Background Audit and feedback continues to be widely used as a strategy to improve professional practice. It appears logical that healthcare professionals would be prompted to modify their practice if given feedback that their clinical practice was inconsistent with that of their peers or accepted guidelines. Yet, audit and feedback has not been found to be consistently effective. Objectives To assess the effects of audit and feedback on the practice of healthcare professionals and patient outcomes. Search strategy We searched the Cochrane Effective Practice and Organisation of Care Group's register up to January 2001. This was supplemented with searches of MEDLINE and reference lists, which did not yield additional relevant studies. Selection criteria Randomised trials of audit and feedback (defined as any summary of clinical performance over a specified period of time) that reported objectively measured professional practice in a healthcare setting or healthcare outcomes. Data collection and analysis Two reviewers independently extracted data and assessed study quality. Quantitative (meta-regression), visual and qualitative analyses were undertaken. Main results We included 85 studies, 48 of which have been added to the previous version of this review. There were 52 comparisons of dichotomous outcomes from 47 trials with over 3500 health professionals that compared audit and feedback to no intervention. The adjusted RDs of non-compliance with desired practice varied from 0.09 (a 9% absolute increase in non-compliance) to 0.71 (a 71% decrease in non-compliance) (median = 0.07, inter-quartile range = 0.02 to 0.11). The one factor that appeared to predict the effectiveness of audit and feedback across studies was baseline non-compliance with recommended practice. Reviewer's conclusions Audit and feedback can be effective in improving professional practice. When it is effective, the effects are generally small to moderate. The absolute effects of audit and feedback are more likely to be larger when baseline adherence to recommended practice is low.

Audit and feedback: effects on professional practice and healthcare outcomes

In this randomized, double-blind, placebo-controlled trial, 1065 patients were assigned to receive yearly intravenous zoledronic acid (at a dose of 5 mg), and 1062 patients were assigned to receive placebo. The infusions were first administered within 90 days after surgical repair of a hip fracture. All patients (mean age, 74.5 years) received supplemental vitamin D and calcium. The median follow-up was 1.9 years. The primary end point was a new clinical fracture. Results The rates of any new clinical fracture were 8.6% in the zoledronic acid group and 13.9% in the placebo group, a 35% risk reduction with zoledronic acid (P = 0.001); the respective rates of a new clinical vertebral fracture were 1.7% and 3.8% (P = 0.02), and the respective rates of new nonvertebral fractures were 7.6% and 10.7% (P = 0.03). In the safety analysis, 101 of 1054 patients in the zoledronic acid group (9.6%) and 141 of 1057 patients in the placebo group (13.3%) died, a reduction of 28% in deaths from any cause in the zoledronic acid group (P = 0.01). The most frequent adverse events in patients receiving zoledronic acid were pyrexia, myalgia, and bone and musculoskeletal pain. No cases of osteonecrosis of the jaw were reported, and no adverse effects on the healing of fractures were noted. The rates of renal and cardiovascular adverse events, including atrial fibrillation and stroke, were similar in the two groups. Conclusions An annual infusion of zoledronic acid within 90 days after repair of a low-trauma hip fracture was associated with a reduction in the rate of new clinical fractures and with improved survival. (ClinicalTrials.gov number, NCT00046254.)

/pdf/zoledronic-acid-and-clinical-fractures-and-mortality-after-3fcy691ral.pdf

Zoledronic acid and clinical fractures and mortality after hip fracture

Background
Educational meetings are widely used for continuing medical education. Previous reviews found that interactive workshops resulted in moderately large improvements in professional practice, whereas didactic sessions did not.

Objectives
To assess the effects of educational meetings on professional practice and healthcare outcomes.

Search methods
We updated previous searches by searching the Cochrane Effective Practice and Organisation of Care Group Trials Register and pending file, from 1999 to March 2006.

Selection criteria
Randomised controlled trials of educational meetings that reported an objective measure of professional practice or healthcare outcomes.

Data collection and analysis
Two authors independently extracted data and assessed study quality. Studies with a low or moderate risk of bias and that reported baseline data were included in the primary analysis. They were weighted according to the number of health professionals participating. For each comparison, we calculated the risk difference (RD) for dichotomous outcomes, adjusted for baseline compliance; and for continuous outcomes the percentage change relative to the control group average after the intervention, adjusted for baseline performance. Professional and patient outcomes were analysed separately. We considered 10 factors to explain heterogeneity of effect estimates using weighted meta-regression supplemented by visual analysis of bubble and box plots.

