Gout is a type of arthritis (inflammation of the joints) that mostly affects men age 40 and older. It is nearly always associated with elevated blood uric acid levels (hyperuricemia). At elevated uric acid levels , crystals may develop and accumulate in joints causing inflammation and pain, the characteristic symptoms of gout. These crystals are called mono-sodium urate crystals (MSU).


Gout is often divided into four symptomatic stages:

  • Asymptomatic hyperuricemia.
  • Acute gouty arthritis.
  • Intercritical gout.
  • Chronic tophaceous gout.

Asymptomatic Hyperuricemia

Asymptomatic hyperuricemia, in which MSU slowly builds up, always precedes gout and is considered the first stage of the disorder. It lasts for an average of 30 years.

Note: Hyperuricemia does not inevitably lead to gout. In fact, less than 20% of the hyperuricemic population develops the full-blown gouty arthritis.

Acute Gouty Arthritis

Acute gouty arthritis occurs with the first symptoms of gout. Gout typically affects the toes and fingers first.

The symptoms of acute gout arthritis are described as follows:

  • Severe pain at and around the joint.. The area can be so tender that walking and even the weight of bed sheets can be unbearable. The pain usually takes eight to 12 hours to develop. In many cases the attack occurs late at night or early in the morning.
  • Swelling may extend beyond the joint, indicating fluid build-up.
  • The skin over the affected area is often red, shiny, and tense. After a few days it may start to peel.
  • Chills and mild fever, loss of appetite, and feelings of ill health may occur with an attack.

Intercritical Gout

Intercritical gout is the term used to describe the periods between attacks. The first attack is usually followed by a complete remission of symptoms, but left untreated, gout nearly always recurs at some point in the future.

Chronic Tophaceous Gout

When gout remains untreated, the intercritical periods typically become shorter and shorter, and the attacks, although sometimes less intense, can last longer. Over the long term (about 10 to 20 years) gout may become a chronic disorder with constant low-grade pain and mild or acute inflammation. Gout may eventually affect several joints, including those that may have been free of symptoms at the first appearance of the disorder. In rare cases, the shoulders, hips, or spine are affected.

With chronic elevated uric acid levels, the mono-sodium urate crystals may form painless deposits under the skin. They are called Tophi (singular tophus). They form at the helix of the outer ear (the curved ridge along the edge of the ear), forearm, elbow or knee, or hands or feet. Tophi may cause pain and stiffness in the affected joint. Eventually, they can also erode cartilage and bone, ultimately destroying the joint. Large tophi under the skin of the hands and feet can give rise to deformities.

Gout is one of the most common types of arthritis. Gout is estimated to affect about 2.1 million Americans (1.56 million men and 550,000 women). The prevalence of gout has been rising in recent decades, not only in America but in other developed countries, possibly because of dietary and lifestyle changes, greater use of medications that cause hyperuricemia, and an aging populations.

Risk Factors

The risk factors for gout, of which there are several, are identical to those for hyperuricemia.

  • Age – Gout usually first occurs in middle-aged adults and becomes increasingly prevalent as people age.
  • Gender – Men are significantly at higher risk for gout. In males, uric acid levels rise substantially at puberty with a first attack typically between the ages of 30 and 50 years. It is more common in African American men compared with Caucasian men.

Before menopause women have a significantly lower risk for gout than men, possibly because of the actions of estrogen. After menopause the risk increases in women so that after age 60 the incidence is equal in men and women, and after 80, gout occurs more often in women.

  • Family History – A fairly substantial proportion of patients with gout (10% to 20%) has a family history of the arthritic condition.

Major Risk Factors

  • Obesity Research suggests a clear link between body weight and uric acid levels; obesity may be an especially important risk factor for gout in men.
  • Hypertension and Diuretics The use of diuretics, which are agents used to treat high blood pressure, are highly associated with gout.
  • Alcohol Use – Alcohol use is highly associated with gout in younger adults. Binge drinking particularly increases uric acid levels. It appears to play less of a role among elderly patients, especially among women with gout.


Gout is classified as either primary (the most common type) or secondary, depending on the cause of the associated hyperuricemia. In both types of gout, between 70% and 95% of hyperuricemia cases are the result of under-excretion of uric acid in the kidneys, rather than uric acid overproduction.

Primary Gout

More than 99% of primary gout cases are referred to as idiopathic, meaning that the cause of the hyperuricemia cannot be determined. They are most likely due to a combination of hormonal and genetic factors that cause metabolic abnormalities resulting in excess uric acid. The remaining 1% of primary gout cases are traceable to either of two rare inherited enzyme defects that affect purine synthesis in the cells.

Secondary Gout

In secondary gout, hyperuricemia is caused by drug therapy or medical conditions other than an inborn metabolic disorder

MedicationsThe list of drugs that cause hyperuricemia is long. They include the following:

  • Thiazide diuretics (the “water pills” used to control hypertension). These agents are very highly associated with gout. In fact, 75% of elderly-onset gout patients report the use of diuretics.
  • Pyrazinamide (used to treat tuberculosis).
  • Cyclosporine (given to transplant recipients to prevent organ rejection).
  • Low dose (not high dose) aspirin may reduce uric acid excretion and increase the chance for hyperuricemia.
  • Niacin

Alcohol Use Alcohol use is a major contributor to gout and increases uric acid levels in three ways:

  • By providing a dietary source of purines (the compounds from which uric acid is formed).
  • By intensifying the body’s production of uric acid.
  • By interfering with the kidneys ability to excrete uric acid.

