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Gout and
Hyperuricemia
apt. Farisa Luthfiana, S.Farm, M.Clin.Pharm
Capaian Pembelajaran
Setelah mengikuti matakuliah ini mahasiswa mampu:
1. Memahami patofisiologi RA
2. Memahami terapi rasional pada berbagai kasus RA
3. Mampu mengidentifikasi dan menyelesaikan permasalahan terkait
pengobatan RA
Tujuan Pembelajaran
Mahasiswa mampu memilih terapi (b) farmakologi atau
pengobatan(c) dengan tepat (d), termasuk terapi non farmakologis,
menentukan pedoman pemilihan obat, rekomendasi dosis, monitoring
efek samping, pertimbangan farmakokinetik, dan interaksi obat
dengan obat lainnya.
Key Concepts
01
Etiology
02
Algoritma
03
Drug
information
04
Case Study
05
Summary
06
TABLE OF CONTENT
Key Concepts
01
KEY CONCEPTS
In the absence of a history of gout, asymptomatic hyperuricemia is not
usually treated
Acute gouty arthritis may be treated effectively with short courses of
highdose nonsteroidal anti-inflammatory drugs (NSAIDs), corticosteroids, or
colchicine
Initiation of a xanthine oxidase inhibitor may be considered in patients with
gout and one of the following indications for urate-lowering therapy (ULT):
(a) two or more gout attacks per year,
(b) the presence of one or more tophus,
(c) a history of urolithiasis,
(d) high-risk comorbidities including chronic kidney disease, hypertension,
ischemic heart disease, or heartvfailure,
(e) first diagnosis of gout at age <40 years,
(f) serum uric acidvconcentrations >8.0 mg/dL.
KEY CONCEPTS
According to the treat-to-target approach supported by the American
College of Rheumatology (ACR) and European League Against Rheumatism
(EULAR) Guidelines, the goal serum urate concentration is less than 6 mg/dL
[less than 357 μmol/L], or less than 5 mg/dL [less than 297 μmol/L] if signs
of gout persist at a concentration of 6 mg/dL.
Xanthine oxidase inhibitors are preferred agents for the prophylaxis of
recurrent gout attacks because they are effective in both underexcreters
and overproducers of uric acid.
Uricosuric drugs are contraindicated for patients with impaired kidney
function (a creatinine clearance less than 45-50 mL/min).
Due to increased risk of acute kidney injury when used as monotherapy,
lesinurad is only approved to be taken in combination with a xanthine
oxidase inhibitor.
KEY CONCEPTS
Low-dose colchicine, NSAID, or corticosteroid therapy should be
administered during the first 6 months of urate-lowering therapy (ULT) to
minimize the risk of acute gout attacks that may occur during this initiation
period..
Uric acid nephrolithiasis should be treated with adequate hydration (2-3
L/day), a daytime urine-alkalinizing agent, and 60 to 80 mEq/day (mmol/day)
of potassium bicarbonate or potassium citrate..
Patients with hyperuricemia or a history of gouty arthritis should undergo
comprehensive evaluation for signs and symptoms of cardiovascular
disease, and aggressive management of cardiovascular risk factors (eg,
weight loss, reduction of alcohol intake, control of blood pressure, glucose,
and lipids) should be attempted.
Definition and
etiology
02
Prognostic
Asymptimatic
Hiperuricemia Intercritical
phase
Tophaceous Gout
Uric Acid
Nephrolithiasis
Acute
Definition
The term gout describes a heterogeneous clinical spectrum of
diseases including elevated serum urate concentration
(hyperuricemia), recurrent attacks of acute arthritis
associated with monosodium urate (MSU) crystals in
synovial fluid leukocytes, deposits of monosodium urate
crystals (tophi) in tissues in and around joints, interstitial
kidney disease, and uric acid nephrolithiasis
A decline in the urinary excretion of
uric acid to a concentration
below the rate of production
leads to hyperuricemia and an
increased miscible pool of
sodium urate.
Overproduction of
Uric Acid
Underexcretion of
Uric Acid
Metabolism product
Cause Gout Hiperuricemia
Algoritma
03
EULAR Evidence-Based
Recommendations for
Gout:
Diagnostic Principles
Management Gout
Acute Maintanance
Analgetic/
antiinflamation
Analgetic Urate
Lowering
Therapy
Algorithm for management of an acute gout attack. (Algorithm
derived from 2017 ACP, 2016 EULAR and 2012 ACR gout guidelines.)
Acute Gouty Arthritis
Management of Hyperuricemia in Gout (maintenance)
Algorithm for management of hyperuricemia in gout. (Algorithm derived from 2017 ACP, 2016 EULAR and 2012 ACR goutguidelines.)
Drug
information
04
Uric acid pathway and targets of drug
action. (HGPRT, hypoxanthine-
guanine phosphoribosyltransferase;
PRPP, phosphoribosyl
pyrophosphate.)
Xantin Oxidase
Inhibitor
Xanthine oxidase inhibitors
reduce uric acid
by impairing the ability of
xanthine oxidase to convert
hypoxanthine to xanthine
and xanthine to uric acid
Uricosuric Drugs
Uricosuric drugs increase the
renal clearance of uric acid
by inhibiting postsecretory renal
proximal tubular
reabsorption of uric acid.
