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Acute Gout Care
Although nonpharmacologic measures, such as ice pack application and rest of the involved
joints, can be helpful, the mainstay of acute gout care is the administration of
anti-inflammatory drugs such as
nonsteroidal anti-inflammatory drugs (NSAIDs), colchicine, and
glucocorticoids.
The choice of these options largely
depends on the patients’ comorbidities, concurrent medications,and previous response if
recurrent flares. Early initiation of antiinflammatories helps abort or reduce the severity of
flares. Thus,for recurrent flares in established gout patients, patients can beprovided a supply
of their medications ready to start at the first sign of a flare.
# NSAIDs are used most often in individuals without complicating comorbidities; NSAIDs given
in full anti-inflammatory doses are effective in the vast majority of patients (e.g., indomethacin,
25–50 mg tid; naproxen, 500 mg bid; ibuprofen, 800 mg tid;and celecoxib, 800 mg followed by
400 mg 12 h later, then 400 mg bid).
# Oral colchicine is also effective, particularly if used early in a gout flare. A low-dose regimen
(1.2 mg with the first sign of a flare,followed by 0.6 mg in 1 h and subsequent-day dosing
depending on
response) is as effective as, and better tolerated than, the formerly used higher-dose regimens.
Colchicine is eliminated from the body through P-glycoprotein (also known as MDR1) in the
liver, small intestine, and kidneys as well as via enteric and hepatic cytochrome P450 3E4
(CYP3A4). As such, the dose, particularly for prolonged
use, is reduced among patients with renal disease or when used with P-glycoprotein or CYP3A4
inhibitors such as clarithromycin
or tacrolimus; additional caution is warranted among patients with hepatorenal impairment.
# Glucocorticoids given as an intramuscular injection or orally (e.g., prednisone, 30–50 mg/d
as the initial dose and gradually tapered with the resolution of the attack) can be effective even
in polyarticular gout. For a single joint or a few involved joints,intraarticular glucocorticoid
injection is effective and well tolerated.
# With the central role of the inflammasome and IL-1β in gout flares,anakinra is a useful option
when other treatments are contraindicated or have failed.
URATE-LOWERING THERAPY
Ultimate control of gout requires correction of the underlying chronic hyperuricemia, the central
cause for gout.
Attempts to normalize serum urate to a subsaturation point (typically, <300–360 μmol/L [5.0–6.0
mg/dL]) to prevent recurrent gout flares and eliminate tophi are critical and entail a commitment
to urate-lowering regimens that are required usually for life.
Urate-lowering drug therapy should be considered when, as in most patients, the
hyperuricemia cannot be corrected by risk factor interventions (control of body weight,
healthy diet, limitation of alcohol use,
decreased consumption of fructose-rich foods and beverages, and avoidance of thiazide and
loop diuretics).
The decision to initiate urate-lowering drug therapy usually is made considering
● the number of gout flares (urate lowering may be cost-effective with more than two
attacks yearly),
● severity and duration of flares,
● quality of life, or
● the patient’s willingness to commit to lifelong therapy.
Urate-lowering therapy should be initiated in any patient who already has subcutaneous
tophi or chronic gouty arthritis or known uric acid stones.
Allopurinol, a xanthine oxidase inhibitor, is the first-line urate-lowering drug among gout
patients. Allopurinol can be given in a single morning dose, starting at 100 mg daily or less and
titrating up (to 800 mg daily) to achieve a target serum urate level
<5–6 mg/dL (i.e., a subsaturation point of MSU crystals). In patients with chronic kidney disease
(CKD), the starting allopurinol dose should be lowered depending on the CKD levels; for
example, with
an estimated glomerular filtration rate of 30–45 mL/min, one would
start at 50 mg daily and titrate up slowly. Starting at a low dose and
titrating up reduces the risk of severe cutaneous adverse reactions
(SCARs), including Stevens-Johnson syndrome and toxic epidermal necrolysis, as well as the
risk of gout flares associated with
rapid serum urate reduction due to introduction of urate-lowering therapy. Allopurinol is
generally well tolerated, but mild cutaneous reactions can develop in ~2% of users.
SCARs to allopurinol are rare but can be life-threatening, and thus, appropriate precaution is
advised. Presence of CKD, higher allopurinol initial dosing (e.g., >100 mg daily in CKD
patients), and HLA-B*
5801 carriage are important risk factors; older age and female sex are also associated with a
higher risk of SCARs. As the HLA-B*5801 carriage rate is substantially higher among Southeast
Asians (except for
Japanese descendants), Pacific Islanders/Native Hawaiians, and
blacks than whites or Hispanics (leading to racial disparity in the risk of SCARs), screening for
HLA-B*5801 should be performed before starting allopurinol in those Asians and blacks. If
patients carry the HLA-B*5801 allele, an alternative urate-lowering agent should be
administered.
