Education Lab

The Patient With Gout

The case: A 47-year-old man presents with a 10-year history of gout. He is interested in the prevention of further attacks because these have been increasing in frequency and severity during the past year. He currently takes tramadol, if needed, for pain.

His physical exam is unremarkable with no evidence of tophi or joint tenderness. Laboratory data is as follows:

  • Sedimentation rate: 16 mm/hr
  • Serum uric acid: 9.8 mg/dL
  • Liver and kidney function: normal
  • Blood counts: normal; and
  • Radiographs of the hands and feet show no evidence of gout.

Key Supporting Information

Gout is a major health problem in the United States; it affects 8.3 million people, which is approximately 4% of the adult population. Although gout is well understood and has good therapeutic options, it tends to be poorly managed with insufficient patient evaluation, inappropriate use of traditional and new medications, and low patient compliance.

According to 2006 guidelines issued by the European League Against Rheumatism (EULAR), gout patients should be treated with both nonpharmacological and pharmacological approaches. Patients should be counseled about dietary and lifestyle changes such as avoiding foods with high purines (including meats, sardines, anchovies, beans, lentils and beverages high in fructose), weight reduction and avoidance of alcohol.

Following publication of the 2006 EULAR gout guidelines, significant evidence on gout has accumulated and new treatments for patients with gout have become available. The 2011 recommendations for the diagnosis and management of gout and hyperuricemia have been published and it is the objective of the 2011 guidelines to update the 2006 recommendations. The revised 2011 recommendations are based on the Grading of Recommendations Assessment, Development and Evaluation approach as an evidence-based strategy for rating quality of evidence and grading strength of recommendation in clinical practice.

Data continue to support the decision to diagnose gout using clinical characteristics rather than mandating monosodium urate crystal identification. However, new investigations have shown that limiting the diagnostic process to the typical signs and symptoms of gout may fail to identify women with the disease.

Gout is caused by the deposition of monosodium urate crystals. Approximately 50% of patients demonstrate radiographic bony changes, usually 6 years to 8 years after the initial attack. These changes depend on the sites where the urate crystals are deposited.

Tophi deposition in the hallux
Figure. Tophi deposition in the hallux is shown.

Image: Codario RA

The feet and hands are commonly involved and can occur in an asymmetric, polyarticular pattern. Although urate is not inherently radio-opaque, the varying densities seen on radiographs are caused by calcium precipitation with the urate crystals. Tophi, which are soft tissue masses caused by the deposition of urate crystals, are typically located in the periarticular area along the extensor surface, but may be intra-articular or not associated with the joint at all. The Figure illustrates tophi deposition in the hallux.

Although studies have shown a serum uric acid (SUA) level of greater than 6 mg/dL is a significant risk factor for gout, it is not always a reliable diagnostic tool because approximately 14% of patients with acute gout present with SUA levels of less than 6 mg/dL. Strong associations have been demonstrated between gout and metabolic syndrome, cardiovascular disease (CVD), and chronic kidney disease (CKD), such that diagnosing and managing comorbid conditions has become an integral part of disease management.

The use of nonpharmacologic measures, particularly dietary aspects, has become more sophisticated. It is more widely recognized that gout therapy relies on good patient education. Effective management of an acute attack requires that treatment is begun within hours of first symptom onset. Low-dose colchicine (1.2 mg as soon as possible, followed by one dose of 0.6 mg 1 hour later) or a nonsteroidal anti-inflammatory drug should be implemented. Oral corticosteroids can also be effective.

For most patients, a target SUA level between 5 mg/dL and 6 mg/dL is safe and effective. Prophylactic treatment to control acute gout attacks is an essential aspect of gout therapy. Changes in modern lifestyle, including diets rich in animal fat and fructose-sweetened drinks, have contributed to the increasing prevalence of gout and many of its comorbid conditions, such as obesity, hypertension, metabolic syndrome and cardiovascular disease. A recent survey indicated patients with gout had an average of four comorbidities; up to 10% of patients presented with greater than seven comorbidities. The intricate interplay of gout and associated comorbid conditions adds complexity to diagnosis and disease management, requiring a balancing act between controlling the metabolic imbalance causing hyperuricemia and gout while addressing multiple contributing or secondary comorbidities.

