Does this patient have Gout?
Gout is a disease resulting from deposition of monosodium urate (MSU) crystals in the joints and connective soft-tissues in the setting of sustained hyperuricemia (serum uric acid >6.8 mg/dL). Classically, the initial manifestation of gout is acute monoarthritis characterized with abrupt onset of exquisite pain and swelling of the joint (commonly in the first metatarsophalangeal joint, called “podagra”).
Gout has a predilection for lower extremity joints, but any joint can be affected. Oligoarticular and polyarticular presentations can occur, usually in the later stages of the disease and/or in the elderly.
Systemic symptoms such as fevers, chills, malaise, and leukocytosis can accompany acute gout. Other key components of gout flares include: maximal pain in 4-12 hours, recurrent pattern of similar attacks, and marked impairment of physical function. If untreated, spontaneous resolution can occurs in 3-10 days in patients with early disease, and 10-20 days in those with late/chronic disease.
Older adults, particularly women, may present with polyarticular involvement, which may be mistaken for rheumatoid arthritis; a tophus may also be mistaken for a rheumatoid nodule, or Heberden’s nodes.
Tophi, which are collections of MSU crystals, are pathognomonic for gout. Tophi accumulate in the joints, tendon sheaths, bursae, and subcutaneous tissues. Deposits can also occur in connective other tissues such as the renal pyramids, heart valves, and/or sclerae. Tophi appear as asymmetric white to yellow firm swellings under the skin usually of the ear pinnae, ulnar aspect of forearm, fingers, and Achilles’ tendon.
Gout flares are predicated on perturbation of serum uric acid (sUA) levels. These perturbations occur during acute illnesses, surgery, trauma, dehydration, fasting, or medication changes (e.g. introduction of diuretics, or initiation/discontinuation of urate-lowering therapy (ULT)).
Dietary indiscretions from food high in purine content (i.e. red meat, shellfish, and alcohol, particularly beer) elevate sUA levels and trigger an acute gout flare. Predictors of the development of clinical gout, other than the high sUA, include: hypertension, the use of thiazides and/or loop diuretics, obesity, and a high alcohol intake, all of which appear to contribute in an additive manner to the risk of gout.
Gout in special populations can present with atypical features, or have an aggressive natural history. These include:
Gout in women (more likely to present with advanced disease, with tophi within Heberden’s nodes of osteoarthritis, and frequently flare in the context of diuretic use).
Early-onset gout (onset before age 25, strong family history of gout and/or nephrolithiasis, and may be associated with genetic or enzymatic diseases of purine metabolism).
Transplantation gout (related to cyclosporine or tacrolimus use).
Chronic refractory gout (CRG) is a deforming, disabling phase of the disease, as a result of failure to respond to ULT, suboptimal ULT dose titration, their intolerance to available medications, or the presence of several comorbidities that limit treatment with the approved ULT agents.
The differential diagnosis of acute gout includes: septic arthritis, other crystal-related arthritis (e.g. calcium pyrophosphate dehydrate (CPPD) disease, basic calcium phosphate (BCP), calcium oxalate (CaOx) spondyloarthropathies, or rheumatoid arthritis.
Gout can be confused with cellulitis because of associated periarticular or bursal erythema during acute flares.
What tests to perform?
The diagnostic “gold-standard” for gout and other crystal-induced arthropathies is a diagnostic arthrocentesis and evaluation of the synovial or bursal fluid under compensated polarized light microscopy for the presence of MSU-crystals, or other types of crystals. It is essential to exclude the presence of septic arthritis by performing a gram-stain and culture of the synovial or bursal fluid.
The diagnostic standard for gout is visualization of monosodium urate crystals (MSU) from a synovial or bursal fluid aspirate, and/or tophaceous deposits, and/or from a tissue biopsy.
MSU-crystals are characteristically needle-shaped, and on compensated polarized microscopy, appear as bright, negatively birefringent crystals (yellow when parallel to the axis of slow vibration, and blue when perpendicular to this axis). Figure 1.
