In gout, monosodium urate crystals are deposited in tissue, causing inflammation and sudden severe pain, usually in a single joint. It occurs in three or four out of 1,000 persons, and 90% to 95% of patients are men over age 30. One in four have a family history of gout. Once called a rich man's disease because of its association with overindulgence in food and alcohol, this metabolic disorder can be exacerbated by poor diet. Primary gout is the result of overproduction or underexcretion of uric acid. Secondary gout is the result of myeloproliferative diseases, lead poisoning, enzyme deficiencies, or renal failure. Left untreated, gout may lead to a chronic arthritis.

Its reputation associates gout with overeating (especially meats), overindulgence in alcohol, and being overweight, but it can strike at any time and for no apparent reason. The mechanism is excessive uric acid production, decreased uric acid excretion, or both. Primary disease is an inborn error of metabolism attributed to several biochemical defects. Secondary disease is a complication of acquired disorders such as leukemia or the use of certain drugs.

• Family history of gout
• Obesity
• Hypertension
• Stress resulting from a fracture or surgical procedure
• Thiazide diuretics
• Drinking alcohol
• Polynesian heritage
• Diabetes
• Renal failure

• Pain in a single joint, often at the base of the great toe, but can be in other joints of the feet, fingers, wrists, elbows, knees, and ankles
• "Exquisite" pain and tenderness
• Swelling, heat, and stiffness of joint
• Shiny red or purple coloration of joint
• Fever up to 39°C (102.2°F) with or without chills
• Begins in hours and may subside over a few days or up to three weeks
• In later attacks, may see tophi (accumulations of urate just beneath the skin) in hands, feet, olecranon, prepatellar bursa, and in external parts of ears.
• Untreated, attacks will be more frequent and more severe

• Pseudogout
• Rheumatoid arthritis
• Osteoarthritis
• Cellulitis
• Infectious (acute pyogenic) arthritis
• Sarcoidosis
• Multiple myeloma
• Hyperparathyroidism
• Hand–Schüller–Christian disease
• Chronic lead intoxication
• Lead toxicity

Metatarsophalangeal joint is most commonly affected and appears red, swollen, hot, and exquisitely painful to touch. History may reveal recent food and alcohol excess, surgery, infection, physical or emotional stress, use of diuretics, certain chemicals, or uricosuric drugs. Fever is common, along with tachycardia, local desquamation, and sometimes pruritus. Tophi may be found in later attacks, as can progressive functional loss and disability and possibly gross deformities. Hyperuricemia with typical history of monarticular acute arthritis is usually sufficient for diagnosis.

• Serum uric acid level—Hyperuricemia greater than 7.5 mg/dL (unless uricosuric drugs are being taken) may be present but is not in itself diagnostic.
• Erythrocyte sedimentation rate (ESR) is elevated during attack.
• White blood cell count (WBC) is mildly elevated during attack.

• Urate crystals in synovial membrane
• Tophi present in some patients

Plain radiograph to rule out other disorders; no typical findings in early disease, but late disease may show punched-out lesions (tophi) and joint destruction.

Synovial aspirate is cloudy and markedly inflammatory, with urate crystals (needle-shaped and birefringent under polarized light).

Microscopic gout crystals seen in synovial fluid.

Gout is often completely controlled by proper treatment.

• Nonsteroidal anti-inflammatory drugs (NSAIDs) for pain and inflammation
• Abstinence from alcohol
• Dietary restrictions (avoid fat, alcohol, sardines, anchovies, scallops, organ meats, sweetbreads, cocoa, spinach, asparagus, eggs, oatmeal, and mushrooms)
• Medication to reduce the amount of uric acid produced or to promote its excretion