Main results
In updating the review, 49 new studies were identified for inclusion. A total of 81 trials involving more than 11,000 health professionals are now included in the review. Based on 30 trials (36 comparisons), the median adjusted RD in compliance with desired practice was 6% (interquartile range 1.8 to 15.9) when any intervention in which educational meetings were a component was compared to no intervention. Educational meetings alone had similar effects (median adjusted RD 6%, interquartile range 2.9 to 15.3; based on 21 comparisons in 19 trials). For continuous outcomes the median adjusted percentage change relative to control was 10% (interquartile range 8 to 32%; 5 trials). For patient outcomes the median adjusted RD in achievement of treatment goals was 3.0 (interquartile range 0.1 to 4.0; 5 trials). Based on univariate meta-regression analyses of the 36 comparisons with dichotomous outcomes for professional practice, higher attendance at the educational meetings was associated with larger adjusted RDs (P < 0.01); mixed interactive and didactic education meetings (median adjusted RD 13.6) were more effective than either didactic meetings (RD 6.9) or interactive meetings (RD 3.0). Educational meetings did not appear to be effective for complex behaviours (adjusted RD -0.3) compared to less complex behaviours; they appeared to be less effective for less serious outcomes (RD 2.9) than for more serious outcomes.

Authors' conclusions
Educational meetings alone or combined with other interventions, can improve professional practice and healthcare outcomes for the patients. The effect is most likely to be small and similar to other types of continuing medical education, such as audit and feedback, and educational outreach visits. Strategies to increase attendance at educational meetings, using mixed interactive and didactic formats, and focusing on outcomes that are likely to be perceived as serious may increase the effectiveness of educational meetings. Educational meetings alone are not likely to be effective for changing complex behaviours.

Continuing education meetings and workshops: effects on professional practice and health care outcomes

Epidemiology is the study of the distribution and determinants of disease in human populations. Over the past decade there has been considerable progress in our understanding of the fundamental descriptive epidemiology (levels of disease frequency: incidence and prevalence, comorbidity, mortality, trends over time, geographic distributions, and clinical characteristics) of the rheumatic diseases. This progress is reviewed for the following major rheumatic diseases: rheumatoid arthritis (RA), juvenile rheumatoid arthritis, psoriatic arthritis, osteoarthritis, systemic lupus erythematosus, giant cell arteritis, polymyalgia rheumatica, gout, Sjogren's syndrome, and ankylosing spondylitis. These findings demonstrate the dynamic nature of the incidence and prevalence of these conditions – a reflection of the impact of genetic and environmental factors. The past decade has also brought new insights regarding the comorbidity associated with rheumatic diseases. Strong evidence now shows that persons with RA are at a high risk for developing several comorbid disorders, that these conditions may have atypical features and thus may be difficult to diagnose, and that persons with RA experience poorer outcomes after comorbidity compared with the general population. Taken together, these findings underscore the complexity of the rheumatic diseases and highlight the key role of epidemiological research in understanding these intriguing conditions.

/pdf/epidemiological-studies-in-incidence-prevalence-mortality-4xq1rtiol6.pdf

Epidemiological studies in incidence, prevalence, mortality, and comorbidity of the rheumatic diseases

Context The risk of bacterial infection is increased in patients treated with drugs that inhibit tumor necrosis factor α (TNF-α). Little is known about the reactivation of latent viral infections during treatment with TNF-α inhibitors. Objective To investigate whether TNF-α inhibitors together as a class, or separately as either monoclonal anti–TNF-α antibodies (adalimumab, infliximab) or a fusion protein (etanercept), are related to higher rates of herpes zoster in patients with rheumatoid arthritis. Design, Setting, and Patients Patients were enrolled in the German biologics register RABBIT, a prospective cohort, between May 2001 and December 2006 at the initiation of treatment with infliximab, etanercept, adalimumab, or anakinra, or when they changed conventional disease-modifying antirheumatic drug (DMARD). Treatment, clinical status, and adverse events were assessed by rheumatologists at fixed points during follow-up. Main Outcome Measures Hazard ratio (HR) of herpes zoster episodes following anti–TNF-α treatment. Study aims were to detect a clinically significant difference (HR, 2.0) between TNF-α inhibitors as a class compared with DMARDs and to detect an HR of at least 2.5 for each of 2 types of TNF-α inhibitors, the monoclonal antibodies or the fusion protein, compared with conventional DMARDs. Results Among 5040 patients receiving TNF-α inhibitors or conventional DMARDs, 86 episodes of herpes zoster occurred in 82 patients. Thirty-nine occurrences could be attributed to treatment with anti–TNF-α antibodies, 23 to etanercept, and 24 to conventional DMARDs. The crude incidence rate per 1000 patient-years was 11.1 (95% confidence interval [CI], 7.9-15.1) for the monoclonal antibodies, 8.9 (95% CI, 5.6-13.3) for etanercept, and 5.6 (95% CI, 3.6-8.3) for conventional DMARDs. Adjusted for age, rheumatoid arthritis severity, and glucocorticoid use, a significantly increased risk was observed for treatment with the monoclonal antibodies (HR, 1.82 [95% CI, 1.05-3.15]), although this risk was lower than the threshold for clinical significance. No significant associations were found for etanercept use (HR, 1.36 [95% CI, 0.73-2.55]) or for anti–TNF-α treatment (HR, 1.63 [95% CI, 0.97-2.74]) as a class. Conclusion Treatment with monoclonal anti–TNF-α antibodies may be associated with increased risk of herpes zoster, but this requires further study.

