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Gout is essentially a rheumatic disease that results from deposition of uric acid crystals (monosodium urate) within tissues, fluids and joints of the body.
There may be an overproduction or under excretion of uric acid in a process called hyperuricemia. Underexcretion is the most common cause and is thought to account for 80–90% of hyperuricemia.
Uric acid is a metabolic product resulting from the metabolism of purines. Purines are found in human DNA and RNA as well as in certain foods. Some foods such as alcohol, high protein foods as well as some medications may precipitate gout.
Gout comes as acute or sudden attacks. Acute gout shows up as a red, hot, and swollen joint accompanied with excruciating pain.
Recurrent bouts of flare ups of acute gout can lead to a degenerative and progressive form of chronic or long term arthritis called gouty arthritis.
There may be long periods of normalcy between two attacks of acute gout. Gout also raises the risk of developing kidney stones.
There are four stages of gout. The first stage is an asymptomatic stage where there are no overt symptoms. However, the uric acid levels are high and there is presence of deposition of crystals in tissues.
The second stage is acute gout or acute flares when urate crystals in one or more joints cause acute inflammation. There is pain, redness, swelling, and warmth over the joint lasting days to weeks.
Typically the joint of the great toe is affected first in around half of the persons with gout. Uric acid levels may be normal in about half of patients with an acute flare.
The phase between two acute flares is the next stage. The person with gout continues to have hyperuricemia with continued joint damage. With progression of the disease the period between two acute flares tends to reduce.
The next stage is chronic gout or gouty arthritis. There is soreness and a dull pain in the affected joints. There may also be presence of lumps or tophi that are urate crystals deposited in soft tissue usually seen over elbows, ears, or ends of the fingers.
Risk factors for gout include:-
Gout is diagnosed with a great degree of confirmation and accuracy by aspiration or withdrawal of the fluid within the affected joint and examining it for urate crystals.
Urate crystals are also seen within the tophi. Infection must be excluded before diagnosis of gout is made.
Treatment aims at relieving the pain during an acute attack as well as prevents future attacks and the formation of tophi and kidney stones.
The initial pain and inflammation during acute flares is well treated by nonsteroidal anti-inflammatory drugs or NSAIDs. To reduce inflammation drugs like colchicines and steroids may be used.
The patient is advised to lose weight, avoid alcohol and reduce the intake of foods that are high in purines and change the medications that may increase the risk of gout.
To prevent future attacks drugs like Allopurinol are used that reduce the production of uric acid in the body. Probenecid similarly helps the kidneys remove uric acid.
Rheumatoid arthritis and gout are relatively common diseases. However, it is rare to find both diseases co-existing together in an individual patient.
Further diagnosis of RA in a gout patient is complicated because 10% of patients with RA have high blood levels of uric acid while 30% of patients with gout along with tophi have a low titre or level of rheumatoid factor.
To confirm presence of both conditions there should be Rheumatoid factor positivity, joint erosion and damage typical of RA, presence of histologically confirmed rheumatoid nodule along with recurrent attacks of gout with identification of monosodium urate (MSU) crystals in the joints.