RA—especially in men who smoke.13 Of interest, nicotine must be inhaled to confer risk—smokeless tobacco did not increase the risk of chronic inflammatory diseases.14 It is largely unclear how inhaled nicotine does this.

Two independent studies15 16 show an increased risk of smoking in patients with axial spondyloarthritis and psoriatic arthritis (PsA). Recently three independent studies15,–,17 have shown an increased risk of severe disease in patients with axial spondyloarthritis and psoriatic arthritis (PsA) who are or were smokers. The results of these studies point largely in the same direction but one recent study on PsA came to a different result.18 However, earlier studies19 had also reported an increased risk conferred by smoking. The cardiovascular risk profile of patients with ankylosing spondylitis (AS) has recently been described in a meta-analysis.20 Having spondyloarthritis was found strongly to predict early coronary artery bypass grafting.21 A number of studies has shown that smoking is associated with poor outcome in patients with established AS.22,–,26 For the first time, a clear negative effect of smoking is now reported in 647 patients with early inflammatory back pain and possible spondyloarthritis.15 In that study, smoking was associated with an earlier onset of back pain, higher disease activity, worse functional status and quality of life, more frequent inflammation of the sacroilliac joints and spine as assessed by MRI, and more frequent structural lesions of the sacroilliac joints and spine as assessed by radiographs using the modified SASSS. As those patients had a short disease duration not much damage had occurred as yet.

Psoriasis is a chronic skin disease that affects 2–3% of the population. PsA, a frequent inflammatory joint condition that belongs largely to the spectrum of spondyloarthritis, affects approximately 20–25% of patients with psoriasis. The prevalence of the metabolic syndrome is high among individuals with psoriasis.27 Past association studies in patients with psoriasis28 and PsA29 have suggested a worsening effect of smoking on the disease. Now, the association between smoking status, duration and intensity of smoking and incidence of PsA has been studied in 94 874 participants from the Nurses’ Health Study II over a 14-year time period.16 During 1 303 970 person-years of follow-up, 157 incident PsA cases were identified. Among total participants, smoking was associated with an elevated risk of PsA. Compared with never smokers, the relative risk was 1.5 for past smokers and 3.1 for current smokers. With increasing smoking duration or pack-years, the risk of PsA, especially for the more severe phenotypes increased. This confirms earlier studies with similar results30 indicating comparable mechanisms in PsA and in RA.

Taken together, the interactions between environmental factors and the onset, the course and outcomes of rheumatic diseases are getting increasingly complex, and it is becoming increasingly clear how detrimental the influence of smoking is on most of these diseases. The role of rheumatologists is to inform their patients about these facts and the risks associated, and to encourage patients to quit smoking. Except in RA, the pathogenetic basis of the influence of smoking has remained largely unclear to date.

The benefits of quitting smoking begin as soon as an individual stops, and there are evaluated programmes to help give up smoking.31 However, the advantages of the cessation of smoking in patients with rheumatic diseases have not been prospectively assessed as yet.

Of note, in patients with Crohn’s disease cessation of smoking is thought to have an effect size similar to a medical intervention with azathioprine.32 Of interest, smoking causes opposing effects on ulcerative colitis and Crohn’s disease. The odds ratio of developing ulcerative colitis for smokers compared with lifetime non-smokers is thus 0.41, while smokers with Crohn’s disease have a more aggressive course of the disease.32

European League Against Rheumatism recommendations for cardiovascular risk management in patients with arthritis have recently been published.33 According to these the rheumatologist is in charge of identifying the risk of cardiovascular disease in patients with inflammatory rheumatic diseases. Who is in charge of treating that risk needs to be decided within each healthcare system. In any case, a close cooperation between the general practitioner and the rheumatologist seems warranted to achieve best patient care.

Ref:  Ann Rheum Dis. May 2012.

Objectives To investigate the association of smoking with various clinical, functional and imaging outcomes in patients with early axial spondyloarthritis (SpA).

Although the systematic measurement of disease activity facilitates clinical decision making in rheumatoid arthritis (RA), no recommendations currently exist on which measures should be applied in clinical practice in the US. The American College of Rheumatology (ACR) convened a Working Group (WG) to comprehensively evaluate the validity, feasibility, and acceptability of available RA disease activity measures and derive recommendations for their use in clinical practice.

