Gout (metabolic arthritis) is a type of joint inflammation (arthritis) caused by the crystallization of uric acid in tendons, surrounding tissues and joints, due to the high concentration of uric acid in the body. Crystallization of uric acid causes an inflammatory reaction.
Gout represents one of several types of arthritis when the cause of the disease is known. The disease’s cause is the crystallization of uric acid in the connective tissue of the joint, joint spaces, cartilage, tendons, or all the above places. Uric acid is a byproduct of the breakdown of urine consisting of waste and salt from our body.
In normal situations, uric acid is eliminated by urination and urination. When the body increases uric acid release, or if the kidneys do not function properly and remove uric acid from the body, its concentration in the blood increases.
This condition is called hyperuricemia. Hyperuricemia is not a disease, and anyone can have it without any symptoms. However, as uric acid is poorly soluble in water, in the conditions of hyperuricemia, uric acid crystals form and thus develop gout, and disease occurs.
History of gout
Gout is a disease that attacks older, genetically predisposed people and has always been known. Perhaps the oldest known form of arthritis, gout, was described as early as Hippocrates in the 5th century BC.
At one time, the term “gout” meant all arthritis forms. It was also known as the “disease of kings” because of the connection between gout and a rich diet full of meat delicacies and alcoholic beverages. The clear connection between the debauched life and gout was easily discernible. Since the cause of gout has been unknown for a very long time, it is no wonder that many patients who suffered from gout from their disease created special mythology.
Namely, it was considered that gout protects against other, more dangerous diseases, such as insanity. In the eighteenth century, gout was at the peak of its epidemiological prevalence and was considered a “sign of sublimity and nobility.” As a certain Lord Chesterfield put it, “gout is a disease of the Lord … while rheumatism is a disease of the stablemen.”
The connection between gout and uric acid was clear as early as the 19th century. Still, the exact biochemical mechanisms of uric acid production in the body were only known in the 1960s, which led to effective gout therapy. On the other hand, gout is the easiest form of arthritis to treat and control.
Epidemiology of gout
The prevalence of gout in Europe and the US is approximately 0.2%, although hyperuricemia in this population occurs in about 5% of cases. The prevalence of gout is increasing and is mostly seen in developed countries. Gout occurs more in men than in women (10: 1), rarely occurs before adulthood in young people indicates a defect of specific enzyme ), and rarely occurs in premenopausal women. The prevalence in older women increases with the increased use of diuretics.
Uric acid levels begin to increase after puberty and are higher in men than in women until menopause. There is a normal distribution of serum urate (SU) in the population with changes in the distribution at the upper end of the population spectrum.
Hyperuricemia is defined as a urate level higher than the two standard deviations from the mean (420 μmol / L in men, 360 μmol / L in women). This is a concentration close to the solubility limit of urate.
Gout pathology and pathophysiology
The underlying pathological substrate of gout is inflammation of the joints and surrounding tissue. Inflammation is caused by urate (uric acid) crystals located in the inflammatory area that the immune system recognizes as foreign bodies (a mechanism identical to inflammation around a thorn).
Uric acid is a normal component of the human body. It is a degradation product of purine bases (adenine and guanine). It is poorly soluble in water at the root of the disease.
If the level of urate in the blood reaches a value two to three times higher than normal, the crystallization of urate into tiny crystals begins. This crystallization occurs in the joints, primarily in the big toe joints. Sediments of tiny uric acid microcrystals are called tophi.
The concentration (“level”) of urate in the blood (actually the whole body, but measured in the blood) can increase for two reasons: increased urate production and decreased urate excretion.
If the breakdown of these bases is increased in the body, then an excessive amount of uric acid occurs and consequently an increase in its level in the blood (hyperuricemia). The causes of this condition can be defects in the enzymes of purine base metabolism, increased cell destruction due to radiotherapy or chemotherapy tumors. Also, certain types of food, such as offal, can cause increased uric acid production.
The mechanisms of glomerular filtration, tubular reabsorption, and tubular secretion are involved in the kidneys’ excretion of uric acid. Of all the filtered uric acid in the urine, only 10% ends. Urinary uric acid excretion in the urine may be impaired due to kidney disease or drugs that block urate excretion (some diuretics, acetylsalicylic acid, pyrazinamide, nicotinic acid, and alcohol), and hyperuricemia may occur. These drugs should therefore not be used in gout or hyperuricemia.
How inflammation occurs
Even small amounts of urate crystals in the joints cause a strong inflammatory reaction, followed by the joints’ pain and swelling. Namely, leukocytes come to the area of urate crystallization and try to phagocytose the crystals, thinking that it is a foreign body. Phagocytosis increases lactic acid concentration, which further stimulates the crystallization of urate. Inflammatory reactions lead to severe pain and all the symptoms of gout.