The MSU crystals are usually intracellular during acute attacks; extracellular crystals are commonly present in synovial fluid obtained between gout attacks (intercritical periods).
Synovial fluid in acute gout can appear from translucent to cloudy, has low viscosity, and is consistent with moderate to severe inflammation: leukocyte counts in the range of 5,000 to 80,000 cells/mm3 (average between 15,000 and 20,000 cells/mm3), with neutrophils >90%. This overlaps with findings in septic arthritis or pseudogout.
Joint aspiration with Gram’s staining and culture must be performed if high suspicion of septic joint, even if MSU-crystals are identified in synovial/bursal fluid, as bacterial infection can coexist with any crystal-associated arthritis.
Neutrophilia and elevated inflammatory markers can reflect a systemic inflammatory response.
Prolonged hyperuricemia is a biochemical prerequisite for the development of gout. Hyperuricemia is defined as a sUA greater than 6.8 mg/dL, which exceeds the soluble concentration of MSU in body fluids. Above this level, MSU deposition in joint and soft-tissue occurs, leading to tophi formation over time.
Clinical laboratories define hyperuricemia as a serum urate level that is greater than two standard deviations above the mean value in a gender and age-matched healthy population (the upper limit of normal by this standard is 8.0-8.5 mg/dl, which misses a large proportion of hyperuricemic patients).
During an acute gout attack, sUA may be normal. The sUA level should not be used to confirm or rule out gout flares, as these can be normal during an acute flare. Its role should only be supportive, possibly to establish a pre-test probability for gout. It is useful, however, for following the effects of urate-lowering therapy to attain sUA “target to treat”.
The vast majority of hyperuricemic patients will not develop gout.
Radiographic changes are late features of gout, being apparent years after the onset or when it has progressed to tophaceous stages. In early disease, this may show nonspecific soft tissue swelling.
Changes suggestive of gouty arthritis on plain radiography are: erosive arthropathy without periarticular osteopenia, marginal “punched-out” erosions with overhanging edges, subcortical cysts, and calcified tophi.
A study in which radiographic findings for gout were compared with clinical diagnosis of gout and other arthropathies found that having at least one radiographic finding of gout was 31% sensitive and 93% specific.
CT, including the newer Dual-Energy CT, offer excellent visualization of tophi deposits, but their use has been primarily limited to estimation of “tophi burden”, although not for diagnosis.
MRI is useful for early detection of tophi, bony erosions, and synovial involvement. It has limited use due to its high cost and has not been adopted as a standard measure in the diagnostic workup of gout.
The use of high resolution (8-16 MHz) ultrasound (MSUS) can be considered “point of care technology” for a quick and accurate bedside evaluation of gout. Ultrasonographic findings have been described at the very early stages of gout, even in those with asymptomatic hyperuricemia, suggesting active, subclinical tophus formation (Figure 2 and Figure 3).
In established gout, high-resolution ultrasonographic MSUS findings include a “double-contour sign” (layering of MSU over the surface of the hyaline cartilage) (Figure 2). Tophi appear as hyperechoic and bright dotted foci (Figure 3).
A study found that the presence of bright stippled foci and/or hyperechoic areas seen on US indicated gout with a great sensitivity (96%), whereas the specificity was limited (73%). These bright stippled foci and hyperechoic (cloudy) areas, representing monosodium urate MSU deposits of different sizes, were found to be reliable features in the diagnosis of gout. US is much more sensitive than conventional X-ray, but less specific.
Thus, MSUS often provides additional diagnostic information in patients with clinical suspicion of gout when laboratory findings and X-ray results are negative or inconclusive. MSUS facilitates differentiation between MSU and CPPD crystal deposition diseases and is far more sensitive than plain radiography for early disease detection.
Advantages of MSUS include good early disease detection, low cost, portability, and absence of radiation exposure, but require a sonographer skilled in musculoskeletal evaluations.
How should patients with gout be managed?