The strong positive correlations between SUA/gout and hypertension, CVD, stroke, cardiovascular mortality, type 2 diabetes, metabolic syndrome and kidney disease have been further established with numerous large cohort study results published since 2005. Modifiable comorbidities and risk factors should be addressed as an important part of the management of patients with gout. However, addressing comorbidities can be challenging because many of the typical comorbidities seen in the context of gout result in contraindications to the medications required for the treatment of the disease. Medications used to treat comorbid conditions may have positive effects on gout. Due to the mild uricosuric effects of losartan or fenofibrate, these medications may be of benefit in patients with hypertension or hyperlipidemia and gout. Conversely, the close association between gout and comorbid conditions may allow for comorbidity management through the treatment of hyperuricemia and gout. Thus, urate-lowering therapy has been associated with a reduction in the risk of CVD, slowing the progression of kidney disease and diminishing the severity of proteinuria in patients with type 2 diabetes.

Learning Objectives:

Upon successful completion of this educational activity, participants should be better able to assess acute gout.

Click here to see this Education Lab Activity.

Overview

Author(s)/Faculty: Ronald A. Codario, MD, FACP, FNLA, RPVI, CCMEP
Source: Healio Rheumatology Education Lab
Type: Monograph
Articles/Items: 7
Release Date: 7/15/2015
Expiration Date: 7/15/2016
Credit Type: CME
Number of Credits: 1
Cost: Free
Provider: Vindico Medical Education

CME Information

Provider Statement: This continuing medical education activity is provided by Vindico Medical Information.
Support Statement: No commercial support for this activity.
Target Audience: This activity is designed for rheumatologists and other health care professionals involved in the treatment of patients with rheumatological disorders.

The case: A 47-year-old man presents with a 10-year history of gout. He is interested in the prevention of further attacks because these have been increasing in frequency and severity during the past year. He currently takes tramadol, if needed, for pain.

His physical exam is unremarkable with no evidence of tophi or joint tenderness. Laboratory data is as follows:

  • Sedimentation rate: 16 mm/hr
  • Serum uric acid: 9.8 mg/dL
  • Liver and kidney function: normal
  • Blood counts: normal; and
  • Radiographs of the hands and feet show no evidence of gout.

Key Supporting Information

Gout is a major health problem in the United States; it affects 8.3 million people, which is approximately 4% of the adult population. Although gout is well understood and has good therapeutic options, it tends to be poorly managed with insufficient patient evaluation, inappropriate use of traditional and new medications, and low patient compliance.

According to 2006 guidelines issued by the European League Against Rheumatism (EULAR), gout patients should be treated with both nonpharmacological and pharmacological approaches. Patients should be counseled about dietary and lifestyle changes such as avoiding foods with high purines (including meats, sardines, anchovies, beans, lentils and beverages high in fructose), weight reduction and avoidance of alcohol.

Following publication of the 2006 EULAR gout guidelines, significant evidence on gout has accumulated and new treatments for patients with gout have become available. The 2011 recommendations for the diagnosis and management of gout and hyperuricemia have been published and it is the objective of the 2011 guidelines to update the 2006 recommendations. The revised 2011 recommendations are based on the Grading of Recommendations Assessment, Development and Evaluation approach as an evidence-based strategy for rating quality of evidence and grading strength of recommendation in clinical practice.

Data continue to support the decision to diagnose gout using clinical characteristics rather than mandating monosodium urate crystal identification. However, new investigations have shown that limiting the diagnostic process to the typical signs and symptoms of gout may fail to identify women with the disease.

Gout is caused by the deposition of monosodium urate crystals. Approximately 50% of patients demonstrate radiographic bony changes, usually 6 years to 8 years after the initial attack. These changes depend on the sites where the urate crystals are deposited.

