Gwen Sascha Fernandes

Long-term persistence and adherence on urate-lowering treatment can be maintained in primary care-5-year follow-up of a proof-of-concept study

Objectives. To evaluate the persistence and adherence on urate‐lowering treatment (ULT) in primary care 5 years after an initial nurse‐led treatment of gout. Methods. One hundred gout patients initiated on up‐titrated ULT between March and July 2010 were sent a questionnaire that elicited information on current ULT, reasons for discontinuation of ULT if applicable, medication adherence and generic and disease‐specific quality‐of‐life measures in 2015. They were invited for one visit at which height and weight were measured and blood was collected for serum uric acid measurement. Results. Seventy‐five patients, mean age 68.13 years (s.d. 10.07) and disease duration 19.44 years (s.d. 13), returned completed questionnaires. The 5‐year persistence on ULT was 90.7% (95% CI 81.4, 91.6) and 85.3% of responders self‐reported taking ULT ≥6 days/week. Of the 65 patients who attended the study visit, the mean serum uric acid was 292.8 &mgr;mol/l (s.d. 97.2). Conclusion. An initial treatment that includes individualized patient education and involvement in treatment decisions results in excellent adherence and persistence on ULT >4 years after the responsibility of treatment is taken over by the patients general practitioner, suggesting that this model of gout management should be widely adopted.

Cardiovascular disease and osteoarthritis: common pathways and patient outcomes.

Osteoarthritis (OA) and cardiovascular disease (CVD) are the two most prevalent conditions in the population aged over 70 in developed countries. Both conditions share common risk factors, in particular age and body mass index. However, the very high level of co‐occurrence of both diseases cannot be accounted by common risk factors alone.

Prevalence of knee pain, radiographic osteoarthritis and arthroplasty in retired professional footballers compared with men in the general population: a cross-sectional study

Objectives To determine the prevalence of knee pain, radiographic knee osteoarthritis (RKOA), total knee replacement (TKR) and associated risk factors in male ex-professional footballers compared with men in the general population (comparison group). Methods 1207 male ex-footballers and 4085 men in the general population in the UK were assessed by postal questionnaire. Current knee pain was defined as pain in or around the knees on most days of the previous month. Presence and severity of RKOA were assessed on standardised radiographs using the Nottingham Line Drawing Atlas (NLDA) in a subsample of 470 ex-footballers and 491 men in the comparison group. The adjusted risk ratio (aRR) and adjusted risk difference (aRD) with 95% CI in ex-footballers compared with the general population were calculated using the marginal model in Stata. Results Ex-footballers were more likely than the comparison group to have current knee pain (aRR 1.91, 95% CI 1.77 to 2.06), RKOA (aRR 2.21, 95% CI 1.92 to 2.54) and TKR (aRR 3.61, 95% CI 2.90 to 4.50). Ex-footballers were also more likely to present with chondrocalcinosis (aRR 3.41, 95% CI 2.44 to 4.77). Prevalence of knee pain and RKOA were higher in ex-footballers at all ages. However, even after adjustment for significant knee injury and other risk factors, there was more than a doubling of risk of these outcomes in footballers. Conclusions The prevalence of all knee osteoarthritis outcomes (knee pain, RKOA and TKR) were two to three times higher in male ex-footballers compared with men in the general population group. Knee injury is the main attributable risk factor. Even after adjustment for recognised risk factors, knee osteoarthritis appear to be an occupational hazard of professional football.

Use of prescription analgesic medication and pain catastrophizing after total joint replacement surgery

OBJECTIVE To survey the use of analgesic medication 4.8 years after total joint replacement (TJR) surgery and assess the determinants of medication usage. PATIENTS AND METHODS Of 852 patients who had undergone TJR for osteoarthritis were recruited from secondary care. Participants (mean age, 73.7 years) responded to a questionnaire on medication use, physical function and pain (WOMAC, VAS and body pain), pain catastrophizing and illness behaviour (somatization). RESULTS Only 37% of study participants were not on any pain relief medication, 25.1% were taking opioids, 6.9% were taking prescription NSAIDs and 25.9% were taking only non-prescription analgesics. Use of NSAIDs correlated with presence of back pain, body pain and high illness behaviour. The strongest associations with use of opioids were severe joint pain, high pain catastrophizing, body and back pain. After adjustment for covariates plus presence of pain, catastrophizing remained significantly associated with higher risk of opioid use (OR = 1.66, 95% CI: 1.13-2.43, p < 0.009) and of other prescription medication that can be used to treat pain (anti-depressants, anti-epileptics and hypnotics) (OR = 2.52, 95% CI: 1.61-3.95, p < 0.0005). CONCLUSIONS Use of opioid medication 4 years post-TJR is very high in our study population. In addition to joint, back and body pain, a major contributor to opioid use is pain catastrophizing. Our data suggest that current opioid and other analgesic prescribing patterns may benefit from considering the catastrophizing characteristics of patients.

Traits associated with central pain augmentation in the Knee Pain in the Community (KPIC) cohort

Abstract This study aimed to identify self-report correlates of central pain augmentation in individuals with knee pain. A subset of participants (n = 420) in the Knee Pain and related health In the Community (KPIC) baseline survey undertook pressure pain detection threshold (PPT) assessments. Items measuring specific traits related to central pain mechanisms were selected from the survey based on expert consensus, face validity, item association with underlying constructs measured by originating host questionnaires, adequate targeting, and PPT correlations. Pain distribution was reported on a body manikin. A “central pain mechanisms” factor was sought by factor analysis. Associations of items, the derived factor, and originating questionnaires with PPTs were compared. Eight self-report items measuring traits of anxiety, depression, catastrophizing, neuropathic-like pain, fatigue, sleep disturbance, pain distribution, and cognitive impact were identified as likely indices of central pain mechanisms. Pressure pain detection thresholds were associated with items representing each trait and with their originating scales. Pain distribution classified as “pain below the waist additional to knee pain” was more strongly associated with low PPT than were alternative classifications of pain distribution. A single factor, interpreted as “central pain mechanisms,” was identified across the 8 selected items and explained variation in PPT (R2 = 0.17) better than did any originating scale (R2 = 0.10-0.13). In conclusion, including representative items within a composite self-report tool might help identify people with centrally augmented knee pain.

