IRA

Perhimpunan Reumatologi Indonesia
Indonesian Rheumatology Association

Is My Joint Pain Due To Gout? Get to know Gout

Gout is often blamed if a person experiences joint pain. Not only among patients who experience it, even some doctors who see patients with pain themselves still think so. This is obtained from a survey of approximately 200 general practitioners some time ago. In fact, joint pain due to gout is only a small part of all existing joint pain complaints. In addition, there is an opinion in society to avoid green vegetables and nuts if there is joint pain, either due to gout or not, this is not scientifically proven. Likewise, uric acid-lowering drugs (allopurinol) are often mistakenly used for complaints of joint pain, even though these drugs cannot relieve pain, even their effects sometimes cause more pain, or can even cause severe allergic reactions, kidney damage and even death.

Not all rheumatism or joint pain is a result of gout Rheumatism is a collection of diseases with disorders of the bone-muscle system (musculoskeletal) and joints, including disorders of the connective tissue. There are more than 100 types of diseases that can cause muscle and joint pain, and rheumatic disease due to increased uric acid levels in the blood (hyperuricemia) is only one of the various diseases that exist. Data from the rheumatology clinic of Hasan Sadikin Hospital in Bandung during January to December 2010, showed that approximately 73% of joint pain patients who came for treatment had osteoarthritis, known as calcification and not due to uric acid. Only about 3.3% had joint pain caused by elevated uric acid levels, also known as gouty arthritis. The prevalence of gouty arthritis in the world is around 1-2% and has increased twofold compared to the previous two decades. In Indonesia, the prevalence of gout arthritis is not known with certainty and varies considerably from one region to another. A study in Central Java found a prevalence of gouty arthritis of 1.7% while in Bali, a prevalence of hyperuricemia was 8.5%.

What is Gouty Arthritis?
Gouty arthritis is an inflammatory disease of the joints that can be very painful, accompanied by swelling, warmth, sometimes redness of the affected joint and difficulty moving. This disease is caused by the deposition of monosodium urate (MSU) crystals in the joints that trigger an inflammatory reaction. This situation is closely related to increased levels of uric acid in the blood (hyperuricemia), but people who experience hyperuricemia do not necessarily suffer from gouty arthritis.

Increased uric acid levels in a person’s blood are related to two factors, namely overproduction or decreased uric acid secretion (underexcretion) through the kidneys or a combination of both.

Who can be affected?
Gouty arthritis is commonly seen in men of all ages, most commonly in the fifth or sixth decade, but in women it is generally seen in the elderly (elderly) or after menopause. Factors that can increase the risk of gout arthritis include: comorbid diseases such as obesity, high blood pressure (hypertension), and a high-purine diet and alcohol consumption. In addition, certain drugs can cause a decrease in uric acid excretion. (for example: diuretic drugs used in people with heart disease or pyrazinamides used in people with tuberculosis).

It is important to recognize this disease
If not treated properly, gouty arthritis can cause recurring attacks, chronic joint disease accompanied by the formation of tofus (lumps filled with uric acid crystals) and can cause various complications in addition to damage to the joints themselves. Complications that may arise are heart disease, kidney disease (kidney stones or impaired kidney function), and decreased quality of life and work productivity due to pain, disability due to joint contractures and increased medical costs.

Gouty arthritis consists of 4 phases, namely:
Asymptomatic hyperuricemia (without symptoms):
If the uric acid concentration is more than the normal limit in the blood, it tends to be saturated, this is called hyperuricemia, which is> 7 g / dL in men and> 6g / dL in women. In this phase the increase in uric acid is not accompanied by clinical symptoms. There is no need for uric acid-lowering drugs in this phase, unless the uric acid level is very high.

Acute gouty arthritis: Symptoms include an acute (sudden) attack, the joint becomes painful, warm, swollen, red, and difficult to move. Pain increases to a peak in 8-12 hours. The joint involved in the first attack is generally one joint and the most commonly affected is the base of the big toe (90%), the other joints: the ankles, knees and rarely the wrists, fingers and elbows. The classic sign is that the sufferer is in so much pain that it is difficult to walk or wear shoes. Sometimes accompanied by general symptoms of fever, chills or weakness. Examination of uric acid levels in the blood at the time of the attack can increase or it can be normal, due to the concentration, especially in the joints. The natural course of untreated gouty arthritis will resolve on its own in a few hours to 1-2 weeks. Checking the uric acid level in the blood is recommended after 2 weeks of an acute attack because it shows the true uric acid level. The first attack and subsequent attacks are generally more than a year old. Further attacks will increase in frequency and pain longer, and involve more than one joint.