https://jamanetwork.com/journals/jama/articlepdf/183405/joc90006_737_744.pdf

Risk of Herpes Zoster in Patients With Rheumatoid Arthritis Treated With Anti–TNF-α Agents

Objective

To evaluate the risk of serious bacterial infections associated with tumor necrosis factor α (TNFα) antagonists among rheumatoid arthritis (RA) patients.



Methods

A retrospective cohort study of US RA patients enrolled in a large health care organization identified patients who received either TNFα antagonists or methotrexate (MTX). Administrative data were used to identify hospitalizations with possible bacterial infections; corresponding medical records were abstracted and reviewed by infectious disease specialists for evidence of definite infections. Proportional hazards models evaluated time-dependent infection risks associated with TNFα antagonists.



Results

Hospital medical records with claims-identified suspected bacterial infections were abstracted (n = 187) among RA patients who received TNFα antagonists (n = 2,393; observation time 3,894 person-years) or MTX (n = 2,933; 4,846 person-years). Over a median followup time of 17 months, the rate of hospitalization with a confirmed bacterial infection was 2.7% among the patients treated with TNFα antagonists compared with 2.0% among the patients treated with MTX only. The multivariable-adjusted hazard ratio (HR) of infection among the patients who received TNFα antagonists was 1.9 (95% confidence interval [95% CI] 1.3–2.8) compared with patients who received MTX only. The incidence of infections was highest within 6 months after initiating TNFα antagonist therapy (2.9 versus 1.4 infections per 100 person-years; multivariable-adjusted HR 4.2, 95% CI 2.0–8.8).



Conclusion

The multivariable-adjusted risk of hospitalization with a physician-confirmed definite bacterial infection was ∼2-fold higher overall and 4-fold higher in the first 6 months among patients receiving TNFα antagonists versus those receiving MTX alone. RA patients were at increased risk of serious infections, irrespective of the method used to define an infectious outcome. Patients and physicians should vigilantly monitor for signs of infection when using TNFα antagonists, particularly shortly after treatment initiation.

Risk of serious bacterial infections among rheumatoid arthritis patients exposed to tumor necrosis factor alpha antagonists.

In a previous study by our group (1), we observed a significantly increased risk of being hospitalized with a serious bacterial infection among patients with rheumatoid arthritis (RA) who were treated with tumor necrosis factor α (TNFα) antagonists compared with patients with RA who received methotrexate (MTX). Although we showed that this risk was increased during the entire study period (median duration of followup 17 months), the risk was highest within the first 6 months after beginning treatment with the TNFα antagonist. Given our further interest in characterizing drug-specific risks, we evaluated the comparative effects of antibody-based and non–antibody-based TNFα antagonists on the risk of being hospitalized with a bacterial infection.

Extending our previously published analysis (1), we defined cohorts of patients with RA who had at least 2 International Classification of Diseases, Ninth Revision, Clinical Modification diagnosis codes for RA (714.x, excluding 714.3) and were receiving either infliximab or adalimumab, etanercept, or MTX without a TNFα antagonist. Because the number of patients receiving adalimumab (n = 118) was insufficient to permit meaningful conclusions, these patients were excluded from this analysis. All patients exposed to TNFα antagonist were new users, defined as having at least 6 months of nonexposure to these drugs prior to the first filled prescription. Patients were considered at risk of infection within 90 days of the most recent filled prescription for the drug of interest. Patients who were exposed to multiple TNFα antagonists during the same window of risk were excluded.

In a sensitivity analysis, shorter risk windows were used (i.e., 30 days for etanercept and MTX, and 60 days for infliximab). Given our previously observed increased risks within the first 6 months of starting a biologic agent, we separately considered exposure time within and beyond 6 months. Using methods previously described (1), serious bacterial infections were initially identified through administrative claims data. Following nationwide medical record abstraction of hospital records, infections were confirmed independently by infectious disease physicians who were blinded to the medication lists for each hospitalization. Incidence rates, crude and adjusted incidence rate ratios, and 95% confidence intervals were computed for patients who received infliximab and etanercept compared with those who received MTX.

