Anti-Gout Drugs

INTRODUCTION

• Gout is a common and complex form of arthritis that can affect anyone. It’s characterized by sudden, severe attacks of pain, swelling, redness, and tenderness in the joints, often the joint at the base of the big toe.
• It is a metabolic disorder characterized by hyperuricemia. Purine is metabolized to uric acid by xanthine oxidase. In gout patients either increased in uric acid production or unable to excrete uric acid normally.
• So an excess of uric acid in the blood, this uric acid combines with sodium and forms sodium urate, which accumulates in typical sites like kidneys, cartilage, joints, and ears.
• Uric acid is the final product of the metabolism of endogenous and exogenous purine in man. An excess of uric acid, measured in the plasma as sodium urate, constitutes hyperuricemia.
• This excess may be caused by an overproduction or under excretion of urate. It is influenced by genetic and environmental factors and may be classified as primary (mainly idiopathic) or secondary.
• An increase in urate production may be caused by excessive dietary purine intake, certain cancers or their treatment, or, more rarely, enzyme defects of purine metabolism.
• Reduced urate excretion may be caused by renal disease, hypertension, or the intake of certain drugs such as thiazide diuretics. Other factors contributing to hyperuricemia include hyperlipidemia, obesity, alcohol consumption, and lead exposure.
• A gout is a form of inflammatory arthritis that develops in some people who have high levels of uric acid in the blood.
• The acid can form needle-like crystals in a joint and cause sudden, severe episodes of pain, tenderness, redness, warmth, and swelling.
• Gout is caused initially by an excess of uric acid in the blood, or hyperuricemia.
• Uric acid is produced in the body during the breakdown of purines – chemical compounds that are found in high amounts in certain foods such as meat, poultry, and seafood.

CLASSIFICATIONS OF DRUGS USE IN THE TREATMENT OF GOUT

Drugs that act in Acute Gout:

• Drugs which inhibits neutrophils migration in joint: Colchicines.
• Drugs that inhibit inflammation and pain: NSAIDs, Prednisolone.

Drugs used in Chronic Gout:

• Drugs that inhibit uric acid synthesis: Allopurinol, Febuxostat.
• Drugs that increase uric acid excretion: Probenecid, Sulphinpyrazone, Benzhromarone.

Therapeutic Uses:

• Antigout drugs in chronic and acute gout.
• Secondary hyperuricemia.

ADR:

• Hypersensitivity reaction, Skin rashes, Arthralgia, Pain, Fever, hepatitis, GIT distress, Nausea, Peripheral neuritis, Cataract formation.

Probenecid:

• Increased uric acid excretion by inhibiting its active reabsorption from renal tubules. The result increased uric acid excretion. Uricosuric effect.

Therapeutic Uses:

• Chronic gout.
• Hyperuricemia.

ADR:

• Git distress, Allergic dermatitis, dyspepsia, nephritic syndrome.

Sulfinpyrazone:

• Increased uric acid excretion by inhibiting its active reabsorption from renal tubules. The result increased uric acid excretion. Uricosuric effect.

Therapeutic Uses:

• Chronic gout
• Hyperuricemia

ADR:

• GIT disturbance, Nausea, Vomiting, hyperuricemia.

Prednisolone:

MOA:

• Inhibits gene transcription of COX₂, cytokines, interleukins, as a result, produce relief from inflammation.
• Increase release and synthesis of annexin-1, which is potent anti-inflammatory to cells hence produce anti-inflammatory actions.
• Symptomatic pain relief.
• Inhibition of chemotactic migration of leucocytes.

ADR:

• Prolonged use leads to toxic effects.

Therapeutic Uses:

• Acute gout.
• Hyperuricemia.

NSAIDs:

MOA:

• NSAIDs reduce inflammation and pain but it does not have any effect on disease progression.

• Inhibits pain sensation-Analgesic action.
• Reduced capillary permeability, decreased tissue edema-Anti inflammatory action.
• These release Prostaglandins which are responsible for inflammation, pain, etc.
• COX inhibitors cause inhibition of COX enzyme and inhibit the conversion of arachidonic acid into PGG₂ later PGG₂ to PGH₂, PGI₂, PGE₂, PGF₂α, and PGD₂. So inhibits pain sensation-Analgesic action, decreased tissue edema-Anti inflammatory action.
• Symptomatic pain relief
• Inhibition of chemotactic migration of leucocytes.
• Inhibits crystal urate formation.

Therapeutic Uses:

• Acute gout
• Hyperuricemia

Adverse Effects:

• Nausea, Vomiting, Constipation, Diarrhea, Dizziness, Edema, Kidney failure, Ulcers.

Colchicines:

• Drugs which inhibits neutrophils migration in joint. Inhibition of chemotactic migration of leucocytes.
• Relief from gout.

Therapeutic Uses:

• Acute gout.
• Hyperuricemia.

ADR:

• GIT disturbance, Nausea, Vomiting, hyperuricemia.

Make sure you also check our other amazing Article on : NSAIDs