By: Michael Russel
What is gouty arthritis? Gout is a term which pertains to the presence of characteristic crystals in tissues and joints. Gouty arthritis is the result of an inflammatory response mounted against these characteristic crystals in joints. As a result of that, the affected joints become swollen, red and painful.
The joints most frequently affected by gouty arthritis are the first metacarpal phalangeal joint or the thumb joint and the first metatarsal phalangeal joint or the joint of the big toe. Other joints may be affected as well and these include the knee joints, shoulder joints and rarely, the hip joints.
What are the symptoms of gouty arthritis? Initial symptoms include sudden and rapid swolling of a single joint, the most common joint being the joint of the big toe, giving rise to a painful, red and swollen big toe, which occasionally may be confused with an infection. Other joints may also be affected in similar ways, although that is not common.
What are the causes of gouty arthritis? Gouty arthritis occurs when excess uric acid deposits in joints, forming characteristic crystals (known as monosodium urate crystals). In a normal person, the rate of uric acid production (waste product of cellular metabolism) equates to the rate of uric acid excretion (through the kidneys).
In people with gouty arthritis, the rate of excretion is markedly reduced, which leads to excessive accumulation of uric acid in the body and subsequently, in the joint. In certain subgroups of people with gouty arthritis, the rate of uric acid production greatly exceeds excretion and thus excess uric acid accumulates in the body.
Factors that increase uric acid production include excessive consumption of shellfish and alcohol, obesity; some medications can increase uric acid levels, examples include aspirin, diuretics and immunosuppressants. On the other hand, kidney failure will reduce rate of excretion and thus causes an accumulation of uric acid in the body.
What are at risks of getting gouty arthritis? Gouty arthritis affects 1% of the population. 10% of older men have gout. Gout is more common in men than women. However, in women after menopause, the risk is similar to that of men. Gouty arthritis is strongly associated with kidney disease, hypertension, hyperlipidemia, obesity and diabetes. People who have a family history of gout are at risk of getting gout themselves too.
How is gouty arthritis diagnosed? Gouty arthritis is diagnosed by identifying typical features of an acute attack. Gouty arthritis should be suspected when a patient experiences sudden joint swelling and severe pain, usually followed by pain-free periods between attacks.
Definitive diagnosis of gouty arthritis is based on identifying characteristic crystals (known as monosodium urate crystals) in joint fluid under a microscope, which the physician extracts using a needle from an affected joint. Measurement of uric acid level in the blood is not necessary in the diagnosis of gouty arthritis, as uric acid levels are often elevated in people who do not have gout.
How is gouty arthritis treated? In an acute attack, gouty arthritis is treated with colchicine and non-steroidal anti-inflammatory drugs (NSAIDs) which include indomethacin and naproxen. Corticosteroids, given orally or by injection, can be useful in dampen the inflammatory response in acute attack.
Allopurinol, which blocks the production of uric acid in the body, has no role in an acute attack. However, it's use in normalizing blood uric acid level between attacks and to prevent acute gouty arthritis is invaluable.
In conclusion: Gouty arthritis is the result of inflammation caused by deposition of characteristic crystals in joints. There are many causes of gouty arthritis, all of which fall under two big umbrellas, either there is an excess production, or a decrease excretion of uric acid.
Risk factors that predispose an individual to develop gouty arthritis include obesity, excessive alcohol consumption, kidney disease, certain drugs and so on. Acute attack can be treated with colchicine, NSAIDs and corticosteroids, while prevention can be achieved by taking allopurinol. Allopurinol has no role in an acute attack.