Kidney Insufficiency – Renal (meaning kidney) insufficiency is a major risk factor for gout in older people. This condition results in an impaired ability of the kidneys to eliminate waste products, including uric acid, which then build up in the blood. Hyperuricemia occurs in 30% – 85% of people who have renal insufficiency from kidney transplants or certain medications (eg, immunosuppressive agents or diuretics).

Other Conditions – A number of other conditions can cause gout. They include the following:

  • Over exposure to lead.

Purine-Rich Diet A purine-rich diet rarely causes hyperuricemia, although it may precipitate an attack in some people with existing gout. Such foods include organ meats, red meat, shellfish and alcohol (particularly beer) among others.


Gout symptoms may be precipitated by various conditions:

  • Severe illness (an important trigger). Between 20% to 86% of patients with gout experience a recurrence when they are hospitalized. Gout can be exacerbated by serious conditions that are associated with kidney and heart disease including diabetes, obesity, unhealthy cholesterol levels, and high blood pressure.
  • Stress
  • Infection
  • Joint injury
  • Weight loss
  • Surgery
  • Certain drug treatment (an important trigger)
  • Overindulgence in alcohol or purine-rich foods
  • Over-strenuous exercise. Even a long walk can trigger symptoms in a patient who is not sufficiently physically fit.

Symptoms occur more frequently in the spring, with the peak in April, according to some studies.


A thorough medical history and physical examination can reveal a number of significant indicators to help confirm or rule out gout. Of these, include the joints affected (ie. the big toe) as well as the speed of onset of the arthritis.

Examination of synovial fluid (joint fluid) is the most accurate method for diagnosing gout. The procedure involves extracting fluid from the affected joint with a needle. Ultrasound is frequently used to guide the extraction of fluid. The presence of monosodium urate (MSU) crystals will nearly always confirm a diagnosis of gout. The laboratory can also test the sample for infection.

A blood test is typically done to measure blood uric acid levels. A low level of uric acid in the blood makes a diagnosis of gout much less probable, and a very high level increases the likelihood of gout.

X-rays do not typically reveal any abnormalities during the early stages of gout, and their usefulness where gout is concerned lies in assessing the progress of the disorder in its chronic phase. Another benefit of X-ray is to rule out other similarly presenting arthritic conditions.

Pain and Disability

Left untreated, gout can develop into a painful and disabling chronic disorder. Persistent gout can destroy cartilage and bone, causing irreversible joint deformities and loss of motion.

Treatment Guidelines

There are differing treatment approaches to the various phases of gout, previuosly detailed above. Most involve drug therapy along with lifestyle modification.

Lifestyle Changes

During the period between gout attacks, patients are advised to avoid foods high in purines and to maintain a healthy weight. Patients should also avoid alcohol and reduce any stress. High purine foods include organ meats, red meat and shellfish, among others.

Treatments for Asymptomatic Hyperuricemia

Because asymptomatic hyperuricemia usually does not lead to gout or other health problems, treatment to prevent a first attack of gout is generally inadvisable. In unusual circumstances, when very high uric acid levels threaten the kidney, treatment may be justified.

Treatment of an Acute Attack of Gout

Drug treatments for acute attacks of gout are aimed at relieving pain and reducing inflammation. They should be started as early as possible.

  • In younger, healthy patients without serious medication conditions, nonsteroidal anti-inflammatory drugs (NSAIDs) or COX2 inhibitors are the drugs of choice. (ie. ibuprofen, naproxen, indomethacin, etc…)
  • Corticosteroids may be given both orally or as an injection into the affected joint. Oral corticosteroids (ie. Medrol or Prednisone) can be beneficial in patients who cannot tolerate NSAIDs and may be particularly beneficial for elderly patients or those with kidney problems. Injections into the affected joints provide effective relief for many patients.
  • Colchicine is used in healthy adults only and with caution. It should not be used in patients with severe kidney or liver problems.
  • In severe cases surgery to remove the calcifications or joint replacement is necessary.
  • Rest, applying cold, and protecting the affected joint with a splint can also promote recovery. After the first attack, some physicians advise their patients to keep a supply of medications on hand so that self-medication can begin at the first sign of symptoms of a second acute attack

Preventing Gouty Attacks

After an acute attack patients remain at risk for another for several weeks during the intercritical period. In such cases, low doses of either of the following agents may be used to during this period for prevention.

Drugs Used to Reduce Uric Acid Levels in Chronic Gout

In individuals with recurrent attacks of gouty arthritis physicians will prescribe medications to reduce blood uric acid levels (antihyperuricemic drugs). The goal of antihyperuricemic therapy is to reduce the frequency of attacks and dissolve tophi.

Long-term treatment of hyperuricemia may be recommended for the following situations:

  • Gout with tophi.
  • Recurrent gout (more than 2-3 yearly attacks).
  • Unusually severe attacks or those affecting more than one joint.
  • X-rays showing joint damage from gout.
  • Hyperuricemia is caused by an identifiable inborn metabolic deficiency.

A number of effective antihyperuricemic agents are available.

  • Allopurinol (Zyloprim, Lopurin)– Inhibits uric acid production and is useful for those who overproduce uric acid, who have kidney disorders, or who have kidney stones.
  • Febuxostat (Uloric) – Works by a similar mechanism to allopurinol. Is safer in those with kidney insufficiency
  • Uricosurics – Probenecid and sulfinpyrazone. These are less often used. Discuss with your rheumatologist whether these are right for you.

Allopurinol is rarely associated a life-threatening rash-based disease. Individuals should immediately contact their treating physician if a rash or other symptoms develop while on the medication.