Although gout is often mistaken for joint disease, it is not. Gout is, in fact, a disease of the whole organism. Patients suffering from gout often suffer from high blood pressure, disorders of sugar and cholesterol metabolism, early atherosclerosis, and liver and kidney damage. Gout occurs in about 0.25% of Europe and North America.
In gout, we distinguish between acute gout and chronic gout. In chronic gout, the attack’s intensity is lower, but complete cessation of symptoms rarely occurs. Toffee usually accumulates in the ears, hands, and feet.
Clinical picture of gout
Common gout symptoms are sudden attacks of severe pain, tenderness, redness, heat, and swelling of some joints. Usually, only one joint is affected per attack, especially the big toe joint, but the knee joint, ankle, foot, hand, wrist, and elbow can also be affected.
Uric acid deposits, called tophi, can appear as bumps under the skin around the joints and on the ears’ edges. Uric acid crystals can also collect in the kidneys and cause kidney stones. The inflammation that is part of a gout attack is systemic, so fever, fatigue, and malaise are not uncommon side effects.
As with other known types of arthritis, gout tends to attack certain joints. This is especially the case with the first metatarsal-phalangeal joint (the joint between the big toe and the rest of the foot), which was first attacked in 75% of patients, and was affected in over 90% of cases of this disease.
The ankle, other ankles, and knee are also common locations for gout, as is the elbow’s bursa. In the further course of the disease, multiple joints may be affected without treatment, including the joints of the fingers and wrists. The shoulder girdle is very rarely affected by gout, the hip rarely.
While some gout attacks will resolve quickly and on their own, most will persist for a week, a few weeks, or even longer if left untreated. Since seizures are usually quite painful and usually make it difficult to walk, most patients will seek treatment.
Since gout treatment is lifelong, it is essential to make a definitive diagnosis. In this case, the general practitioner will easily diagnose but can often become two or more possible causes of inflammation in which there are symptoms similar to gout. Ideally, the diagnosis can be made by identifying uric acid crystals in the joint fluid or the urinary fluid mass (tofus).
You can visualize these crystals in a droplet of liquid on a slide observed through a polarizing microscope, which takes precedence over how the crystals “bend” light (polarization). The fluid is aspirated with a needle from the wrist and sent for analysis to the laboratory. The gout crystals have a needle shape and are yellow or blue, depending on their arrangement on the slide.
There may be many circumstances where a test sample is not available, but a diagnosis needs to be made. Therefore, a set of criteria has been set to enable diagnosis. These criteria consider the advantages of gout symptomatology that differ from other types of inflammatory arthritis, such as rheumatoid arthritis.
For example, gout inflammation usually reaches a maximum within 24 hours, while in other types of arthritis, it progresses much more slowly. Similarly, the presence of redness on the skin above the joint, high uric acid levels in the blood, and others, make gout a much more likely diagnosis. A gout diagnosis is made if 6 of the 10 criteria listed in the box below are present.
Diagnosing gout when crystal identification is not possible (ideally, 6 of the 10 listed features will be present):
- Inflammation reaches a maximum within one day (strong acceleration of inflammation).
- The existence of a history of a similar episode of inflammation.
- An arthritis attack on only one joint.
- Redness above the affected joint (gout is a strong inflammation)
- The big toe base’s involvement on one side (the most commonplace of gout attacks).
- Involvement of the joints in the middle of the foot.
- Elevated uric acid levels in the blood picture.
- X-ray findings of joint swelling that are not symmetrical.
- The joint fluid was tested for infection, and the result was negative.
- An X-ray shows characteristic changes for gout, including bone cysts and erosions.
When gout is diagnosed, you should look at its complications. It would help if you looked for cerebral acid accumulations called toffee, which can be found in several locations (see the image gallery below).
The doctor should look at the existence of kidney stones for the history of the disease. Patients with kidney stones and gout are likely to require faster and more aggressive urate-lowering than patients without stones to prevent stones’ recurrence.
Studies have shown that patients with gout have a higher risk of coronary heart disease and should be evaluated for that risk (e.g., laboratory tests for cholesterol and triglycerides).
Treatment of an acute gout attack
Therapy for acute gout attacks:
- Nonsteroidal antirheumatic drugs or COX-2 inhibitors. Examples of NSAIDs: Naproxen 500 mg twice daily, indomethacin 25 mg three times daily. Example of a COX-2 inhibitor: celecoxib 200 mg twice daily. Possible side effects: Increased blood pressure, swelling of the joints, nausea, ulcers (long-term use may increase the risk of heart attacks, but the treatment of gout usually lasts shorter). Use with caution in kidney and liver problems.
