Gout

“The patient goes to bed and sleeps quietly until about two in the morning when he is awakened by a pain which usually seizes the great toe, but sometimes the heel, the calf of the leg or the ankle. The pain resembles that of a dislocated bone … and this is immediately succeeded by a chillness, shivering and a slight fever … the pain … , which is mild in the beginning … , grows gradually more violent every hour …   so exquisitely painful as not to endure the weight of the clothes nor the shaking of the room from a person walking briskly therein.” This is the famous description of acute gout attack by Sir Thomas Sydenham. Sir Thomas Sydenham was a famous physician of his times and he himself suffered from gout.

Introduction

Gout is sometimes referred to as the “disease of kings.” This is because people have incorrectly linked it to the kind of overindulgence in food and wine only the rich and powerful could afford at older time. Gout is the most common inflammatory arthritis in adults. It is one of the most painful forms of arthritis and many people compare gout-associated pain with childbirth or breaking a leg. It is one of the best understood diseases. Gout is a type of crystal related inflammatory arthritis induced by the deposition of monosodium urate (Uric acid) crystals in joints and other tissues. This condition and its complications occur more often in elderly males, women after menopause and people with kidney disease. It is associated with hyperuricemia (a serum urate level of more than 6.8 mg per deciliter). Hyperuricemia is caused either by the overproduction of uric acid or more commonly by decreased excretion by Kidneys. The occurrence of gout is partly genetic. Its prevalence is on the rise due to increase in incidence of hypertension, diabetes, obesity and hypercholesterolemia. Conditions that are associated with hyperuricemia and gout include insulin resistance, the metabolic syndrome, obesity, renal insufficiency, hypertension, congestive heart failure, and organ transplantation. The use of thiazide diuretics, cyclosporine, and low-dose aspirin (<1 g per day) can cause hyperuricemia. Gout may be precipitated by any cause that may cause sudden change in the uric acid concentration in blood. Seafood and beer have both been shown to be powerful foods to cause a sudden increase in uric acid, which can trigger an attack. Other triggers include recent diuretic use, physical trauma, hospitalization and surgery.

Clinical features

Gout has two clinical phases. The first is characterized by intermittent acute attacks as described above. The base of the big toe is the most common joint to be affected, but can also affect ankle/knee/wrist/elbow. It is estimated that 9 out of 10 people with gout will eventually have a gout attack in their big toe. In females, it can present as polyarticular involvement as similar to Rheumatoid arthritis and sometimes may be difficult to diagnose. Without treatment attacks resolve spontaneously over a period of 7 to 10 days. The frequency of the episodes increases with time and with inadequate treatment, transition to the second phase can occur, manifested as chronic tophaceous gout, which often involves acute polyarticular attacks, joints pain and swelling between the attacks and crystal deposition (tophi) in cartilage, joints, bones and soft tissues. Tophi are commonly seen over the hands, feet, elbows and ears. Tophi sometimes breakthrough the skin and appear as white or yellowish white chalky discharge.

Gout not only affects joints but may also get deposited in kidneys and lead to renal failure over a period of time.

Management

Acute Gout

The main aim of therapy for acute gout is rapid relief of pain and disability caused by intense inflammation. Options for managing acute attacks include the use of non-steroidal anti-inflammatory drugs (NSAIDs), colchicines and glucocorticoids. The choice of agent, dose, and duration of therapy is guided by consideration of coexisting illnesses as well as the severity of the gout. These drugs may also be used for the prophylaxis over a period of time for control of acute attacks till the urate lowering drugs bring the uric acid to defined level.

Chronic phase – urate lowering therapy

Three classes of drugs are approved for lowering urate levels: xanthine oxidase inhibitors, uricosuric agents, and uricase agents. Xanthine oxidase inhibitors are the most commonly used drugs and block the synthesis of uric acid and can be used regardless of whether there is overproduction of urate. In this class of drugs, the one most commonly prescribed is allopurinol. Allopurinol hypersensitivity is much less common but can be life-threatening. The majority of patients receive 300 mg of allopurinol daily, but this dose is often inadequate to achieve target urate levels. Daily doses up to 800 mg may be used in patients. In 2009, another xanthine oxidase inhibitor, febuxostat, was approved for the treatment of hyperuricemia in patients with gout. These are started at low dose and increased slowly over a period of several weeks to full strength till the defined urate levels are achieved. They should not be stopped suddenly.  The dose should be adjusted as necessary to maintain a serum urate level below 6 mg per deciliter, which is associated with a reduced risk of recurrent attacks and tophi. Therapy is generally continued indefinitely.

Lifestyle and behavioral interventions

Dietary intake can influence both the development of gout and frequency of flare symptoms. Lifestyle changes may make it easier to manage this lifelong disease. Suggestions include gradual weight loss, avoidance of alcohol and smoking cessation. Avoid consumption of high sugar drinks and foods high in purines; like organ meat, beaf, pork and lamb. The consumption of coffee, vitamin C, low calorie diet and dairy products appears to decrease the risk of attacks. Encourage the use of low fat dairy products and vegetables