Among the patients with RA who were exposed to TNFα antagonists, 850 were exposed to infliximab, and 1,412 were exposed to etanercept. The unexposed comparator cohort included 2,933 patients with RA who were treated with MTX. Etanercept users were younger (mean age 47.8 years; P <0.0001 versus MTX users) than infliximab users (mean age 53.4 years; P < 0.05 versus MTX users) and MTX users (mean age 54.9 years). Infliximab users had more physician encounters in the 6 months prior to therapy (mean 8.2; P < 0.0001 versus MTX users) compared with etanercept users (mean 7.0; P nonsignificant versus MTX users) and MTX users (mean 6.9 months). The pattern of glucocorticoid usage and burden of comorbidity were similar or greater in the unexposed cohort than in the TNFα-exposed cohorts. The absolute number of cases of bacterial infection, person-time, incidence rates, and incidence rate ratios are presented in Table 1. As shown, the incidence of a serious bacterial infection was highest during the first 6 months after initiation of a TNFα antagonist, and this finding was significant only among patients exposed to inflix-imab. There were no significantly increased risks of infection in either the infliximab or etanercept group after the first 6 months following initiation. In our sensitivity analysis using shorter exposure windows, results were similar (data not shown).



Table 1

Incidence rates, crude and adjusted incidence rate ratios, and 95% confidence intervals for bacterial infection in patients treated with infliximab and etanercept compared with MTX, according to time since initiation of TNFα antagonist treatment ...



Our results may help, in part, to explain discordance between the results of prior studies of the risk of bacterial infections associated with TNFα antagonists (1–5). Some of this discordance may result from differences in the patient populations, the methods of outcome ascertainment, use of disease-modifying antirheumatic drugs by patients who were not exposed to TNFα antagonists, and the pattern of glucocor-ticoid use. Based on our results, and adding to this list of factors that may affect associations with biologic agent—related infection, we now suggest that the proportion of individuals exposed to antibody-based TNFα antagonists and the proximity to the time of initiation of the TNFα antagonist may be important factors to consider, although further work is needed to confirm this observation.

We hypothesize that our finding of a significantly increased early risk of infection among individuals exposed to infliximab may relate to the large induction doses routinely given in the first 6 weeks of therapy, although more complex biologic mechanisms such as the ability to bind transmembrane TNF may be important as well. Parenthetically, we note that a similar differential pattern of infection risk has been observed for mycobacterial infection (6). The reduced risks of infection seen with both infliximab and etanercept after 6 months of therapy may also reflect a reduction in the number of patients who are highly susceptible to infection, whereby individuals who experience a serious infection early in the course of therapy may discontinue the drug and no longer be at risk of an infection in later time periods, resulting in a “healthier” cohort later in time. Additionally, it is possible that better control of inflammation with the use of TNFα antagonists ultimately leads to better longer-term outcomes, including a reduced risk of infection.

In summary, we observed that a significantly increased risk of infection occurred shortly after initiation of therapy with a TNFα antagonist; this risk was greatest for patients receiving infliximab, and it did not persist beyond 6 months. Although our overall results may raise concerns about how to balance safety with effectiveness for this important group of agents, this concern is tempered by the relatively low absolute incidence of infection, even within early time periods (incidence rate less than 5 infections per 100 patient-years). Moreover, TNFα antagonists have dramatic efficacy for a majority of patients with RA, and, for many, the expected benefits likely will outweigh even modestly increased risks of associated adverse events.

https://onlinelibrary.wiley.com/doi/pdf/10.1002/art.23050

Drug-specific and time-dependent risks of bacterial infection among patients with rheumatoid arthritis who were exposed to tumor necrosis factor α antagonists

Randomized Trial to Improve Fracture Prevention in Nursing Home Residents

Summary
We studied nursing home residents with osteoporosis or recent fracture to determine the frequency and predictors of osteoporosis treatment. There was wide variation in performance, and both clinical and systems variables predicted use. This study shows that improvement in osteoporosis care is possible and important for many nursing homes.

/pdf/prevalence-and-predictors-of-osteoporosis-treatment-in-2eokbe95b5.pdf

Aiyuan Xie

Papers

Risk of serious bacterial infections among rheumatoid arthritis patients exposed to tumor necrosis factor alpha antagonists.

Drug-specific and time-dependent risks of bacterial infection among patients with rheumatoid arthritis who were exposed to tumor necrosis factor α antagonists

Randomized Trial to Improve Fracture Prevention in Nursing Home Residents

Prevalence and predictors of osteoporosis treatment in nursing home residents with known osteoporosis or recent fracture.