Treatment objectives are:
Rapid and safe resolution of pain and inflammation for acute gout flare.
Limit recurrent attacks.
Inhibit, or prevent progression of crystal deposition, development of chronic gouty synovitis and associated connective tissue and bone destruction.
Prevent disability or loss of function, and improve quality of life.
Treatment strategies for gout revolve around three goals:
Treatment of hyperuricemia.
Treatment of significant co-morbidities such as hypertension, obesity, cardiovascular and kidney disease through lifestyle changes and pharmacologic management.
General treatment principles
Choice of agent, dose, and duration of therapy should be individualized, influenced by factors such as renal, hepatic, cardiovascular, gastrointestinal disease, coagulation status, and severity of gout.
Adjunctive measures include:
Resting the affected joint.
Polyarthritis flares require more intensive therapy than monoarthritis.
Anti-inflammatory therapy is more effective if started within 36 hours. Therapies started after 72 hours have little lesser impact on the course of the gout flare. “Treat-to-target” strategy with goal sUA to less than 6 mg/dL, and less than 5 mg/dL for those patients with tophi deposits
Urate lowering therapy (ULT) should not be initiated during an acute flare of gout, as it may prolong the flare. However, once established, do not stop ULT during acute gout flares.
Antihyperuricemic therapy in gout is most effective when continued lifelong. Direct treatment of asymptomatic hyperuricemia is not yet evidence-based.
A diagnosis of gout should prompt evaluation for potentially modifiable risk factors (e.g. dietary habits) and associated coexisting co-morbidities (e.g. hypertension, hyperlipidemia, cardiovascular disease) that may require further intervention.
Compliance and adherence to prescribed therapy needs to be ensured for successful outcomes. Patient education is paramount for successful treatment and drug-compliance.
Anti-inflammatory treatment options include: non-steroidal anti-inflammatory drugs (NSAIDs), including selective cyclooxygenase-2 (COX-2) inhibitors, glucocorticoids (intra-articular or systemic), ACTH (ACTHAR) and colchicine (Colcrys).
Urate-lowering therapy is achieved most commonly with xanthine oxidase inhibitors (i.e. allopurinol, febuxostat), uricosuric agents (e.g. probenecid), or recombinant uricase (e.g. pegloticase) for patients with chronic refractory gout. The goal of all ULT is to prevent disease progression by reducing the total body urate burden.
Off-label, and investigational therapies (i.e. anti-interleukin 1 [IL-1] drugs) are available.
Neutrophils and other inflammatory cells.
Proinflammatory cytokines such as IL-1.
Inflammasome (a multi-protein complex generated in macrophages which produces the active form of interleukin-1 beta [IL-1β], a potent inducer of inflammation).
Treatment for acute gouty inflammation
Several NSAIDs (listed below) have been demonstrated in clinical trials to be effective in acute gout:
Naproxen 500 mg PO for 5 days (or 750-1000 mg PO daily for 3 days then 500-750 mg total daily for 4-7 days).
Indomethacin 150-200 mg PO daily for 3 days then 75-100 mg PO daily for 4-7 days.
Sulindac 300-400 mg PO daily for 7-10 days.
Indomethacin 150-200 mg PO daily for 3 days then 75-100 mg PO daily for 4-7 days.
Avoid NSAIDs in patients with renal or hepatic failure, patients at risk of gastrointestinal hemorrhage, congestive heart failure, and in those on chronic anticoagulants (i.e. warfarin).
First-line treatment when NSAIDs and high doses of colchicine are not viable options due to substantial renal dysfunction. Glucocorticoids may be a safer alternative, especially for the elderly (for short-term use):
Prednisone 30-60 mg daily for 3 days, then taper by 10-15 mg/day every 3 days to discontinuation.
Oral prednisolone 35 mg PO daily for 5 days (found to be comparable to NSAIDs).
Medrol dose pack (for less severe flares).
In severe acute polyarticular gout, a short course of intravenous methylprednisolone (100-150 mg for 1-2 days) may be warranted.