- Corticosteroids. Examples: prednisolone 40 mg on the first day, 30 mg on the second day, 20 mg on the third day, 10 mg on the fourth day. Possible side effects: Increased blood pressure, elevated blood sugar, mood swings. Short-term use, such as this one for gout, is generally much better tolerated. Contraindications: diabetics.
- Colchicine. Example: 0.6 mg of colchicine orally once per hour until improvement or diarrhea occurs. Do not exceed 4-5 doses. Possible side effects: Other choices are more commonly used due to frequent diarrhea problems (lower doses are often better tolerated for prevention). Use with caution in kidney and liver problems.
- Topical steroid injections. Example: Different doses are used depending on the size of the affected joint, and many preparations are available. Possible side effects: in 1-2% of cases, local reactions to injections may occur, and the condition of the joint may temporarily worsen the next day. In diabetics, a single local injection can temporarily raise blood sugar levels.
Gout is a chronic disease. Therefore, the key part of therapy is actually preventing disease attacks. Here, the therapy is causal. It tries to reduce uric acid production (reduction of meat intake) or increase its excretion in the urine (drugs and abstinence from alcohol and some drugs).
The second aspect is an acute attack of the disease, i.e., developing a disabling inflammatory reaction. Here is the backbone of anti-inflammatory therapy, and it is used to suppress inflammation. But without removing urate from the body, you cannot stop the inflammation completely.
In the treatment of gout, it is important to adhere to dietary measures – reduce the intake of foods rich in purines (meat, offal), abstain from alcohol, and drink large amounts of fluid so that the daily volume of urine is more than 2 liters so that uric acid is excreted as thoroughly as possible. Organism.
In gout’s medical treatment, we distinguish between drugs used to prevent gout and drugs for relieving pain in an acute gout attack when it has already occurred.
For prevention are used:
- uricosurics that stimulate uric acid secretion (probenecid, sulfinpyrazone and benzbromarone)
- uricostatics that block uric acid production from urate (allopurinol)
For the treatment of an acute attack of gout can be used:
- nonsteroidal antirheumatic drugs (NSAIDs)
The practice of treating an acute attack
Taking care of an acute gout attack is very different from preventing future attacks. Drugs used for prevention, such as allopurinol, can actually worsen an acute attack, so their application should be waited for until the attack resolves, sometimes for several weeks. Several measures can help deal with an acute gout attack.
One principle is that treating an acute attack should begin immediately after the onset of the attack, as rapid treatment is often rewarded with rapid improvement. If an acute attack is allowed to last longer than a day before treatment begins, the response to treatment can be much slower.
Physical measures can sometimes help with an acute attack. It is important not to strain the foot if the gout attack is located in the lower extremities. Ignoring an acute attack can lead to a prolonged duration of the attack. Applying ice topically proved to be useful (no longer than 10 minutes) not to damage the skin).
Nonsteroidal antirheumatic drugs and COX-2 inhibitors
Nonsteroidal antirheumatic drugs and COX-2 inhibitors are the main therapy in acute gout attacks in patients in whom, of course, they are not contraindicated. These drugs include agents like naproxen, ibuprofen, celecoxib, indomethacin, and many others. They reliably reduce inflammation and pain in gout. However, patients with ulcers, hypertension, coronary heart disease, and fluid retention must be cautious, even with short-term drug administration (3-7 days) required to resolve an acute attack.
The doses of NSAIDs needed to address acute gout attacks are slightly higher, as a complete anti-inflammatory effect is required (some examples are given in the text). For example, over-the-counter doses, for example, ibuprofen 200 mg, two tablets three times a day, are often not enough.
Corticosteroids, such as prednisone and methylprednisolone, are anti-inflammatory agents quite effective against gout attacks. Anti-inflammatory steroids differ in action and side effects from male sex hormone steroids.
Anti-inflammatory steroids have long-term risks, such as bone loss and infection, but the risk of short-term use (3-7 days) is relatively low. These agents can cause an increase in blood pressure and blood sugar so that they can be a problem for patients with uncontrolled hypertension or uncontrolled diabetes mellitus.
Colchicine has a greater role in preventing gout attacks than in the treatment of acute attacks. However, this drug is still used for seizures and is quite beneficial for some people. An essential characteristic of colchicine is its specificity. For example, it can help deal with an acute attack, but it does not help with a recurrent one rheumatoid arthritis.
