Key Points
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Surprisingly, instances of suboptimal treatment of gout remain frequent, even in this era of expanded and well-understood treatment options. These include errors in medication use and dosages and inadequate use of the laboratory and diagnostic approaches.
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Common diagnostic and therapeutic errors include infrequent use of diagnostic joint aspiration and crystal analysis, infrequent monitoring of serum urate, and failure to achieve an adequate target level for serum urate.
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Inappropriate dosings of allopurinol and colchicine, particularly in those with renal dysfunction, are the most common medication errors.
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Higher number of outpatient visit days, more primary care or rheumatology visits, and lower comorbidities are associated with better gout care patterns.
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Efforts aimed at improving quality of care should first focus on high-risk patients such as elderly patients and those with higher comorbidity load, most severe forms of gout, and polypharmacy. Multimodal low-cost interventions are most likely to be associated with improvements that are sustainable and can be implemented in multiple health care systems.
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Data from several studies confirmed gaps in quality of care, pertaining to both treatment and laboratory monitoring and for both effectiveness and safety.
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Most significant gaps were evident in lack of monitoring of serum urate levels after starting urate-lowering therapy, failure to achieve target serum urate, use of inappropriate doses of allopurinol, and lack of use of colchicine or NSAID prophylaxis when starting allopurinol.
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These quality care gaps can be overcome by systems-based interventions, although patient- and physician-based interventions may also help.
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The quality gaps present opportunity for improvement in quality of gout care.
Grant support: This material is the result of work supported by the resources and the use of facilities at the VA Medical Center, Birmingham ,Alabama, USA.
Financial conflict: There are no financial conflicts related to this work. J.A.S. has received speaker honoraria from Abbott; research and travel grants from Allergan, Takeda, Savient, Wyeth, and Amgen; and consultant fees from Savient, URL Pharmaceuticals, and Novartis.
The views expressed in this article are those of the authors and do not necessarily reflect the position or policy of the Department of Veterans Affairs or the United States government.
Introduction
Gout, characterized by acute and chronic inflammatory arthritis, affects up to 3% to 4% of the adult population in the United States (see Chapter 6 ), with a similar prevalence in most Western countries. Furthermore, the prevalence of gout in the United States may have approximately doubled in the past 20 years with the greatest increase occurring in males that are 65 or older. Gout accounts for significant health care burden and costs. A diagnosis of gout was associated with 1.4 million outpatient visits in the United States in 2002. A recent study estimated that $27 million is spent annually for care of new acute gout cases in the United States. Thus, gout is a significant problem with public health implications.
Effective treatment options for acute and chronic gout have been available for more than half a century, yet instances of suboptimal treatment of gout remain frequent. A simulation study found that urate-lowering therapy is cost-effective in most scenarios and cost-saving in the patients with two or more acute gout attacks per year. Although new approaches are currently being developed for the treatment of gout, treating symptomatic gout with available therapies is still a major concern. Available treatment options for gout include nonsteroidal antiinflammatory drugs (NSAIDs), corticosteroids (oral, parenteral, and intraarticular), colchicine, urate-lowering medications such as allopurinol, febuxostat, and pegloticase, and uricosurics such as probenecid. With currently available therapies being effective in a majority of the patients, efficacy needs to be balanced against safety in a given patient, especially in the elderly patients with bone marrow, liver, or kidney problems. Many patients with gout continue to experience recurrent gouty attacks, which has a negative impact on health-related quality of life, function, mobility, and social roles. Thus, there is an urgent need for improving the quality of care (QOC) for patients with gout.
In this chapter, we describe the results of a systematic review of the published literature regarding compliance with evidence-based QOC indicators for gout and errors in medication use and laboratory monitoring in gout. Using the search terms “gout,” “quality of care,” “treatment guidelines,” “recommendations,” “medical errors,” and similar terms, an experienced librarian from the Cochrane musculoskeletal group (L.F.) performed a systematic search in the following databases in July 2010: (1) Ovid MEDLINE 1950 to June week 1 2010; (2) EMBASE 1980 to 2010 week 23; and (3) The Cochrane Library (including Cochrane database of systematic reviews, DARE, CENTRAL, HTA database, and NHS EED), second quarter 2010. We previously published a review of studies on QOC in gout, and several studies included in this chapter were also included in the previous review. This chapter provides an updated systematic review of studies of QOC in gout.
Definition and Measurement of Quality of Care
The Agency for Health Care Research (AHRQ) defines quality of care as the “degree to which health care services for individuals and populations increase the likelihood of desired health outcomes and are consistent with current professional knowledge.” QOC for gout has been frequently measured using quality indicators (QIs) since the description of 10 gout QIs by Mikuls et al. in 2004. These QIs for gout related to medication prescription, laboratory monitoring, and behavioral modifications were derived using evidence-based UCLA appropriateness method using a panel of rheumatologists and internists. QIs are process measures of health care quality. QIs are easily measurable since they have well-defined numerator and denominator, easily extractable from readily available health care data. Prior to description of QIs for gout, QOC was measured based on what was accepted as appropriate treatment regimens and laboratory monitoring in patients with gout. The gout QIs cover the spectrum of gout management, including both effectiveness/efficacy and safety/adverse events. Efficacy QIs consist of treatment of acute gouty arthritis, urate-lowering therapies to prevent gouty arthritis flares and damage from tophaceous deposits, behavioral modification to prevent gout and gouty flares, antiinflammatory prophylaxis during the initiation of urate-lowering therapy for the prevention of acute gouty flares, and serum urate monitoring. Safety QIs address the areas of safety related to adverse events related to use of colchicine, NSAIDs, and urate-lowering therapy.