Intra-articular steroid injections are useful when only 1-2 joints are involved.
Avoid use if septic arthritis has not been excluded. Use with caution in patients with hyperglycemia.
Colchicine binds to a tubulin, which inhibits microtubule elongation and function, and which suppresses inflammation by inhibiting neutrophil adhesion and migration. More recently, colchicine also inhibits the inflammasome that promotes the maturation of inflammatory cytokines Interleukin 1β (IL-1β). Although oral colchicine has long been used, it was only recently approved in 2009, by the Food and Drug Administration (FDA) for use in patients with acute gout. It is now marketed under the brand name Colcrys.
In a randomized trial, colchicine (Colcrys, at a dose of 1.2 mg at the onset of a flare, followed by 0.6 mg 1 hour later) was significantly more likely than placebo to result in a reduction in pain of 50% or more 24 hours later. This regimen had efficacy similar to that of a high-dose regimen (1.2 mg, then 0.6 mg per hour for 6 hours), with fewer gastrointestinal side effects.
Dose should be adjusted based on creatinine clearance for prophylaxis.
Avoid in patients with creatinine clearance <10 ml/min, patients on hemodialysis (colchicine is not dialyzable), patients with clinically significant hepatic or hepatobiliary dysfunction, and those with combined hepatic and renal disease.
Use colchicine with caution and regular toxicity monitoring in patients on statins (combined use may synergistically potentiate myopathy). Gastrointestinal toxicity (diarrhea, which can be severe, and nausea) is the most common adverse event.
COX-2 selective NSAIDs (e.g. celecoxib 200 mg po bid for 3 days, then 200 mg daily for 4-7 days). Use with caution in patients at risk for clinically significant gastrointestinal adverse effects, including active peptic ulcer. May increase risk of cardiovascular events.
Synthetic ACTH (not universally available ACTHAR) may be used as an off-label use.
For refractory gout, the IL-1 cytokine inhibitor anakinra given 100 mg subcutaneously for 3 days had good results in a small pilot study, wherein there was rapid, significant symptom relief within 48 hours of injection.
Canakinumab (IL-1β inhibitor) proved to be superior to intramuscular triamcinolone in preliminary studies of patients who had contraindications to NSAIDs or colchicine. The FDA has not approved this medication for gout, although it has requested the manufacturing company for additional clinical data.
Rilonacept, another IL-1 inhibitor given by subcutaneous weekly injections, is currently in phase three trials for prevention of gout flares during the start of ULT. This showed marked reduction in acute flares during the first 16 weeks after ULT initiation and dose escalation.
Treatment for chronic gouty arthritis
Long-term management of gouty arthritis includes dietary restrictions and education, with the additional use of ULT.
Urate-lowering therapy (ULT) is indicated for hyperuricemic patients with a confirmed diagnosis of gout, plus the following:
Frequent > 1 gout attack per year, or:
Uric acid overproducing state, daily uric acid excretion greater than 1000 mg
Uric acid urolithiasis, or:
Presence of tophi, or:
Severe, difficult to treat, or refractory attacks, or:
Chronic, advanced gouty arthritis.
Gout with chronic renal disease.
Gout with major organ transplant.
These ULT may all cause hypersensitivity, and carry the risk of mobilization flares. Thus, prophylaxis for recurrent flares must be instituted when initiating or titrating these medications.
The xanthine oxidase inhibitors can both cause elevated transaminase levels and require ongoing monitoring. Monitoring of sUA is ideally done every 6 months to attain and maintain sUA at less than 6 mg/dL.
A xanthine oxidase inhibitor that is effective and widely used for urate-lowering for the past four decades.
FDA approval is for dosages 100-800 mg/day, however general usage of allopurinol seldom exceed 300 mg/day. Treating to target of sUA <6 mg/dL often requires doses greater than 300 mg/day.
Rash may develop in 2% of patients, and is dose-dependent. Rarely, patients can develop a Steven-Johnson-like reaction (allopurinol hypersensitivity syndrome), which can be fatal.