Unfortunately, the use of colchicine for an acute attack requires a higher dose, often 0.6 mg every hour, and sometimes 6 doses are required. After receiving 3 or more doses, diarrhea is likely, universal in higher doses. Diarrhea makes oral colchicine a less effective alternative to acute attacks in most patients. Also, if a patient has abnormal kidney or liver function, colchicine can build up in the body and act toxic, such as suppressing blood cell production.
In the past, colchicine has also been used intravenously, in addition to oral administration. Intravenous use can be very effective and does not cause diarrhea in this way. Still, it must be used with extreme caution, as a dosing error can cause the cessation of blood cell production in the bone marrow, making the drug potentially fatal. This is why colchicine is so rarely used intravenously today.
Topical injections of corticosteroids may be a great option if the patient has only one joint attack. Preparations include methylprednisolone acetate, tramquinoline, and betamethasone. Of these drugs, betamethasone has the shortest effect in the joint, but gout tends to limit itself over a few weeks, so that this short-term option can be relatively successful.
The advantage of betamethasone is the reduced likelihood of a temporary flare-up of the disease the day after the injection, which is a common side effect of topical steroid injections. Local injections also carry a small risk of infection in the joint. However, it is advantageous if the disease has not yet been definitively diagnosed, as synovial fluid can be aspirated with the same needle for analysis.
Diet when gout occurs
Uric arthritis (gout) is a disease that can be significantly aggravated by a wrong diet and lead to an acute attack of the disease and severe pain. Your food should contain a sufficient amount of carbohydrates, you should avoid fats, and protein should be used within the limits of need (1 gram per kilogram of body weight).
In particular, avoid:
– all animal offal (liver, kidneys, heart, brain, lungs, pancreas), freshly prepared or already industrially processed
– all dishes and sauces made from animal offal
– canned meat
– dried meat and sausages
– fresh and processed (canned) bluefish
– hard alcohol
Avoid as much as possible:
– meat of beef, pork, mutton, and game
– beans, peas, lentils, spinach
– mushrooms (fresh, dried, and canned)
– wine and beer
– coffee, tea
– sharp spices, pickled food
Consume in moderation:
– veal, poultry, domestic rabbit meat
– milk, cheese, butter, margarine
– turnips, artichokes, celery, cucumbers
Allowed without restrictions:
– all other vegetables
– All fruit
– all types (fresh and dried) of cereals, bread, and flour products
– all kinds of soups and cooked green vegetables
It is recommended:
– plenty of fluids (water and naturally drained juices)
Sweet juices cause gout
New research has shown that women who regularly consume drinks rich in fructose, such as sweetened soft drinks and orange juice, are more likely to develop gout.
Researchers at Boston University School of Medicine reviewed data collected on nearly 80,000 women who participated in one large study over a 22-year period.
Gout is an excruciating condition in which urate, a chemical substance produced in the metabolism of amino acids, is not completely excreted from the body but accumulates in the joints.
During the study, a diagnosis of gout was made in 778 women.
The researchers found that women who consumed sugar-fortified beverages daily had a 1.7-fold higher risk of developing gout than women who consumed such beverages less frequently than once a month.
They also observed that women who consume orange juice daily have a 1.4 times higher risk of developing this disease.
The research results were presented at the annual meeting of the American Society of Rheumatology and were presented by Dr. Hyon Choi, a rheumatologist from the University of British Columbia.
“From a public health standpoint, we are particularly concerned about sugar-fortified beverages, as their consumption has increased significantly over the past few years,” explained Dr. Choi.
“Our research has shown that the risks associated with fructose-enriched beverages are comparable to the risks associated with alcoholic beverages, which are already known to cause gout,” he concluded.
Another study presented at the same meeting found that gout incidence in the U.S. is likely to have increased over the past two decades.
Gout is a common disease and seems to be becoming more common. For treatment to be effective, it is important to make the correct diagnosis as early as possible and start therapy as soon as possible. Other conditions (e.g., pseudogout), which can mimic gout, should definitely be ruled out by identifying crystals from the joint fluid whenever possible.
Treating gout without pharmacotherapy is very important, such as avoiding standing on the foot when it is inflamed and adhering to a diet to reduce purine intake and lose weight if necessary. For acute gout attacks, the key is to get treatment as quickly as possible and choose the least likely medications to cause side effects.
For chronic gout prevention, the essential message is that current treatments work in the vast majority of patients and are generally well tolerated. Patients must understand the four stages of gout because they are different for each stage. Patients must be consulted well and report any frequency changes in gout attacks.
A general practitioner can often act without the need to consult a rheumatologist. Still, you should consider consultation if the diagnosis is unclear, or there are doubts about the choice of therapy, or seizures continue, and related side effects.