Febuxostat is a newer xanthine oxidase
inhibitor that is predominantly metabolized by glucuronide formation and oxidation in the liver
and considered to not require dose
adjustment in moderate to severe chronic kidney disease. It has also been used in patients
who carry the HLA-B*
5801 allele.
Uricosuric agents such as probenecid are considered second-line urate-lowering therapies for
gout and can be used in patients with good renal function either alone or in combination with
xanthine
oxidase inhibitors such as allopurinol. Probenecid can be started at a dose of 250 mg twice daily
and increased gradually as needed up to 3 g/d to achieve and maintain a target serum urate
level. Probenecid is generally not effective in patients with serum creatinine levels >177 μmol/L
(2 mg/dL).
Benzbromarone (not available in
the United States) is another uricosuric drug that is more effective in patients with CKD.
In contrast to thiazide and loop diuretics,
which increase serum urate levels and trigger gout attacks, other drugs used to treat common
comorbidities of gout can also help
lower serum urate levels, including losartan, amlodipine, fenofibrate, and sodium-glucose
cotransporter-2 inhibitors.
Pegloticase is a pegylated uricase that is available for patients who do not tolerate
or fail full doses of other treatments.
Urate-lowering drugs are generally not initiated during active ongoing gout flares, given
the potential worsening of the flare by acutely lowering serum urate levels. However,
urate-lowering therapy can be started during the resolution phase of or after a gout flare,
together with anti-inflammatory prophylaxis (e.g., colchicine 0.6 mg one to two times daily or
naproxen 250 mg twice daily) to reduce the risk of the flares that often occur with the initiation of
urate-lowering therapy. These paradoxical flares are presumed to be inflammatory reactions
to MSU crystals shed from dissolution of organized MSU deposits (synovial tophi) induced
by rapid
serum urate reduction . As such, faster urate reduction has been associated with higher risk
of flares in clinical trials of
urate-lowering drugs. Continuing concomitant anti-inflammatory
prophylaxis is usually recommended until the patient is normouricemic and without gouty
attacks for 3–6 months or tophi disappear.
Reference : Harrison's Principles of Internal Medicine 21st edition

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Acute Gout Care & Urate Lowering Therapy .pdf

  • 1. Acute Gout Care Although nonpharmacologic measures, such as ice pack application and rest of the involved joints, can be helpful, the mainstay of acute gout care is the administration of anti-inflammatory drugs such as nonsteroidal anti-inflammatory drugs (NSAIDs), colchicine, and glucocorticoids. The choice of these options largely depends on the patients’ comorbidities, concurrent medications,and previous response if recurrent flares. Early initiation of antiinflammatories helps abort or reduce the severity of flares. Thus,for recurrent flares in established gout patients, patients can beprovided a supply of their medications ready to start at the first sign of a flare. # NSAIDs are used most often in individuals without complicating comorbidities; NSAIDs given in full anti-inflammatory doses are effective in the vast majority of patients (e.g., indomethacin, 25–50 mg tid; naproxen, 500 mg bid; ibuprofen, 800 mg tid;and celecoxib, 800 mg followed by 400 mg 12 h later, then 400 mg bid). # Oral colchicine is also effective, particularly if used early in a gout flare. A low-dose regimen (1.2 mg with the first sign of a flare,followed by 0.6 mg in 1 h and subsequent-day dosing depending on response) is as effective as, and better tolerated than, the formerly used higher-dose regimens. Colchicine is eliminated from the body through P-glycoprotein (also known as MDR1) in the liver, small intestine, and kidneys as well as via enteric and hepatic cytochrome P450 3E4 (CYP3A4). As such, the dose, particularly for prolonged use, is reduced among patients with renal disease or when used with P-glycoprotein or CYP3A4 inhibitors such as clarithromycin or tacrolimus; additional caution is warranted among patients with hepatorenal impairment. # Glucocorticoids given as an intramuscular injection or orally (e.g., prednisone, 30–50 mg/d as the initial dose and gradually tapered with the resolution of the attack) can be effective even in polyarticular gout. For a single joint or a few involved joints,intraarticular glucocorticoid injection is effective and well tolerated. # With the central role of the inflammasome and IL-1β in gout flares,anakinra is a useful option when other treatments are contraindicated or have failed. URATE-LOWERING THERAPY Ultimate control of gout requires correction of the underlying chronic hyperuricemia, the central cause for gout.