The incidence of severe cutaneous adverse reactions to allopurinol have been reported to be higher in populations such as the Han Chinese, Thai, and Korean patients, particularly in association with the HLA-B58:01 genotype. This is associated with HLAB-38 haplotypes.
Slow initiation and titration schedule is recommended, and dose reductions may be necessary in patients with renal impairment.
Febuxostat is a non-purine analogue, which is structurally different from allopurinol that inhibits xanthine oxidase; there have been no reports of cross-reactive toxicities.
In the CONFIRMS trial, 40 mg of febuxostat had similar effectiveness as 300 mg allopurinol, but 80 mg dose of febuxostat outperformed allopurinol. Unlike with allopurinol, there currently is no recommendation for dose reduction in mild to moderate renal impairment.
Uricosuric agents can be added on, or used as second-line therapy: probenecid is used occasionally, but is contraindicated in low GFR states, history of kidney stones, or a state of uric acid overproduction is established. Benzbromarone is a potent uricosuric agent with restricted use, and is not currently available in the US.
Pegloticase is an infusible uric acid-lowering medication recombinant uricase, which was FDA-approved in 2010 for use in recalcitrant gout or patients who have large, refractory tophaceous deposits.
Humans have a mutational inactivation of the urate oxidase (uricase) gene, in contrast to non-primate mammals. In effect, humans excrete uric acid as the end product of purine metabolism, rather than the more soluble allantoin. Pegloticase is a mammalian recombinant uricase conjugated to monomethoxypolyethylene glycol (PEG).
The “PEGylation” of the uricase enzyme prolongs its half-life, and reduces immunogenicity. This “PEGylated” uricase enzyme completes the final step in the purine catabolic pathway, creating a soluble form of urate, which lacks the potential to precipitate.
Pegloticase is given intravenously, resulting in rapid dissolution of MSU. It may rapidly resolve tophi and control chronic synovitis in patients with severe chronic refractory gout.
The pegloticase package insert includes warnings for anaphylaxis, infusion reactions, gout flares, and congestive heart failure. Patients should be monitored closely for all four reactions.
Gout flares, infusion reactions, and anaphylaxis are among the prominent risks of this potent therapy.
Loss of uric acid-lowering effect is predictive of infusion reactions, especially when the sUA levels rise to >6.0mg/dL. Thus, sUA level should be measured prior to each infusion. If sUA has risen to greater than 6 mg/dL after an initial decline, pegloticase should be discontinued. Consider drug cessation due to the risk of serious infusion reactions or anaphylaxis.
What happens to patients with gout?
It is currently estimated that there are 8.3 million diagnoses of gout in the United States. Prevalence has been generally cited as five cases per 1000 persons in the United States. Incidence is rising, reflecting increased longevity, co-morbid diseases, and increased use of medications that promote hyperuricemia (e.g. low dose aspirin, thiazide diuretics).
Gout is more common in Filipino or Polynesian ethnicity.
Male to female ratio is 4:1; onset in males is between the fourth and sixth decades of life (between ages 35-50). Other studies report a male:female ratio ranging from 7:1 to 20:1. In women, onset is usually after menopause, due to loss of uricosuric effect of estrogens.
Humans do not express the enzyme uricase which degrades uric acid; an end product of purine nucleotide catabolism.
In the majority, hyperuricemia is due to impaired renal uric acid excretion, rather than urate overproduction – which can largely occur in the setting of genetic or enzymatic defects in purine metabolism.
Hyperuricemia and gout are associated with other co-morbidities: obesity, hypertension, cardiovascular disease, kidney disease, and the metabolic syndrome. Three forms of hyperuricemia-induced renal disease are recognized, which may progress to end-stage renal disease: acute urate nephropathy, chronic urate nephropathy, and uric acid nephrolithiasis that occurs in 10-25% of all patients with gout.