Methods

The Rheumatoid Arthritis Clinical Disease Activity Measures Working Group conducted a systematic review of the literature to identify RA disease activity measures. Using exclusion criteria, input from an Expert Advisory Panel (EAP), and psychometric analysis, a list of potential measures was created. A survey was administered to rheumatologists soliciting input. The WG used these survey results in conjunction with the psychometric analyses to derive final recommendations.

Results

Systematic review of the literature resulted in identification of 63 RA disease activity measures. Application of exclusion criteria and ratings by the EAP narrowed the list to 14 measures for further evaluation. Practicing rheumatologists rated 9 of these 14 measures as most useful and feasible. From these 9 measures, the WG selected 6 with the best psychometric properties for inclusion in the final set of ACR-recommended RA disease activity measures.

Conclusion

We recommend the Clinical Disease Activity Index, Disease Activity Score with 28-joint counts (erythrocyte sedimentation rate or C-reactive protein), Patient Activity Scale (PAS), PAS-II, Routine Assessment of Patient Index Data with 3 measures, and Simplified Disease Activity Index because they are accurate reflections of disease activity; are sensitive to change; discriminate well between low, moderate, and high disease activity states; have remission criteria; and are feasible to perform in clinical settings.

Ref:  Arth Care Res.  May 2012.

Aromatase inhibitors are the standard of care for the treatment of most postmenopausal women with early stage hormone-receptor-positive breast cancer. 1 These drugs, in general, have a favourable side-effect profile, and are not associated with increased gynaecological or thromboembolism risks compared with selective oestrogen receptor modulators. The side-effects of aromatase inhibitors relate to the musculoskeletal system—loss of areal bone mineral density (BMD) and an increased risk of fracture …

Ref:  Lancet.  Feb 2012.

Summary

Knee-replacement surgery is frequently done and highly successful. It relieves pain and improves knee function in people with advanced arthritis of the joint. The most common indication for the procedure is osteoarthritis. We review the epidemiology of and risk factors for knee replacement. Because replacement is increasingly considered for patients younger than 55 years, improved decision making about whether a patient should undergo the procedure is needed. We discuss assessment of surgery outcomes based on data for revision surgery from national joint-replacement registries and on patient-reported outcome measures. Widespread surveillance of existing implants is urgently needed alongside the carefully monitored introduction of new implant designs. Developments for the future are improved delivery of care and training for surgeons and clinical teams. In an increasingly ageing society, the demand for knee-replacement surgery will probably rise further, and we predict future trends. We also emphasise the need for new strategies to treat early-stage osteoarthritis, which will ultimately reduce the demand for joint-replacement surgery.

Ref:  Lancet. Apr 2012.

Introduction

The purpose of this study was to compare urate-lowering (UL) efficacy and safety of daily febuxostat and allopurinol in subjects with gout and serum urate (sUA) ? 8.0 mg/dL in a six-month trial.

Methods

Subjects (n = 2,269) were randomized to febuxostat 40 mg or 80 mg, or allopurinol 300 mg (200 mg in moderate renal impairment). Endpoints included the proportion of all subjects with sUA <6.0 mg/dL and the proportion of subjects with mild/moderate renal impairment and sUA <6.0 mg/dL. Safety assessments included blinded adjudication of each cardiovascular (CV) adverse event (AE) and death.

Results

Comorbidities included: renal impairment (65%); obesity (64%); hyperlipidemia (42%); and hypertension (53%). In febuxostat 40 mg, febuxostat 80 mg, and allopurinol groups, primary endpoint was achieved in 45%, 67%, and 42%, respectively. Febuxostat 40 mg UL was statistically non-inferior to allopurinol, but febuxostat 80 mg was superior to both (P < 0.001). Achievement of target sUA in subjects with renal impairment was also superior with febuxostat 80 mg (72%; P < 0.001) compared with febuxostat 40 mg (50%) or allopurinol (42%), but febuxostat 40 mg showed greater efficacy than allopurinol (P = 0.021). Rates of AEs did not differ across treatment groups. Adjudicated (APTC) CV event rates were 0.0% for febuxostat 40 mg and 0.4% for both febuxostat 80 mg and allopurinol. One death occurred in each febuxostat group and three in the allopurinol group.

Conclusions

Urate-lowering efficacy of febuxostat 80 mg exceeded that of febuxostat 40 mg and allopurinol (300/200 mg), which were comparable. In subjects with mild/moderate renal impairment, both febuxostat doses were more efficacious than allopurinol and equally safe. At the doses tested, safety of febuxostat and allopurinol was comparable.

Ref:  Arth Res Ther.  Apr 2010.

Ref:  Ann Rheum Dis. Apr 2012.