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Gout Symptoms, Causes, and Treatments


Gout is a type of inflammatory arthritis caused by the deposition of uric acid (monosodium urate) crystals in the joint and non-joint spaces. It results from hyperuricemia, which is an elevated uric acid level in the bloodstream.

What are the first symptoms of a gout attack?

The first symptoms of gout are usually the sudden onset of pain, warmth, swelling, redness, tenderness, and decreased range of motion in one or more joints. A full-blown gout attack can build up over a few hours.

Gout symptoms mimic an infection, so your health care provider must carefully differentiate between the two conditions.

At what joints does gout occur?

Although a gout attack can occur anywhere, including the foot, ankles, knees, and elbows, the first toe's metatarsophalangeal (MTP) joint is the most common spot.

The first attack frequently occurs at night, with the person waking up and noticing the symptoms, possibly by the touch of the bedsheet.

Do the symptoms of gout resolve quickly or persist over time?

Gout can be acute (24 hours or less) or chronic (more than 24 hours). The symptoms of chronic gout can last days, weeks, or years, and there can be a repeating pattern of acute attacks (flare-ups) and remissions.

How common is gout?

It is estimated that gout affects 9.2 million people in the United States. Men develop gout at an earlier age, 30 to 50 years old, compared to women, due to the hormone estrogen increasing uric acid clearance (removal); thus, women usually develop gout after menopause, once estrogen levels are lower.

What is the mechanism of gout?

Excess uric acid in the bloodstream, called hyperuricemia, causes uric acid to leave the bloodstream and enter the joint space, forming uric acid crystals. The crystals are pointed in shape and described as "spike-like."

Our bodies treat the uric acid crystals as foreign pathogens, like bacteria or viruses, and attack the crystals. When this occurs, white blood cells are drawn to the area; this is why gout mimics an infection with redness, warmth, and swelling.

It must be noted that even though hyperuricemia causes gout, only 36% of people with hyperuricemia actually develop gout.

What are the joint complications from gout?

Sometimes, there are hard lumps of uric acid crystals, called tophi, that form in the joint. When these tophi are present, they can destroy the bone and cartilage (fibrous material that cushions the joint).

What causes hyperuricemia (increased uric acid in the bloodstream)?

Our bodies develop hyperuricemia either from producing too much uric acid or not enough excretion (removal) of uric acid by the kidneys. It has been referenced that 10% of gout cases are from the body’s overproduction of uric acid, while 90% of gout cases are from kidney underexcretion.

A: Overproduction of uric acid

Purine is a chemical compound broken down to form uric acid; thus, excess amounts of purines in our bodies result in an increased level of blood uric acid.

High amounts of purines usually result from too many purines in our diet. Foods and drinks that contain high levels of purines include:

  • Red meats, turkey, and organ meats like liver
  • Seafood such as scallops, mussels, trout, haddock, tuna, sardines, and anchovies
  • Vegetables including mushrooms, spinach, and cauliflower
  • Alcohol, especially beer

B: Decreased uric acid kidney excretion can result from the following issues:

  • Kidney disease
  • Hypothyroid (low thyroid levels)
  • Medications, especially the diuretics furosemide (Lasix) and thiazide types
  • Certain toxins like lead

How is the diagnosis of gout made?

Your physician or medical provider will take a history, perform a physical exam, order laboratory tests, and order diagnostic imaging.

A: The history is essential regarding the onset of joint symptoms since there is a sudden onset of significant pain, along with the other symptoms.

B: As mentioned above physical exam for gout can demonstrate tenderness, red discoloration, warmth, swelling, and decreased range of motion in one or more joints.

C: Laboratory tests can assist with ruling out other conditions:

  • White blood cell (WBC) count is elevated with an infection.
  • An erythrocyte sedimentation rate (ESR) test screens for some inflammatory conditions.
  • Rheumatoid factor (RF) and antinuclear antibody (ANA) tests evaluate for arthritis.
  • Blood urea nitrogen (BUN) and creatinine levels evaluate kidney function.

A serum (blood) uric acid level is essential since it is elevated with gout. However, an elevated uric acid level does not always exist: some cases of gout have a normal serum uric acid level. In these cases, the excess uric acid has already moved into the joint and is crystallized, leading to a normal serum uric acid level.

D: Radiographical tests

Plain x-rays can be helpful to rule out other forms of arthritis. The tophi of chronic gout can be seen on x-rays.

Ultrasound can be useful by revealing urate crystals in the joint and tophi.

E: Joint aspiration may be necessary, in which a needle is placed into the joint to withdraw fluid. Then, the fluid is viewed under a microscope, with a specialized polarized light, and the uric acid crystals can be visualized.

What is the treatment for acute gout?

Colchicine is the mainstay of treatment of acute gout. It is an anti-inflammatory that decreases swelling and the build-up of uric acid crystals. Common side effects of colchicine include nausea and diarrhea. Colchicine works best if taken within 24 hours of an acute gout attack.

Non-steroidal anti-inflammatory drugs (NSAIDs), either by prescription or over the counter, can relieve symptoms. The most traditionally used NSAID for gout used to be indomethacin, because of its strength, but now other NSAIDs have been found to work just as well.

Aspirin, also known as acetylsalicylic acid (ASA), should not be used since it can raise the body's uric acid level.

Corticosteroids, taken as oral prednisone or by injection, can be used.

Are there additional medications used for chronic gout?

  • Allopurinol prevents the breakdown of purines, decreasing the levels of serum uric acid.
  • Probenecid increases uric acid removal by the kidneys.

Other treatments consist of ice, elevation, and increased fluid intake.

Conclusion

Since the joint damage from gout, including tophi, is irreversible, the treatment is to tend to the acute gout attack and prevent future gout attacks.

Key take-aways:

  • Gout is caused by uric acid crystals deposited into the joints.
  • Symptoms include the sudden onset of tenderness, red discoloration, warmth, swelling, and decreased range of motion in one or more joints.
  • Gout is caused by high levels of uric acid in the bloodstream (hyperuricemia), either from the body's overproduction (10%) or the kidney's underexcretion (90%).
  • Medication treatments for acute and chronic gout include colchicine, non-steroidal anti-inflammatories (NSAIDs), corticosteroids, allopurinol, and probenecid.

Bibliography

Pittman, Joel R., and Michael H. Bross, 'Diagnosis and Management of Gout,' American Family Physician, 59.7 (1999), 1799–1806

Yip, Kevin, and Jessica Berman, ‘What Is Gout?’, JAMA, 326.24 (2021), 2541 <https://doi.org/10.1001/jama.2021.19770>

Zhang, Wei-Zheng, ‘Why Does Hyperuricemia Not Necessarily Induce Gout?’, Biomolecules, 11.2 (2021), 280 <https://doi.org/10.3390/biom11020280>

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