Urate Lowering Therapy
*Anti-Inflammatory Gout
Prophylaxis during
Initiation of Pharmacologic
Urate-Lowering Therapy
*Interleukin-1 Inhibitors

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gout.pptx

  • 1. Gout and Hyperuricemia apt. Farisa Luthfiana, S.Farm, M.Clin.Pharm
  • 2. Capaian Pembelajaran Setelah mengikuti matakuliah ini mahasiswa mampu: 1. Memahami patofisiologi RA 2. Memahami terapi rasional pada berbagai kasus RA 3. Mampu mengidentifikasi dan menyelesaikan permasalahan terkait pengobatan RA
  • 3. Tujuan Pembelajaran Mahasiswa mampu memilih terapi (b) farmakologi atau pengobatan(c) dengan tepat (d), termasuk terapi non farmakologis, menentukan pedoman pemilihan obat, rekomendasi dosis, monitoring efek samping, pertimbangan farmakokinetik, dan interaksi obat dengan obat lainnya.
  • 6. KEY CONCEPTS In the absence of a history of gout, asymptomatic hyperuricemia is not usually treated Acute gouty arthritis may be treated effectively with short courses of highdose nonsteroidal anti-inflammatory drugs (NSAIDs), corticosteroids, or colchicine Initiation of a xanthine oxidase inhibitor may be considered in patients with gout and one of the following indications for urate-lowering therapy (ULT): (a) two or more gout attacks per year, (b) the presence of one or more tophus, (c) a history of urolithiasis, (d) high-risk comorbidities including chronic kidney disease, hypertension, ischemic heart disease, or heartvfailure, (e) first diagnosis of gout at age <40 years, (f) serum uric acidvconcentrations >8.0 mg/dL.
  • 7. KEY CONCEPTS According to the treat-to-target approach supported by the American College of Rheumatology (ACR) and European League Against Rheumatism (EULAR) Guidelines, the goal serum urate concentration is less than 6 mg/dL [less than 357 μmol/L], or less than 5 mg/dL [less than 297 μmol/L] if signs of gout persist at a concentration of 6 mg/dL. Xanthine oxidase inhibitors are preferred agents for the prophylaxis of recurrent gout attacks because they are effective in both underexcreters and overproducers of uric acid. Uricosuric drugs are contraindicated for patients with impaired kidney function (a creatinine clearance less than 45-50 mL/min). Due to increased risk of acute kidney injury when used as monotherapy, lesinurad is only approved to be taken in combination with a xanthine oxidase inhibitor.
  • 8. KEY CONCEPTS Low-dose colchicine, NSAID, or corticosteroid therapy should be administered during the first 6 months of urate-lowering therapy (ULT) to minimize the risk of acute gout attacks that may occur during this initiation period.. Uric acid nephrolithiasis should be treated with adequate hydration (2-3 L/day), a daytime urine-alkalinizing agent, and 60 to 80 mEq/day (mmol/day) of potassium bicarbonate or potassium citrate.. Patients with hyperuricemia or a history of gouty arthritis should undergo comprehensive evaluation for signs and symptoms of cardiovascular disease, and aggressive management of cardiovascular risk factors (eg, weight loss, reduction of alcohol intake, control of blood pressure, glucose, and lipids) should be attempted.
  • 11. Definition The term gout describes a heterogeneous clinical spectrum of diseases including elevated serum urate concentration (hyperuricemia), recurrent attacks of acute arthritis associated with monosodium urate (MSU) crystals in synovial fluid leukocytes, deposits of monosodium urate crystals (tophi) in tissues in and around joints, interstitial kidney disease, and uric acid nephrolithiasis
  • 12. A decline in the urinary excretion of uric acid to a concentration below the rate of production leads to hyperuricemia and an increased miscible pool of sodium urate. Overproduction of Uric Acid Underexcretion of Uric Acid Metabolism product Cause Gout Hiperuricemia
  • 16. Algorithm for management of an acute gout attack. (Algorithm derived from 2017 ACP, 2016 EULAR and 2012 ACR gout guidelines.) Acute Gouty Arthritis
  • 17. Management of Hyperuricemia in Gout (maintenance) Algorithm for management of hyperuricemia in gout. (Algorithm derived from 2017 ACP, 2016 EULAR and 2012 ACR goutguidelines.)
  • 19. Uric acid pathway and targets of drug action. (HGPRT, hypoxanthine- guanine phosphoribosyltransferase; PRPP, phosphoribosyl pyrophosphate.)
  • 20. Xantin Oxidase Inhibitor Xanthine oxidase inhibitors reduce uric acid by impairing the ability of xanthine oxidase to convert hypoxanthine to xanthine and xanthine to uric acid Uricosuric Drugs Uricosuric drugs increase the renal clearance of uric acid by inhibiting postsecretory renal proximal tubular reabsorption of uric acid. Urate Lowering Therapy *Anti-Inflammatory Gout Prophylaxis during Initiation of Pharmacologic Urate-Lowering Therapy *Interleukin-1 Inhibitors