Skip to Main Content

++

SOURCE

++

Source: Ernst ME, Fravel MA. Gout and hyperuricemia. In: DiPiro JT, Talbert RL, Yee GC, Matzke GR, Wells BG, Posey LM, eds. Pharmacotherapy: A Pathophysiologic Approach. 10th ed. New York, NY: McGraw-Hill; 2017. http://accesspharmacy.mhmedical.com/content.aspx?bookid=1861&sectionid=146069254. Accessed May 16, 2017.

++

DEFINITION

++

  • Elevated serum uric acid concentration (>7 mg/dL [416 μmol/L] in men or >6 mg/dL [357 μmol/L] in women)

++

ETIOLOGY

++

  • Idiopathic.

  • Increased activity of phosphoribosyl pyrophosphate (PRPP) synthetase.

  • Deficiency of hypoxanthine–guanine phosphoribosyl transferase (HGPRT)

  • Myeloproliferative and lymphoproliferative disorders.

  • Cytotoxic drug therapy.

  • Medications:

    • Diuretics.

    • Nicotinic acid.

    • Salicylates (<2 g/day)

    • Ethanol.

    • Pyrazinamide.

    • Levodopa.

    • Ethambutol.

    • Cyclosporine.

++

PATHOPHYSIOLOGY

++

  • Abnormalities in enzyme systems that regulate purine metabolism may result in overproduction of uric acid.

    • Increased activity of PRPP synthetase.

    • Deficiency of HGPRT

  • Uric acid overproduction may occur because of increased breakdown of tissue nucleic acids in myeloproliferative and lymphoproliferative disorders.

  • Cytotoxic drug therapy also leads to overproduction of uric acid.

  • Drugs can decrease renal clearance of uric acid.

++

EPIDEMIOLOGY

++

  • Hyperuricemia and gouty arthritis are more common in men than in women.

  • Risk of developing hyperuricemia increases with age.

++

RISK FACTORS

++

  • Renal insufficiency.

  • Metabolic syndrome.

  • Hypertension.

  • Pre-eclampsia or eclampsia.

  • Acidosis.

  • Hyperparathyroidism.

  • Hypothyroidism.

++

CLINICAL PRESENTATION

++
SIGNS AND SYMPTOMS
++

  • Patients may be asymptomatic or present with signs and symptoms of acute attack of gouty arthritis or nephropathy (see Gouty Arthritis).

++

DIAGNOSIS

++
MEANS OF CONFIRMATION AND DIAGNOSIS
++

  • Obtain medical history to determine whether patient has symptoms and to identify causes and comorbid conditions.

++
LABORATORY TESTS
++

  • Elevated serum uric acid level (>7 mg/dL [416 μmol/L] in men or >6 mg/dL [357 μmol/L] in women.

  • Obtain:

    • Complete blood count (CBC)

    • Serum electrolytes.

    • Blood urea nitrogen.

    • Creatinine.

    • Glucose.

    • Liver function tests.

    • Fasting lipid profile.

    • Calcium and phosphorus.

    • Thyroid-stimulating hormone.

  • Consider 24-hour urine collection for creatinine and uric acid to determine whether patient is overproducing or underexcreting uric acid.

++
DIFFERENTIAL DIAGNOSIS
++

++

DESIRED OUTCOMES

++

  • Prevent attacks of acute gouty arthritis.

  • In some cases, normalize serum uric acid concentration.

  • Goal of urate-lowering therapy: achieve and maintain serum uric acid concentration <6 mg/dL (357 μmol/L) and preferably <5 mg/dL (297 μmol/L).

++

TREATMENT: GENERAL APPROACH

++

  • Consider uric-acid lowering therapy in patients with history of recurrent acute gouty arthritis and significantly elevated serum uric acid concentration.

  • Urate-lowering therapy should not begin until 6–8 weeks after resolution of acute gout episode.

  • Reduction of serum urate concentration can be accomplished by decreasing uric acid synthesis (xanthine oxidase inhibitors) or by increasing renal excretion of uric acid (uricosurics).

  • Give colchicine 0.6 mg once daily for at least ...

Pop-up div Successfully Displayed

This div only appears when the trigger link is hovered over. Otherwise it is hidden from view.