Pharmacotherapy of _____GOUT AND HYPERURICEMIA___
Pharmacotherapy of _____GOUT AND HYPERURICEMIA___
Thomas Tran, PharmD Candidate 2007
|Epidemiology |( A direct correlation is seen between serum uric acid concentration and both incidence and prevalence of gout |
| |- Incidence of gout varies from 20 to 35 per 100,000 persons with an overall |
| |prevalence of 1.6 to 13.6 per thousand |
| |- Prevalence increases with age (especially in men) |
| |- Men are affected by gout approximately 10 times more often than women |
|Disease State | ( Gout describes a disease spectrum including: |
|Definition |-Hyperuricemia |
| |-Recurrent attacks of acute arthritis |
| |-Presence of urate crystals in synovial fluid |
| |-Deposits of urate crystals in tissues (tophi) |
| |-Interstitial renal disease |
| | |
| |( Gout is a rapid onset of excruciating pain, swelling, and inflammation of a joint, |
| |particularly the metatarsal phalanges of first toe. |
| | |
| |( Hyperuricemia may be an asymptomatic condition with an increased serum uric acid level as the only apparent abnormality. |
| | |
| |( Normal serum urate concentration values are 6.8 mg/dL for men and 6.0 mg/dL for women |
| | |
| |( Serum urate concentration values for hyperuricemia |
| |-Men: > 7 mg/dL |
| |-Women: > 6 mg/dL |
|Patho-physiology |( Determine whether the patient is an overproducer or underexcretor of uric acid |
| | |
| |( About 10% of the patients who develop gout are overproducers and the rest are |
| |underexcretors. |
| | |
| |( Purines from which uric acid is produced originates from 3 sources: |
| |Dietary purine |
| |Conversion of tissue nucleic acid to purine nucleotides |
| |De novo synthesis of purine bases. |
| | |
| |( There are two enzymatic abnormalities which result in the overproduction of uric acid |
| |Increase in the activity of phosphoribosyl pyrophosphate (PRPP) synthetase, which leads to increased PRPP concentration, and thus increased|
| |uric acid production. |
| |Deficiency of hypoxanthine guanine phosphoribosyl transferase(HGPRT) which leads to increased metabolism of guanine and hypoxanthine to |
| |uric acid. |
| | |
| |( Underexcretion of uric acid occurs when the decline in urinary excretion of uric acid is |
| |below the rate of production |
| | |
| |( Some factors which can contribute to the underexcretion of urate include: |
| |-Renal insufficiency |
| |-Lead intoxication |
| |-Ethanol |
| |-Diuretics |
| |-Hypothyroidism |
| | |
|Clinical Presentation |Asymptomatic Hyperuricemia |
| |( Is defined as an abnormally high serum urate level, without gouty arthritis or nephrolithiasis. |
| |( Hyperuricemia predisposes patients to both gout and nephrolithiasis, but does not warrant therapy in the asymptomatic patient. |
| | |
| |Acute Gouty Arthritis |
| |( Characterized by the sudden onset of pain, erythema, limited ROM and swelling of the involved joint. |
| |( The peak incidence of acute gout occurs between 30 and 50 years of age. |
| |( First attacks are monoarticular in 90 percent. |
| |( In more than 50% of patients, the first MTP joint is the initial joint involved. |
| |( Joint involvement includes the MTP joint, the instep/forefoot, the ankle, the knee, the wrist |
| |and the fingers. |
| |( Conditions that can precipitate an attack include: |
| |-Stress and trauma |
| |-Alcohol ingestion |
| |-Infections and surgery |
| |-Uric acid-lowering agents that can rapidly lower serum uric acid levels |
| |-Drugs known to elevate serum uric acid concentrations |
| | |
| |Intercritical Gout |
| |( Consists of the asymptomatic phase of the disease following recovery from acute gouty |
| |arthritis. |
| | |
| |Tophaceous Gout |
| | |
| |( Recurrent acute attacks can lead to chronic tophaceous gout. |
| |( It consists of progressive cartilage and bone erosion and deposition of tophi |
| |( Tophi are deposits of sodium urate (large enough to be seen on radiographs) and may occur |