  • 2. Attempts to normalize serum urate to a subsaturation point (typically, <300–360 μmol/L [5.0–6.0 mg/dL]) to prevent recurrent gout flares and eliminate tophi are critical and entail a commitment to urate-lowering regimens that are required usually for life. Urate-lowering drug therapy should be considered when, as in most patients, the hyperuricemia cannot be corrected by risk factor interventions (control of body weight, healthy diet, limitation of alcohol use, decreased consumption of fructose-rich foods and beverages, and avoidance of thiazide and loop diuretics). The decision to initiate urate-lowering drug therapy usually is made considering ● the number of gout flares (urate lowering may be cost-effective with more than two attacks yearly), ● severity and duration of flares, ● quality of life, or ● the patient’s willingness to commit to lifelong therapy. Urate-lowering therapy should be initiated in any patient who already has subcutaneous tophi or chronic gouty arthritis or known uric acid stones. Allopurinol, a xanthine oxidase inhibitor, is the first-line urate-lowering drug among gout patients. Allopurinol can be given in a single morning dose, starting at 100 mg daily or less and titrating up (to 800 mg daily) to achieve a target serum urate level <5–6 mg/dL (i.e., a subsaturation point of MSU crystals). In patients with chronic kidney disease (CKD), the starting allopurinol dose should be lowered depending on the CKD levels; for example, with an estimated glomerular filtration rate of 30–45 mL/min, one would start at 50 mg daily and titrate up slowly. Starting at a low dose and titrating up reduces the risk of severe cutaneous adverse reactions (SCARs), including Stevens-Johnson syndrome and toxic epidermal necrolysis, as well as the risk of gout flares associated with rapid serum urate reduction due to introduction of urate-lowering therapy. Allopurinol is generally well tolerated, but mild cutaneous reactions can develop in ~2% of users. SCARs to allopurinol are rare but can be life-threatening, and thus, appropriate precaution is advised. Presence of CKD, higher allopurinol initial dosing (e.g., >100 mg daily in CKD patients), and HLA-B* 5801 carriage are important risk factors; older age and female sex are also associated with a higher risk of SCARs. As the HLA-B*5801 carriage rate is substantially higher among Southeast Asians (except for Japanese descendants), Pacific Islanders/Native Hawaiians, and blacks than whites or Hispanics (leading to racial disparity in the risk of SCARs), screening for HLA-B*5801 should be performed before starting allopurinol in those Asians and blacks. If
  • 3. patients carry the HLA-B*5801 allele, an alternative urate-lowering agent should be administered. Febuxostat is a newer xanthine oxidase inhibitor that is predominantly metabolized by glucuronide formation and oxidation in the liver and considered to not require dose adjustment in moderate to severe chronic kidney disease. It has also been used in patients who carry the HLA-B* 5801 allele. Uricosuric agents such as probenecid are considered second-line urate-lowering therapies for gout and can be used in patients with good renal function either alone or in combination with xanthine oxidase inhibitors such as allopurinol. Probenecid can be started at a dose of 250 mg twice daily and increased gradually as needed up to 3 g/d to achieve and maintain a target serum urate level. Probenecid is generally not effective in patients with serum creatinine levels >177 μmol/L (2 mg/dL). Benzbromarone (not available in the United States) is another uricosuric drug that is more effective in patients with CKD. In contrast to thiazide and loop diuretics, which increase serum urate levels and trigger gout attacks, other drugs used to treat common comorbidities of gout can also help lower serum urate levels, including losartan, amlodipine, fenofibrate, and sodium-glucose cotransporter-2 inhibitors. Pegloticase is a pegylated uricase that is available for patients who do not tolerate or fail full doses of other treatments. Urate-lowering drugs are generally not initiated during active ongoing gout flares, given the potential worsening of the flare by acutely lowering serum urate levels. However, urate-lowering therapy can be started during the resolution phase of or after a gout flare, together with anti-inflammatory prophylaxis (e.g., colchicine 0.6 mg one to two times daily or naproxen 250 mg twice daily) to reduce the risk of the flares that often occur with the initiation of urate-lowering therapy. These paradoxical flares are presumed to be inflammatory reactions to MSU crystals shed from dissolution of organized MSU deposits (synovial tophi) induced by rapid serum urate reduction . As such, faster urate reduction has been associated with higher risk of flares in clinical trials of urate-lowering drugs. Continuing concomitant anti-inflammatory prophylaxis is usually recommended until the patient is normouricemic and without gouty attacks for 3–6 months or tophi disappear.
  • 4. Reference : Harrison's Principles of Internal Medicine 21st edition