First validation of the gout activity score against gout impact scale in a primary care based gout cohort

OBJECTIVES To validate the gout activity score (GAS) against the gout impact scale in a primary care based gout cohort. METHODS This was a single-centre cross-sectional study. People with gout who participated in previous research at academic rheumatology, University of Nottingham, UK, and consented for participation in future studies were mailed a questionnaire in September 2015. Those returning completed questionnaires were invited to attend for a study visit at which blood was collected and musculoskeletal examination was performed. The Gout Assessment Questionnaire, which contains the gout impact scale (GIS), and short form (SF) 36v2 questionnaires were completed. The GAS3-step-c score was calculated. Spearmans correlation coefficient was calculated to examine correlation between GAS and SF-36 v2, and GIS. Statistical analyses were performed using PASW v22. RESULTS One hundred and two (93% men) of the 150 participants who were mailed a questionnaire attended the study visit. Their mean (SD) age, body mass index, serum uric acid and GAS were 67.94 (9.93) years, 29.96 (4.57) kg/m2, 5.25 (1.75) mg/dl, and 2.99 (0.74) respectively. There was moderate correlation between GAS and gout concern overall, unmet gout treatment need, and gout concern during an attack components of GIS (r=0.306 to 0.453), but no to poor correlation between GAS and summary scores and scales of SF-36 v2 (r=-0.090 to -0.251). CONCLUSION This first study to validate GAS against the GIS found moderate correlation. However, this study did not examine the predictive validity of GAS, and prospective studies are needed before GAS can be used widely.

Contribution of central and peripheral risk factors to prevalence, incidence and progression of knee pain: a community-based cohort study

Summary Aim To explore risk factors that may influence knee pain (KP) through central or peripheral mechanisms. Methods A questionnaire-based prospective community cohort study with KP defined as pain in or around a knee on most days for at least a month. Baseline prevalence, and one year incidence and progression (KP worsening) were examined. Central (e.g., Pain Catastrophizing Scale (PCS)) and peripheral (e.g., significant injury) risk factors were examined. Adjusted odds ratio (OR) and 95% confidence interval (CI) were calculated using logistic regression. Proportional risk contribution (PRC) was estimated using receiver-operator-characteristic (ROC) analysis. Results Of 9506 baseline participants, 4288 (45%) had KP (men 1826; women, 2462). KP incidence was 12% (men 11%, women 13%), and KP progression 19% (men 16%, women 21%) at one year. While both central and peripheral factors contributed to prevalence, central factors contributed more to progression, and peripheral factors more to incidence of KP. For example, although PCS (OR 2.06, 95% CI 1.88–2.25) and injury (5.62, 4.92–6.42) associated with KP prevalence, PCS associated with progression (2.27, 1.83–2.83) but not incidence (1.14, 0.86–1.52), whereas injury more strongly associated with incidence (69.27, 24.15–198.7) than progression (2.52, 1.48–4.30). The PRC of central and peripheral factors were 19% and 23% for prevalence, 14% and 29% for incidence, and 29% and 5% for progression, respectively. Conclusions Both central and peripheral risk factors influence KP but relative contributions may differ in terms of development (mainly peripheral) and progression (mainly central). Further study of such relative contributions may inform primary and secondary prevention strategies.

Professional Football Participation and Mortality

Professional Football Participation and Mortality To t h e Ed i t o r The retrospective cohort study by Dr Venkataramani and colleagues1 found a hazard ratio (HR) for mortality in career National Football League (NFL) players compared with NFL replacement players following NFL retirement of 1.38 (95% CI, 0.95-1.99); P = .09. First, the main conclusion of the authors and editorialists2 was that there was no statistically significant difference in mortality between the 2 groups. The American Statistical Association has warned against interpreting scientific significance using a statistical threshold because of the myriad factors influencing precision of estimates.3 In this case, the study was insufficiently powered to detect a relative mortality hazard less than 1.4.1 The result is an underestimate of a potentially clinically meaningful finding. To put this finding into context, this HR is similar to the association between physical inactivity (HR, 1.43 [95% CI,1.34-1.53]) or hypertension (HR, 1.38 [95% CI, 1.30-1.46]) and mortality.4 Second, we have concerns regarding the study design. Venkataramani and colleagues1 made use of a natural experiment, an often powerful design in observational studies, and compared career NFL players with NFL replacement players, the latter of whom played in the league for a limited time during a strike. The authors suggested this design better isolated the effect of playing in the NFL because replacement players are capable of playing professionally and thus are otherwise similar to career players. However, the NFL replacement players may be a diverse group. For many, their general mortality risk factors, such as income, diet, and exercise, may diverge considerably from those of career NFL players. On the other hand, some NFL replacement players may have more similar exposure to league-specific factors (eg, repeated head trauma) than the study suggested because of ongoing participation in football in other leagues. Thus, the study findings may be biased away from the null (in the case of general mortality risk factors) or toward the null (in the case of league-specific risk factors). Third, the larger issue is whether isolating the effect of playing in the NFL is a useful approach. Prevailing hypotheses about the effects of head trauma posit that it is the accumulation of repeated traumas that is most consequential for health.5 As such, the real question is whether increased longevity of playing American football, rather than playing in the NFL per se, is associated with mortality or other health outcomes.