| |at any site. |
| |( Common sites of occurrence include: |
| |Joints of hands or feet |
| |Helix of the ear |
| |Olecranon bursa |
| |Achilles tendon. |
|Risk Factors | ( Serum urate concentration correlates with age, Scr, BUN, male gender, blood pressure, |
| |body wt, and alcohol intake |
| | |
| |( Dietary sources of purines |
| | |
| |( Disease states: Obesity, CHF, hyperparathyroidism, hypothyroidism, psoriasis, etc (Refer |
| |to attached table 1 for Conditions Associated with Hyperuricemia) |
| | |
| |( Medications: diuretics (thiazides), salicylates (< 2g/day), cyclosporine, etc (Refer to |
| |attached table 2 for Drugs Capable of Inducing Hyperuricemia and Gout) |
| | |
| |( Although no genetic marker has been isolated for gout, the familial nature of gout |
| |strongly suggests an interaction between genetic and environmental factors |
|Diagnosis |Presence of urate crystals in synovial fluid |
| |A tophus proven with urate crystals by chemical means or polarized light microscopy |
| |OR |
| |Presence of 6 of the following 12 clinical lab and X-ray findings: |
| |More than 1 attack of acute arthritis |
| |Maximum inflammation within 1 day |
| |Attack of mono-articular arthritis |
| |Joint redness observed |
| |First MTP joint painful or swollen |
| |Unilateral attack involving 1st MTP joint |
| |Unilateral attack involving tarsal joint |
| |Suspected tophus |
| |Hyperuricemia |
| |Asymmetric swelling within a joint |
| |Subcortical cysts without erosion |
| |Negative culture of joint fluid for microorganisms during attack of acute inflammation |
|Desired Therapeutic |Acute Gouty Arthritis |
|Outcomes* |Relieve acute pain |
| |Relieve acute inflammation |
| | |
| |Recurrent gout |
| |Relieve acute attacks |
| |Prevent acute attacks |
| | |
| |Hyperuricemia |
| |Reduce serum uric acid concentrations to normal ranges |
| |Prevent complications of hyperuricemia |
| |Prevent acute gout attacks |
| |Prevent uric acid nephropathy |
| |Reduce tophi if present |
| | |
| |-DiPiro JT, Talbert RL, Yee GC et al., eds. Pharmacotherapy: A pathophysiological approach. 6th ed |
|*Reference of |-ISAT class notes on Gout and Hyperuricemia |
|Guidelines Used |- Harris MD, Siegel LB, Alloway JA. Gout and hyperuricemia. American Family Physician. 1999; 59:925-34 |
| |-Chan PD, Johnson MT. Treatment Guidelines for medicine and primary care. Current Clinical Strategies Publishing 2006. 268. |
|Treatment Options** | |
| |Non-drug therapy: |
|(Non-drug and Drug |( Dietary changes |
|Therapy – include all |-Low protein/purine diet (stay away from foods like red meat, seafood, tofu, beans) |
|therapeutic |-Drink 2-3 liters a day of fluid |
|classes/agents |( Lifestyle changes |
|available and |-Weight reduction (obesity increases risk of hyperuricemia and gout) |
|preferences per |-Avoid drugs capable of inducing hyperuricemia and gout |
|treatment guidelines) |-Alcohol avoidance |
| | |
| |Drug therapy: |
| |( NSAIDs |
| |( Colchicine |
| |( Xanthine Oxidase Inhibitor |
| |( Uricosuric agents |
|**See Treatment Options|( Corticosteroids |
|Table | |
| | |
| | |
|Monitoring | |
| | |
|(Efficacy and Toxicity |**See Treatment Options Table |
|Parameters) | |
Table 1 Conditions Associated with Hyperuricemia
|Primary gout |Obesity |
|Diabetic ketoacidosis |Sarcoidosis |
|Myeloproliferative disorders |Congestive heart failure |
|Lactic acidosis |Renal dysfunction |
|Lymphoproliferative disorders |Down syndrome |
|Starvation |Lead toxicity |
|Chronic hemolytic anemia |Hyperparathyroidism |
|Toxemia of pregnancy |Acute alcoholism |
|Pernicious anemia |Hypoparathyroidism |
|Glycogen storage disease type 1 |Acromegaly |
|Psoriasis |Hypothyroidism |
TABLE 2 Drugs Capable of Inducing Hyperuricemia and Gout
|Diuretics |Ethanol |Ethambutol |
|Nicotinic acid |Pyrazinamide |Cytotoxic drugs |
|Salicylates ( ................
................
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