Overview of gout
Gout is a type of arthritis that is associated with inflammation and is caused due to crystallization of the uric acid normally present in the body. It affects about 1% of the general population and involves one or more joints in the body. Gout is more common in men aged above 40 years. The joints of the toes are most commonly affected while the heels, ankles, knees, fingers, wrists and elbows may be affected to a lesser extent.1, 2
Signs and Symptoms of gout
Gout may either appear without any provocation (referred to as acute gout or acute gouty arthritis)
may be characterized by frequent attacks of the condition over a period of time (referred to as chronic gouty arthritis or chronic gout).
Acute gout usually affects a single joint or multiple joints of the lower leg. The big toe is most commonly affected. Other sites may include the middle toes, ankle or the knee joints. The pain which often begins in the mornings becomes so severe by night that the individual cannot touch the toes during the flare up. Redness and swelling may be noticed on the affected joints with fever in certain occasions. These features subside within a week’s duration with or without treatment. Some individuals may not have any further such attacks while others may experience such episodes frequently and may progress to develop chronic gout.
Chronic gout is characterized by frequent attacks of acute gout in a year’s duration with completely asymptomatic states in between the attacks. As the condition progresses small nodules of uric acid crystals (tophi) may begin to be deposited in the soft-tissues of the body. The most common sites for such deposition include the helix of the ear, base of the great toe and fingers, wrist, fingers and Achilles tendon. The tophi may develop about 10 or more years after the initial attack of acute gout and cause pain, damage of the soft- tissues of the joints, destruction of the joints and compression of the nerve fibers in that area.1, 2
Causes of gout
The cause of gout has been attributed to increased levels of a chemical substance known as uric acid in the body.
The uric acid is a by-product of certain metabolic reactions taking place in the body and is normally excreted through the kidneys. Any factor that causes either increased production or decreased excretion of uric acid leads to an increase in the uric acid levels in the body, this condition is termed as hyperuricemia. The excess uric acid begins to get deposited in the joints, kidneys (resulting in the formation of kidney stones) and other soft-tissues leading to the signs and symptoms. However, it has to be noted that not all the individuals with hyperuricemia suffer from gout.1
Overproduction of uric acid
The overproduction of uric acid may be observed in case of
- Deficiency of certain enzymes or
- Due to certain underlying disorders such as myeloproliferative diseases, polycythemia vera, severe psoriasis or Paget’s disease.
Decreased excretion of uric acid
Decreased excretion of uric acid may be due to underlying conditions such as
Consumption of drugs such as diuretics, antitubercular drugs and others can also affect the clearance of uric acid in the kidneys.2, 3
Risk Factors for gout
Following are some of the risk factors that are associated with gout4
- Lack of exercise
- Consumption of food such as read meat and sea food that are rich in purine (uric acid is a breakdown product of purine)
- Increased consumption of alcohol
- Consumption of diuretic medication
Diagnosis of gout
The diagnosis is based on the following
- Signs and symptoms
- History of underlying disorders
- The presence of risk factors
- Certain laboratory investigations
A complete examination of the blood, which includes estimation of the various normal parameters of the blood cells along with tests for determination of levels of uric acid in blood and urine, is advised. Radiographs of the affected joints may display evidence of bone destruction with margins of tophi in chronic cases. Analysis of the fluid between the joints or in the tophi may also be advised to confirm the diagnosis.2, 5
Treatment of gout
The aim of the treatment for gout is to reduce the severity of the symptoms during the acute attacks and prevent the progression into chronic states. The pain and swelling may be reduced with the use of nonsteroidal antiinflammatory drugs (NSAIDs) such as indomethacin (indocin). Other prescription drugs that may be advised include colchicine and steroid injections to the affected joints. The increased concentration of uric acid is countered by the administration of specific drugs that belong to the group of uricosuric drugs and allopurinol. The duration, dosage and the type of drug to be used is decided by the doctor based on the severity and stage of gout.1, 2, 6
Alternative therapies for gout
Following have an adjunctive role both in faster remission of gout and prevention of complications.2, 6
- Weight reduction programs
- Moderate exercises
- Decreased consumption of purine-rich foods
- Reduction or discontinuation of alcohol consumption, and control of hypertension and diabetes
Complications of gout
Complications of gout include
- Severe pain
- Deformation of the joints
- Joint destruction
- Carpal tunnel syndrome
- Deposition of uric acid crystals in the various soft-tissues of the body including the kidneys and heart
Prevention of gout
A healthy lifestyle, which includes proper diet with adequate exercise and decreased consumption of alcohol can avoid triggering the condition and also prevent further complications. Following proper instructions from the doctor before consuming medications, especially those medications, which are required to be taken for a long period of time is also helpful.
Living with Gout
Although the acute form of gout may progress to the chronic type, early and proper treatment helps the affected individuals to lead a normal life with minimal complications.
1. Eggebeen AT. Gout: An update. Am Fam Physician. 2007; 76(6): 801–808, 811–812.
2. Pittman JR, Bross MH. Diagnosis and management of gout. Am Fam Physician. 1999; 59(7).
3. Choi HK, Mount DB, Reginato AM. Pathogenesis of gout. Ann Intern Med. 2005; 143: 499–516.
4. Choi HK, Atkinson K, Karlson EW, Curhan G. Obesity, weight change, hypertension, diuretic use, and risk of gout in men: The health professionals follow-up study. Arch Intern Med. 2005; 165: 742––748.
5. Schlesinger N, Diagnosis of gout: Clinical, laboratory, and radiologic findings. Am J Manag Care. 2005; 11: S443–S450.
6. Cannella AC, Mikuls TR. Understanding treatments for gout. Am J Manag Care. 2005; 11: S451–S458.
Written by: healthplus24.com team
Date last updated: February 05, 2015