Any alteration that destabilizes the microenvironment of tophi can provoke an acute attack by causing crystal shedding into the joint space and/or soft-tissue, which then incites the inflammatory cascade (“mobilization flares”). Such alterations include a change in synovial fluid pH, dehydration, or a sudden change in urate concentration.
The natural history of gout is a continuum of stages: asymptomatic hyperuricemia (typically lasts for decades), acute intermittent gout (10 or more years), intercritical gout (asymptomatic periods between acute attacks), and advanced gout (when the intercritical period is no longer free of pain). In the advanced stages, articular and periarticular tophi can be associated with bone erosions and significant joint deformities, contributing to pain, and loss of function, and disability.
Chronic refractory gout (CRG) is a deforming, disabling phase of the disease, as a result of failure to respond to ULT, suboptimal ULT dose titration, their intolerance to available medications, or the presence of comorbidities that contraindicate treatment with approved agents.
How to utilize team care?
Specialty consultation with a rheumatologist is needed if diagnosis or treatment is difficult.
Surgical referral for excision/debridement of tophus is occasionally warranted if it mechanically interferes with limb function. Tophi can ulcerate, which can become secondarily infected; debridement is often necessary prior to curative treatment with antibiotics.
Dietitians (for weight and dietary management), pharmacists (for monitoring of polypharmacy with potential drug interactions, particularly in elderly), and physical/occupational therapists (for functional rehabilitation) may provide valuable adjunctive care.
Are there clinical practice guidelines to inform decision making?
2012 American College of Rheumatology guidelines for management of gout. Part 1: systematic nonpharmacologic and pharmacologic therapeutic approaches to hyperuricemia.
2012 American College of Rheumatology guidelines for management of gout. Part 2: therapy and anti-inflammatory prophylaxis of acute gouty arthritis.
What is the evidence?
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Stamp, LK, Taylor, WJ, Jones, PB. “Starting dose is a risk factor for allopurinol hypersensitivity syndrome: A proposed safe starting dose of allopurinol”. Arthritis Rheum. 2012 Apr 5.
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Terkeltaub, RA, Furst, DE, Bennett, K. “High versus low dosing of oral colchicine for early acute gout flare: Twenty-four-hour outcome of the first multicenter, randomized, double-blind, placebo-controlled, parallel-group, dose-comparison colchicine study”. Arthritis Rheum. vol. 62. 2010 Apr. pp. 1060-8.
Schlesinger, N, De Meulemeester, M, Pikhlak, A. “Canakinumab relieves symptoms of acute flares and improves health-related quality of life in patients with difficult-to-treat Gouty Arthritis by suppressing inflammation: results of a randomized, dose-ranging study”. Arthritis Res Ther. vol. 13. 2011 Mar 25. pp. R53
Becker, MA, Schumacher, HR, Espinoza, LR. “The urate-lowering efficacy and safety of febuxostat in the treatment of the hyperuricemia of gout: the CONFIRMS trial”. Arthritis Res Ther. vol. 12. 2010. pp. R63
Sundy, JS, Becker, MA, Baraf, HS. “Pegloticase Phase 2 Study Investigators. Reduction of plasma urate levels following treatment with multiple doses of pegloticase (polyethylene glycol-conjugated uricase) in patients with treatment-failure gout: results of a phase II randomized study”. Arthritis Rheum.. vol. 58. 2008. pp. 2882-2891.
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Khanna, D, Fitzgerald, JD, Khanna, PP, Bae, S, Singh, MK, Neogi, T, Pillinger, MH, Merill, J, Lee, S, Prakash, S. “American College of Rheumatology. 2012 American College of Rheumatology guidelines for management of gout. Part 1: systematic nonpharmacologic and pharmacologic therapeutic approaches to hyperuricemia”. Arthritis Care Res (Hoboken). vol. 64. 2012 Oct. pp. 1431-46.
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- Does this patient have Gout?
- What tests to perform?
- How should patients with gout be managed?
- What happens to patients with gout?
- How to utilize team care?
- Are there clinical practice guidelines to inform decision making?
- What is the evidence?