Gout QIs are in the IF-THEN-BECAUSE format. An example of a gout QI as described by Mikuls et al. is, “ IF a gout patient is given a prescription for a xanthine oxidase inhibitor, THEN a serum urate level should be checked at least once during the first 6 months of continued use, BECAUSE periodic serum urate measurements are required for appropriate dose adjustments of xanthine oxidase inhibitors (escalations or reductions).”
Search Results
The search identified 680 articles related to the QOC in gout. Eighteen articles qualified for full text review and all were included in the summary synthesis, since there were no exclusions ( Fig. 17-1 ). Two additional articles were identified as pertinent literature not captured in the search. In this chapter, we summarize all the available data in Tables 17-1 and 17-2 and highlight key studies and findings in the narrative.
Type of Study | No. of Patients | Follow-up Duration | |
---|---|---|---|
Petersel and Schlesinger, 2007 | Retrospective cohort | 184 | Not provided |
Neogi et al., 2006 | Prospective case crossover Internet study | 232 | 268 days (SD, 178) |
Dalbeth et al., 2006 | Retrospective | 250 | Not reported |
Annemans et al., 2007, United Kingdom | Retrospective | 7443 | Not reported |
Annemans et al., 2007, Germany | Retrospective | 4006 | Not reported |
Ly, Gow, and Dalbeth, 2007 | Retrospective | 100 | Not reported |
Mikuls et al., 2005 | Retrospective | 63,105 | 3.8 y (SD, 2.8) |
Mikuls et al., 2006 | Retrospective | Not reported, number of medication errors 582,397 | 5-y study |
Sarawate, 2006 | Retrospective | 5942 | 1 y |
Singh, 2007 | Retrospective | 3658 | 2 y |
Singh, 2009 | Retrospective | 643 with new allopurinol | 2 y |
Pal, 2000 | Retrospective | 429 | Not reported |
Smith, 2000 | Retrospective | 73 | Not reported |
Evans, 1996 | Retrospective | 19 | Inpatient stay |
Ho, 1993 | Retrospective | 67 | Inpatient stay |
Stamp, 2000 | Prospective, cross-sectional | 31 | Cross-sectional |
No. of Patients | Age, y, Mean (SD or Range) | Male, % | Body Mass Index, kg/m 2 , mean (SD or range) | Tophaceous Gout, % | Comorbidities | |
---|---|---|---|---|---|---|
Petersel and Schlesinger, 2007 | 184 | 71 (range 40–96 y) | 100% | NR | NR | Heart disease: 15 (19%) Renal insufficiency: 149 (80.9%) |
Neogi et al., 2006 | 232 | 53 (range 23–85) | 81% | 30.8 (17.8–53.5) | 35% | 16% peptic ulcer disease, renal disease, or congestive heart failure |
Dalbeth et al., 2006 | 250 | 56 (range 26–86) | 82% | NR | 134 (53.6%) | 8 patients with end-stage renal failure were excluded; n was originally 258 |
Annemans et al., 2007, United Kingdom | 7443 | 65.6 (SD, 13.8) | 81.6% | NR | NR | Heart disease: 14.5% Renal failure: 9.5% |
Annemans et al., 2007, Germany | 4006 | 58.6 (SD, 13.1) | 80.4% | NR | 16.6% | Heart disease: 16.6% Diabetes: 25.9% Renal failure: 4.8% |
Ly et al., 2007 | 100 | NR | 82% | NR | 56 (56%) | Renal impairment: 44% of acute gout; 100% of chronic gout ∗ |
Mikuls et al., 2005 | 63,105 | 61 (SD,15 y) | 78% | NR | NR | Heart disease: 26% Diabetes: 7% Renal failure: 1% |
Mikuls et al., 2006 | Number of medication errors: 582,397 | NR | NR | NR | NR | NR |
Sarawate, 2006 | 5942 | 57.4 (SD, 14.1) | 76% | NR | 9.1% | Hypertension: 39.8% Coronary artery disease: 24.7% Diabetes: 18.3% Renal impairment: 13% |
Singh, 2007 | 643 | 67.9 (SD, 9.7) | 99% | NR | NR | Mean Charlson score, 2.5 |
Singh, 2009 | 643 | 67.9 (SD, 9.7) | 99% | NR | NR | Mean Charlson score, 2.5 |
Pal, 2000 | 429 | 64.5 y | 80% | NR | NR | NR |
Smith, 2000 | 73 | 77 y | 55% | NR | NR | NR |
Evans, 1996 22 | 19 | 59 y | 80% | NR | NR | Multiple comorbidities including renal and hepatic disease |
Ho, 1993 | 67 | 72 y | 83% | NR | NR | Hypertension: 59%Congestive heart failure: 34% Peptic ulcer disease: 32% |
Stamp, 2000 | 31 | 58 y | 81% | NR; weight 92 kg | 55% | Renal insufficiency: 55% |