Drugs Used in Gout

What are some adverse effects of allopurinol? What should be done if a cutaneous reaction to allopurinol occurs?

It is well tolerated by most patients but some patients can have a hypersensitivity reaction that can cause skin rashes and may lead to Steven-Johnson syndrome. The drugs use should be discontinued

What are the two main strategies for the treatment of gout?

1)Management of the acute attacks of gouty arthritis 2)long-term management of chronic gout.

Allopurinol 1. Mechanism of action 2. Use What does this drug do to tophi? How can this affect the attacks of acute gouty arthritis? How can this be prevented?

1. A purine analog that acts as an inhibitor of xanthine oxidase 2. Used to treat chronic gout by lowering uric acid plasma concentration It causes the dissolution of tophi. The attacks may increase because of the mobilization of the tissue stores of uric acid. By administering NSAIDs or colchicine during the first 4-6 months of allopurinol therapy to reduce the change of an acute attack of gout.

Rasburicase 1. Mechanism of action 2. Use In the US, where is this drug obtained from?

1. Animal derived enzyme that oxidizes uric acid to allantoin, a soluble compound that is easily excreted from the kidneys 2. Used to prevent renal injury caused by rapid lysis of tumor cells and release of free nucleotides (which increases plasma urate levels) in patients receiving chemotherapy. Aspergillus

Glucocorticoids 1. Mechanism of action 2. Use When and how is this used to treat acute gout attacks?

1. Anti-inflammatory and immunosuppressive effects 2. Used to treat attacks of acute gouty arthritis When an attack of acute gouty arthritis is unresponsive to NSAIDs or colchicine depot preparations of glucocorticoids can be injected directly into the site of inflammation.

Colchicine 1. Mechanism of action 2. Use 3. Adverse effects Is this drug safe to use in pregnancy? In which patients should it be used with caution? Is this drug used much anymore?

1. Binds to tubulin which inhibits it polymerization preventing the formation of microtubules. This disrupts the motility of granulocytes and decreases their migration into effected areas and blocks cell division. It also inhibits the release of leukotrienes 2. Used in the treatment of attacks of acute gouty arthritis 3. May cause myopathy neutropenia, aplastic anemia, and alopecia. No Patients with hepatic, renal, or cardiovascular disease. No, because of its troublesome diarrheal AE it has been replaced by NSAIDs

NSAIDs 1. Mechanism of action 2. Use in gout What NSAID is contraindicated in patients with gout and why?

1. Inhibition of COX 2. First-line drug for the treatment of acute gouty arthritis Aspirin: it competes with uric acid for excretion from the proximal tubules of the kidneys which can lead to increased levels of urate in the blood.

Indomethacin 1. Mechanism of action 2. Use in gout

1. NSAID 2. Most popular drug in the treatment of pain for patients suffering from an acute gouty arthritis attack

The aims of therapy for gout are different for each strategy. What is the aim of therapy for the following strategies? 1. Management of the acute attacks of gouty arthritis 2. Management of chronic gout

1. To control pain 2. To achieve normal concentrations of plasma urate

Probenecid 1. Mechanism of action 2. Use 3. Adverse effects In what patients should this drug not be used? Patients taking this drug should be recommended to do what?

1. Uricosuric agent which inhibits uric acid reabsorption in the kidneys 2. Used to treat chronic gout 3. Hypersensitivity reactions In patients with nephrolithiasis as it may form kidney stones. Drink lots of water to minimize the risk of developing kidney stones.

Sulfinpyrazone 1. Mechanism of action 2. Use 3. Adverse effects In what patients should this drug not be used? Patients taking this drug should be recommended to do what?f What drug interaction should be remembered for this drug?

1. Uricosuric agent which inhibits uric acid reabsorption in the kidneys 2. Used to treat chronic gout 3. Hypersensitivity reactions and depression of hematopoesis Because of the possibility of depressing hematopoesis this drug should not be used in patients with underlying blood dyscrasias. Drink lots of water to minimize the risk of developing kidney stones. It can inhibit the metabolism of warfarin.

Gout is a metabolic disorder characterized by what? Does hyperuricemia always lead to gout? What forms sodium urate? What process ensues when the crystals deposit in tissues?

High levels of uric acid in the blood which leads to deposition of sodium urate crystals in tissues and joints. NO - can lead to deposition of sodium urate crystals in jt w/out leading to gout. BUT GOUT is always preceded by hyperuricemia. end product of purine metabolism inflammatory process

What is the interaction between allopurinol, mercaptopurine, and azathioprine?

Mercaptopurine and azothioprine are both metabolized by xanthine oxidase. If a patient starts taking allopurinol their dose of these drugs should be reduced in order to account for this change.

What types of drugs are used for acute gout? What drugs are used for chronic gout?

NSAIDs Colchicine Glucocorticoids 1)agents to decrease uric acid synthesis -allopurinol 2)agents to enhance uric acid secretion = uricosuric agents -probenecid -sulfinpyrazone 3)agents to enhance uric acid metabolism -rasburicase

How do uricosuric agents act to treat chronic gout? What must be given along with these drugs to avoid causing an attack of gout?

They compete with irate for a transporter in the kidneys and inhibit the reabsorption of uric acid. NSAIDs or colchicine