By Neda Amiri, MD, FRCPC, PGY5 (biography and disclosures); Kam Shojania, MD, FRCPC (biography and disclosures)
Part 1: Diagnosing Gout in Primary Care Settings: Do we have to tap?
Kam Shojania: No conflict of interest. Has been involved with: Augurex, Pfizer, UCB, Abbvie, Janssen, Roche, and Celgene.
Mitigating Potential Bias:
- Recommendations are consistent with published guidelines.
- Recommendations are consistent with current practice patterns.
- Treatments or recommendations in this article are unrelated to products/services/treatments involved in disclosure statements.
Neda Amiri: No dislosures.
What care gaps/frequently asked questions I have noticed:
Despite being one of the most common forms of arthritis afflicting adults, optimal care of patients with gout including treatment of acute attacks as well as long-term management is not always achieved. I have noticed primary care providers are hesitant to initiate allopurinol or titrate to an optimal dose, especially in patients with chronic kidney disease.
We covered the diagnosis of gout in the acute setting in a previous “This Changed My Practice” article (http://thischangedmypractice.com/part-1-diagnosing-gout). In this article, we will specifically address the data supporting management of acute and chronic gout.
Data that answers these questions or gaps:
As per American College of Rheumatology (2012) guidelines for the management of gout, the self-reported prevalence of gout in adults is almost 4% (8.3 million people) in the United States. The rising rate has been attributed to the concomitant rise in comorbidities including hypertension, obesity, type 2 diabetes and chronic kidney disease.
In the setting of acute gouty arthritis, monotherapy with NSAIDs (Naproxen, and Indomethacin), Colchicine, or systemic corticosteroids is recommended, particularly if involving one or a few small joints. Guidelines emphasize that oral colchicine is particularly efficacious when started within the first 36 hours of the attack. In absence of renal impairment, the loading dose is 1.2 mg orally, followed by 0.6 mg one hour later. The colchicine is continued at 0.6 mg daily or twice daily until symptoms are resolved. Corticosteroids (oral or intra-articular) are often considered when either the initial therapy fails, or there are more than two joints involved. The dosing of intra-articular steroids depends on the size of the joint. However, for systemic steroids, Prednisone at 0.5 mg/kg per day for five to ten days is recommended. If the pain is severe or if there is polyarticular involvement, combination therapy can be considered. In cases of inadequate response (defined as less than 20% improvement in pain score within 24 hours or <50% improvement after 24 hours), switching to an alternate monotherapy or adding combination therapy is valid. Additional agents such as interleukin-1 inhibitors (anakinra) are available, but their use is limited by cost and access.
In management of hyperuricemia, the etiology and secondary causes should be considered. Patient education regarding lifestyle recommendations should specifically include avoidance of alcohol (particularly beer), meats (high in purine content), and sugar-containing sodas. If possible, urate-elevating medications such as thiazides or loop diuretic should be substituted with other agents.
Indications for initiating uric acid lowering therapy includes: ³2 gout attacks per year, evidence of tophus/tophi on exam or imaging, history of urolithiasis or CKD stage 2 (eGFR <90) or worse. Both allopurinol and febuxostat may be considered as first choice. However, given the higher cost of febuxostat and similar efficacy between the two, allopurinol is used preferentially in Canada. Initial dose is usually 100 mg and titrated every two to four weeks. If the patient has CKD stage 4 (eGFR <30) or worse, 50 mg is used as the initial dose. This approach has been found to be safe in recent trials in patients with CKD. Uric acid should be measured serially (every four weeks) along with creatinine to ensure patients achieve a target uric acid level of 360 umol/L or less. To prevent acute gout attacks at the initiation of therapy (Also referred to as “mobilization gout”), colchicine at a dose of 0.6 mg (daily or twice daily) can be used for the first three to six months.
What I recommend:
- Acute Treatment of Gout: In absence of contraindications or major comorbidities, I use mono or combination therapy with NSAIDs and colchicine in the acute treatment of gout. I use the “loading dose” of colchicine at 1.2 mg, followed by 0.6 mg an hour later, followed by 0.6 mg PO BID until the patient’s symptoms resolve (if no renal impairment).
- In absence of significant clinical improvement (or polyarticular involvement) I inject the active joints with methylprednisolone or I start the patient on prednisone 0.5 mg/kg for 5-10 days; alternatively if there are limited joints involved and they are accessible for injection, I consider glucocorticoid injection.
- Uric acid lowering treatment is indicated in patients who have a) history of renal stones; b) tophi (on exam or imaging); c) more than 2 attacks per year; d) CKD stage 2 or worse (eGFR <90).
- Allopurinol is my first uric acid lowering therapy of choice. I start Allopurinol at 100 mg PO daily and titrated by 100 mg every 2-4 weeks until the serum uric acid goes below 360 umol/L. If the patient has CKD stage 4 (eGFR <30) or worse, I start at 50 mg PO daily, and increase slowly.
- I consider HLA-B*5801 testing in patients who are of Han Chinese, Thai or Korean descent, given the increased risk of Allopurinol hypersensitivity syndrome in those with this HLA subtype.
- Patients who develop a rash with allopurinol can usually be switched to febuxostat 80mg daily.
- I obtain monthly uric acid, creatinine, and liver enzymes to ensure that the target uric acid (below 360 umol/l) is being reached.
- Patients who have an unclear etiology of hyperuricemia, have difficulty reaching their target uric acid levels (especially in the setting of renal impairment) or have adverse events with uric acid lowering therapy should be referred to rheumatology for further assessment and treatment.
- The most common cause of treatment failure in gout is medication non-adherence. Patient education is important to ensure adherence.
Remember that gout is the most common inflammatory arthritis in men and can be successfully managed in almost all patients.
American College of Rheumatology Guidelines for treatment of gout. 2012 http://www.rheumatology.org/Portals/0/Files/Gout_Part_2_ACR-12.pdf
Handouts for Patients:
http://rheuminfo.com: helpful website designed and operated by Canadian Rheumatologists. They have handouts on Colchicine, Allopurinol, NSAIDs for review of side effects, as well as information on gout, and its treatment.“Gout Counseling Tool” for patients: http://rheuminfo.com/wp-content/uploads/2011/04/GOUT_PRESCRIPTION_2011.pdf.
- Becker MA,Fitz-Patrick D, Choi HK, Dalbeth N, Storgard C, Cravets M, Baumgartner S. An open-label, 6-month study of allopurinol safety in gout: The LASSO study. Semin Arthritis Rheum. 2015;45(2):174-83. (View with UBC) DOI: 10.1016/j.semarthrit.2015.05.005
- Stamp LK,O’Donnell JL, Zhang M, James J, Frampton C, Barclay ML, Chapman PT. Using allopurinol above the dose based on creatinine clearance is effective and safe in patients with chronic gout, including those with renal impairment. Arthritis Rheum. 2011 Feb;63(2):412-21. (View with UBC) DOI: 10.1002/art.30119