Tophi deposition in the hallux
Figure. Tophi deposition in the hallux is shown.

Image: Codario RA

The feet and hands are commonly involved and can occur in an asymmetric, polyarticular pattern. Although urate is not inherently radio-opaque, the varying densities seen on radiographs are caused by calcium precipitation with the urate crystals. Tophi, which are soft tissue masses caused by the deposition of urate crystals, are typically located in the periarticular area along the extensor surface, but may be intra-articular or not associated with the joint at all. The Figure illustrates tophi deposition in the hallux.

Although studies have shown a serum uric acid (SUA) level of greater than 6 mg/dL is a significant risk factor for gout, it is not always a reliable diagnostic tool because approximately 14% of patients with acute gout present with SUA levels of less than 6 mg/dL. Strong associations have been demonstrated between gout and metabolic syndrome, cardiovascular disease (CVD), and chronic kidney disease (CKD), such that diagnosing and managing comorbid conditions has become an integral part of disease management.

The use of nonpharmacologic measures, particularly dietary aspects, has become more sophisticated. It is more widely recognized that gout therapy relies on good patient education. Effective management of an acute attack requires that treatment is begun within hours of first symptom onset. Low-dose colchicine (1.2 mg as soon as possible, followed by one dose of 0.6 mg 1 hour later) or a nonsteroidal anti-inflammatory drug should be implemented. Oral corticosteroids can also be effective.

PAGE BREAK

For most patients, a target SUA level between 5 mg/dL and 6 mg/dL is safe and effective. Prophylactic treatment to control acute gout attacks is an essential aspect of gout therapy. Changes in modern lifestyle, including diets rich in animal fat and fructose-sweetened drinks, have contributed to the increasing prevalence of gout and many of its comorbid conditions, such as obesity, hypertension, metabolic syndrome and cardiovascular disease. A recent survey indicated patients with gout had an average of four comorbidities; up to 10% of patients presented with greater than seven comorbidities. The intricate interplay of gout and associated comorbid conditions adds complexity to diagnosis and disease management, requiring a balancing act between controlling the metabolic imbalance causing hyperuricemia and gout while addressing multiple contributing or secondary comorbidities.

The strong positive correlations between SUA/gout and hypertension, CVD, stroke, cardiovascular mortality, type 2 diabetes, metabolic syndrome and kidney disease have been further established with numerous large cohort study results published since 2005. Modifiable comorbidities and risk factors should be addressed as an important part of the management of patients with gout. However, addressing comorbidities can be challenging because many of the typical comorbidities seen in the context of gout result in contraindications to the medications required for the treatment of the disease. Medications used to treat comorbid conditions may have positive effects on gout. Due to the mild uricosuric effects of losartan or fenofibrate, these medications may be of benefit in patients with hypertension or hyperlipidemia and gout. Conversely, the close association between gout and comorbid conditions may allow for comorbidity management through the treatment of hyperuricemia and gout. Thus, urate-lowering therapy has been associated with a reduction in the risk of CVD, slowing the progression of kidney disease and diminishing the severity of proteinuria in patients with type 2 diabetes.

Learning Objectives:

Upon successful completion of this educational activity, participants should be better able to assess acute gout.

Click here to see this Education Lab Activity.

Overview

Author(s)/Faculty: Ronald A. Codario, MD, FACP, FNLA, RPVI, CCMEP
Source: Healio Rheumatology Education Lab
Type: Monograph
Articles/Items: 7
Release Date: 7/15/2015
Expiration Date: 7/15/2016
Credit Type: CME
Number of Credits: 1
Cost: Free
Provider: Vindico Medical Education

CME Information

Provider Statement: This continuing medical education activity is provided by Vindico Medical Information.
Support Statement: No commercial support for this activity.
Target Audience: This activity is designed for rheumatologists and other health care professionals involved in the treatment of patients with rheumatological disorders.