Intercritical gout
This phase is the phase in which the patient is free from pain attacks, or the phase between one attack and the next, lasting an average of 6 months to 2 years. In the second attack onwards this time will be shorter. Although there is no pain, the inflammatory process continues at this stage so that patients who do not get the right treatment will experience more frequent acute attacks and continue at the chronic stage accompanied by the formation of tofus.

Chronic tophaceous gouty arthritis
This chronic (chronic) stage generally develops after approximately 12 years (5-40 years) since the first acute attack of gout. Subcutaneous gouty tofus can be found all over the body: on the fingers, wrists, ears, knees, elbows. Complications of tofus include pain and joint damage and compression of the nerve vessels.

Intercritical gout
This phase is the phase in which the patient is free from pain attacks, or the phase between one attack and the next, lasting an average of 6 months to 2 years. In the second attack onwards this time will be shorter. Although there is no pain, the inflammatory process continues at this phase so that patients who do not get the right treatment will experience more frequent acute attacks and continue at a chronic stage accompanied by the formation of tofus.

Chronic tophaceous gouty arthritis
Chronic stage (chronic) develops generally after approximately 12 years (5-40 years) since the first acute gout attack. Subcutaneous gouty tofus can be found all over the body: on the fingers, wrists, ears, knees, elbows. Complications of tofus include pain and joint damage and compression of the nerve vessels.

Uric acid stones in the kidneys
Besides joint pain, uric acid buildup can also occur in the kidneys and form uric acid stones. The complaint felt by the sufferer is severe back pain (colic) if the stone blocks the urinary tract. Other complaints include stones or sand when urinating, or there is blood in the urine. These uric acid stones can interfere with kidney function and even damage the kidneys, so the patient must undergo dialysis therapy (hemodialysis). Because it is important to evaluate and monitor the kidney function of patients with gout.

How is Gouty Arthritis Management?

Non pharmacological management
Lifestyle modification, including exercise, weight loss for obese people, and low-purine diet can reduce acute gout attacks. Alcohol should be avoided because in addition to increasing production it also interferes with uric acid excretion through the kidneys. Repeated trauma to one joint and dehydration (dehydration) can trigger gout attacks, so it should be avoided.

Foods that contain high purines
-Foods and drinks that contain alcohol: wine, beer, wine, sticky rice, cassava tape, tuak and leavened foods
-Chemist, shrimp, shellfish, crab, lobster (sea food)
-Conserved food (corned beef, sardines)
-Mix (brain, tongue, lungs, liver, tripe, intestines)
-Red meat or meat broth (thick soup)

Studies have found that consumption of purine-rich vegetables, such as cauliflower, spinach, kale and nuts does not increase the risk of developing gout arthritis. During an acute attack, the action that needs to be done is to rest the painful area then first aid can be done by compressing the inflamed area with cold water.

Pharmacologic management
Consult a doctor immediately for management of acute gout attacks. The most important thing is not to take “” stick “or herbal medicines that claim to cure gout, some of which can cause dangerous side effects such as gastrointestinal bleeding and kidney damage. The main principle of therapy is to manage pain and relieve inflammation in acute attacks. In addition, for those who have not or are not currently taking uric acid-lowering drugs (such as allopurinol), do not start taking these drugs during an attack, as this can stimulate the breakdown of uric acid crystals and increase the inflammatory process to become wider. and heavy. Conversely, if you have been diagnosed with gouty arthritis and are on uric acid-lowering drug therapy, then the drug should be continued at the same dose during the attack. Giving drugs to reduce uric acid levels or changing the dose should be done after the acute attack has resolved (approximately 2 weeks). Consult with your doctor about this, do not take uric acid-lowering drugs yourself because allergic reactions and side effects can be quite severe, even to damage kidney function. The doctor will adjust the dose of uric acid lowering medication based on the patient’s kidney function and uric acid levels in their blood. Under certain circumstances uric acid-lowering drugs must be taken for life to prevent recurrent gout attacks and to prevent damage to the kidneys from uric acid stones.

By: dr Laniyati Hamijoyo SpPD-KR, M Kes

The authors are: Consultant Rheumatology / Teaching staff of the Department of Internal Medicine, Faculty of Medicine, University of Padjadjaran / Hasan Sadikin Hospital, Bandung

This article was published in Pikiran Rakyat Daily (22/12/2011)