UPSC MainsMEDICAL-SCIENCE-PAPER-I201510 Marks150 Words
Q18.

Discuss the pharmacotherapy of gout. Describe the rationale of the use of colchicine during acute attack of gout.

How to Approach

This question requires a two-pronged approach. First, a detailed discussion of the pharmacotherapy of gout, encompassing both acute and chronic management. Second, a focused explanation of colchicine's rationale during acute gout attacks, detailing its mechanism of action and specific role. Structure the answer by first outlining the overall pharmacological approach, then detailing acute and chronic therapies, and finally, dedicating a section specifically to colchicine. Include drug names, mechanisms, and potential side effects.

Model Answer

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Introduction

Gout is a common form of inflammatory arthritis caused by hyperuricemia – an elevated level of uric acid in the blood. This leads to the formation of monosodium urate crystals in joints, triggering an acute inflammatory response. Effective management of gout involves both alleviating acute attacks and preventing future episodes through long-term urate-lowering therapy. Pharmacotherapy forms the cornerstone of gout treatment, aiming to reduce pain and inflammation during attacks and lower serum uric acid levels to prevent crystal formation. Understanding the rationale behind each drug’s use is crucial for optimal patient care.

Pharmacotherapy of Gout: An Overview

The pharmacotherapy of gout is broadly divided into two categories: treatment of acute attacks and urate-lowering therapy for chronic management.

Treatment of Acute Gout Attacks

The primary goals during an acute attack are to rapidly reduce pain and inflammation. Several drug classes are employed:

  • Nonsteroidal Anti-inflammatory Drugs (NSAIDs): High-dose NSAIDs (e.g., naproxen, indomethacin) are first-line treatment, inhibiting cyclooxygenase (COX) enzymes and reducing prostaglandin synthesis. Contraindications include renal impairment and gastrointestinal ulcers.
  • Colchicine: Effective if initiated within 24-48 hours of attack onset. Its mechanism is detailed below.
  • Corticosteroids: Used when NSAIDs and colchicine are contraindicated or ineffective. Can be administered orally, intramuscularly, or intra-articularly. Long-term use carries significant side effects.

Urate-Lowering Therapy (ULT) for Chronic Gout

ULT aims to reduce serum uric acid levels below the saturation point (typically <6 mg/dL) to dissolve existing crystals and prevent new formation. Initiation of ULT is *not* done during an acute attack.

  • Xanthine Oxidase Inhibitors (XOIs): Allopurinol and febuxostat are the most commonly used agents. They inhibit xanthine oxidase, an enzyme crucial in uric acid production. Allopurinol can cause hypersensitivity reactions, while febuxostat has a higher cardiovascular risk in some patients.
  • Uricosurics: Probenecid increases uric acid excretion by the kidneys. Requires adequate hydration and is contraindicated in patients with renal impairment.
  • Pegloticase: A recombinant mammalian uricase enzyme that converts uric acid to allantoin, a more soluble and easily excreted product. Reserved for severe, refractory gout.

Rationale for Colchicine Use During Acute Gout Attacks

Colchicine’s mechanism of action is unique. It binds to tubulin, disrupting microtubule polymerization. This inhibits leukocyte migration and adhesion to the joint lining, reducing inflammation. Specifically, it interferes with the inflammasome activation, a key component of the inflammatory cascade in gout.

Colchicine is most effective when started early in an attack, ideally within the first 24-48 hours. However, it has a narrow therapeutic index, meaning the difference between an effective dose and a toxic dose is small. Common side effects include nausea, vomiting, and diarrhea. Its use is often limited by these gastrointestinal effects.

Drug Mechanism of Action Use Side Effects
Colchicine Inhibits leukocyte migration & inflammasome activation Acute gout attacks Nausea, vomiting, diarrhea
Allopurinol Inhibits xanthine oxidase Chronic gout (ULT) Hypersensitivity reactions
Febuxostat Inhibits xanthine oxidase Chronic gout (ULT) Cardiovascular risk

Conclusion

Effective pharmacotherapy of gout requires a tailored approach, addressing both acute inflammation and chronic hyperuricemia. While NSAIDs and corticosteroids provide rapid relief during attacks, urate-lowering therapy is essential for long-term prevention. Colchicine remains a valuable option for acute attacks, particularly when initiated early, despite its potential side effects. Careful patient selection, monitoring, and adherence to treatment guidelines are crucial for optimal outcomes in gout management.

Answer Length

This is a comprehensive model answer for learning purposes and may exceed the word limit. In the exam, always adhere to the prescribed word count.

Additional Resources

Key Definitions

Hyperuricemia
A condition characterized by an elevated level of uric acid in the blood, typically defined as >7 mg/dL. It is a major risk factor for gout.
Inflammasome
A multi-protein complex within cells that activates inflammatory responses. In gout, the NLRP3 inflammasome is activated by monosodium urate crystals, leading to the release of pro-inflammatory cytokines like IL-1β.

Key Statistics

The prevalence of gout has been increasing globally. In the US, it affects approximately 4% of adults, with a higher prevalence in men and individuals with comorbidities like obesity and kidney disease.

Source: National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS), 2023 (knowledge cutoff)

Approximately 60-80% of individuals with gout experience a first attack in the first metatarsophalangeal joint (big toe).

Source: American College of Rheumatology, 2022 (knowledge cutoff)

Examples

Dietary Triggers

A patient with gout may experience an acute attack after consuming a large meal rich in purines, such as red meat, organ meats, or seafood. This increases uric acid production, potentially triggering crystal formation.

Frequently Asked Questions

Can gout be cured?

Gout is not typically "cured," but it can be effectively managed with long-term urate-lowering therapy. Maintaining serum uric acid levels below the saturation point can prevent future attacks and dissolve existing crystals, leading to remission.

Topics Covered

PharmacologyRheumatologyGoutPharmacotherapyColchicine