Although gout usually affects the big toe, it may also affect other joints – the ankles, knees, hands, wrists, and elbows. Unchecked, gout can be a hazardous health condition as the uric acid crystals may eventually be deposited in the soft tissue of the ears, hands and feet, in cartilage, joints, tendons, or elsewhere, forming small, hard lumps called tophi. The crystals can also damage the kidneys. The affected joint starts to ache, then quickly becomes swollen, red, very warm, and extremely painful. Sometimes fever and chills will follow. The skin of the affected area can appear a shiny red or purple. The pain from an acute attack can be excruciating. In some cases, the brush of a sheet can cause howls of pain. The attack usually lasts for a few days, then dies down, and the joint gradually returns to normal.
Tophaceous gout can begin as early as three years or as late as forty years after the initial attack. Each tophus consists of a deposit of urate crystals surrounded by a granuloma made up of mononuclear phagocytes (macrophages) that have developed into epithelial and giant cells. These deposits produce irregular swellings, with the most common site being the helix of the ear. Although the tophi themselves are painless, they often cause progressive stiffness and persistent aching of the affected joint. In the upper extremities, they may cause nerve compressions, as in the case of carpal tunnel syndrome. Tophi in the lower extremities may cause tarsal tunnel syndrome and may erode and drain through the skin.
Renal stones are 1,000 times more prevalent in those with primary gout than in the general population. These stones range in size from that of a grain of sand to massive deposits called staghorn calculi. They also come in a variety of colours, depending on their composition. Some stones consist of pure monosodium urate, while others are of calcium oxalate or calcium phosphate. These stones can form in the collecting tubules, pelvis, or ureters, causing obstruction, dilatation, and atrophy of the more proximal tubules. This will eventually lead to acute renal failure. Stones that form directly in interstitial tissue initiate an inflammatory reaction, leading to chronic renal disease and progressive renal failure. Gout is to be taken very seriously.
Gout was once called the “rich man’s disease” because it was associated with gluttony of food and drink. King Henry VIII is often brought to mind. Today, gout is viewed as a metabolic disorder caused by poor eating habits and an overconsumption of animal proteins. A poor diet can worsen the condition. An increase in fluid intake is advised, especially water. Meat and alcohol should be dramatically reduced, especially red wine and port, which appear to be triggers for gout. Purine-rich foods should also be limited. These include shellfish, oily fish, and dried legumes. It should be noted that taking aspirin can actually slow the excretion of uric acid from the body, thereby aggravating the disease.
The development of gout is related to age, but not caused by it. The disease affects four times more men than women and usually affects men older than age 30 and postmenopausal women. Secondary gout occurs in the elderly. Risk factors for developing gout include a family history, drinking alcohol, high blood pressure, taking certain medications, being overweight, or gaining weight. Other triggers include infections, injury, antibiotics, diuretics, aspirin, and crash dieting.
Gout develops in four stages:
- Asymptomatic gout is diagnosed when serum urate levels rise, but no symptoms are produced. As the disease progresses, it may cause hypertension or nephrolithiasis (kidney stones), and severe back pain.
- The first acute attack strikes suddenly and peaks quickly. Although it generally involves only one joint, this initial attack is extremely painful. The metatarsophalangeal joint of the great toe usually becomes inflamed first (podagra), then the instep, ankle, heel, knee, or wrist joints. Sometimes a low grade fever is present. Mild acute attacks often subside quickly, but tend to recur at irregular intervals. Severe attacks may persist for days or weeks.
- Intercritical periods are the symptom-free periods between gout attacks. Most patients have a second attack within six months to two years, but sometimes can be delayed for many years. Delayed attacks are more common in those who are untreated and tend to be longer and more severe than the initial attack. Such attacks are also polyarticular, that is, invariably affecting many joints, especially in the feet and legs. These attacks are sometimes accompanied by fever. A migratory attack strikes various joints and the Achilles tendon, and is associated with some form of bursitis.
- Chronic polyarticular gout eventually sets in. This final, unremitting stage of the disease is marked by persistent pain with large, subcutaneous tophi in the cartilage, synovial membranes, tendons, and soft tissues. The skin covering the tophi can ulcerate and release pus. Chronic inflammation and tophi deposits precipitate secondary joint degeneration with eventual erosion, deformity, and disability. Kidney involvement leads to renal dysfunction along with hypertension.
Conventional treatment involves a life-long consumption of NSAIDs or other medications to reduce the amount of uric acid production or increase its excretion, as well as the abstinence of alcohol. As mentioned, dietary restrictions will include a low acid diet and one that avoids purine-rich foods (sardines, anchovies, fish roe, shell fish, crab, liver, kidney, sweetbreads, beans, tea, and coffee). The use of herbal diuretics, as well as some anti-rheumatic herbs, will help with this disorder and are less harmful to the body. Celery, boneset, wild carrot, and yarrow are especially useful out of all the diuretics available. A tea of equal parts of burdock root, celery seed, and yarrow taken three times a day over a period of time may also be useful. If there is pain, thuja may be added.
Pseudogout, also known as calcium pyrophosphate dihydrate crystal deposition disease, has only recently been recognized as a form of arthritis. It is caused by deposits of calcium and pyrophosphate crystals in the joints, rather than the uric acid crystals of gout. It is believed that an accumulation of pyrophosphate in the cartilage promotes the formation of the crystals, which may be visible on x-rays. Pyrophosphate is a type of acid produce by the joint tissues and in most cases, forms without an apparent reason, although it does tend to run in families, as does true gout.
Pseudogout is a name that could indicate a fake; but the sudden, goutlike attacks of joint inflammation and pain are very real. These calcium crystals can also be deposited into the cartilage, causing a condition called chondro-calcinosis (Latin for “calcium in the cartilage”). Acute attacks often occur in the knee joints and can be incapacitating for weeks. The disease is not considered to be as serious or painful as gout and is harmless unless the crystals become dislodged. If this happens, inflammation will result, and, if left untreated, can cause long-term damage and pain.
Pseudogout often strikes the knee joint first, then the wrists and ankles, causing pain and swelling with possible destruction of the cartilage. An attack may go on for days or weeks, with the acute phase lasting twelve to thirty-six hours. Or, the pain may flare up in several joints at one time, but is usually less severe and more chronic. Sometimes the pain increases after activity, and sometimes not. Symptoms often disappear without treatment.
Pseudogout usually does not appear before the age of 65 and is rarely seen in anyone under the age of thirty. It seems to affect both men and women equally and usually triggered by surgery, trauma, or stress, but not diet. Even though the crystals contain calcium, drinking milk or eating high-calcium foods does not seem to make a difference. Conventional treatment includes joint aspiration to remove fluid containing the crystals, NSAIDs to manage pain and inflammation, rest, and/or splints during an acute attack. Exercise helps to build muscle strength and restore full motion of the joints after an acute attack. In rare instances, surgery may be necessary to replace a joint that has been badly damaged, extremely painful, or is unstable.