• NSAIDs—such as ibuprofen and indomethacin; IM 50 mg every 8 hours until symptoms resolve (5 to 10 days); avoid if allergic or have active peptic ulcer disease or impaired renal function.
• Colchicine—0.5 to 0.6 mg orally every hour until pain is relieved or nausea or diarrhea appears, then stop drug; usual total dose, 4 to 8 mg; generally only effective for 24 to 48 hours; many side effects, but GI symptoms relieved by IV administration of initial dose of 1 to 2 mg in 10 to 20 ml saline solution; severe toxicity limits usefulness of IV colchicine. Can also be used to prevent future attacks.
• Corticosteroids—dramatic symptom relief in acute attack; best for patients who cannot take NSAIDs. For monarticular disease, give intra-articularly (e.g., triamcinolone, 10 to 40 mg depending on size of joint). For polyarticular disease, give IV (e.g., methylprednisolone, 40 mg daily tapered over seven days) or orally (e.g., prednisone 40 to 60 mg daily tapered over seven days). Do joint aspiration and Gram stain of synovial fluid before giving steroids.
• Analgesics—such as codeine or meperidine for severe pain. Avoid aspirin as salicylates may exacerbate the condition.
• Uricosuric agents—to reduce serum uric acid levels; probenecid (250 mg bid for one week, increased to 500 mg bid) or sulfinpyrazone (100 mg daily initially, gradually increased to 200 to 400 mg daily). Hypersensitivity is indicated by fever and rash (5% of cases) or GI complaints (10%). Maintain daily urine output of at least 2,000 ml and urine pH of at least 6.0; salicylates must be avoided.
• Allopurinol—to reduce serum uric acid levels; 100 mg daily for one week, increased as needed; normal levels often obtained with 200 to 300 mg daily. Use cautiously in renal insufficiency; do not use in asymptomatic hyperuricemia (may precipitate attack). May develop signs ranging from pruritic rash to toxic epidermal necrolysis (rare, yet potentially fatal).

A combination of therapies can be very effective at decreasing both the length and frequency of attacks. Alternative therapies are often most useful in decreasing the frequency and severity of attacks, but may not necessarily offer the best pain relief. Alternative therapies avoid the sometimes toxic effects of some pharmaceutical agents used for gout. Some nutrients may actually exacerbate the condition.

• Avoid obesity. However, it is important to avoid crash dieting and rapid weight loss.
• Avoid alcohol, especially beer, which has a higher purine content than wine or spirits.
• Hydration—Drink plenty of water; dehydration may exacerbate gout.
• Restrict purines in diet—Purines increase lactate production which competes with uric acid for excretion. Foods with a high purine content are beef, goose, organ meats, sweetbreads, mussels, anchovies, herring, mackerel, and yeast. Foods with a moderate amount of purines include meats, poultry, fish, and shellfish not listed above. Spinach, asparagus, beans, lentils, mushrooms, and dried peas also contain moderate amounts of purines.
• Cherries—One half pound of cherries/day (fresh or frozen) for two weeks lowers uric acid and prevents attacks. Cherries and other dark red berries (hawthorn berries and blueberries) contain anthocyanidins that increase collagen integrity and decrease inflammation. 8 to 16 oz. of unadulterated cherry juice per day is also helpful. A lower maintenance dose can be continued for prevention.
• Vitamin C—8 g/day can lead to decreased serum uric acid levels. Note that there is a small subset of patients with gout who will actually get worse with this level of vitamin C.
• Folic acid—10 to 75 mg/day inhibits xanthine oxidase which is required for uric acid production. B12 levels need to be monitored to avoid masking a B12 deficiency.
• EPA (eicosapentaenoic acid) inhibits pro-inflammatory leukotrienes. Dose is 1,500 mg/day.
• Niacin—Avoid niacin in doses greater than 50 mg/day. Nicotinic acid may precipitate an attack of gout by competing with uric acid for excretion.
• Vitamin A—There is some concern that elevated retinol levels may play a role in some attacks of gouty arthritis.

Herbs are generally a safe way to strengthen and tone the body's systems. As with any therapy, it is important to ascertain a diagnosis before pursuing treatment. Herbs may be used as dried extracts (capsules, powders, teas), glycerites (glycerine extracts), or tinctures (alcohol extracts). Unless otherwise indicated, teas should be made with 1 tsp. herb per cup of hot water. Steep covered 5 to 10 minutes for leaf or flowers, and 10 to 20 minutes for roots. Drink 2 to 4 cups/day. Tinctures may be used singly or in combination as noted.

• Devil's claw (Harpagophytum procumbens)—analgesic and anti-inflammatory. Dose is 1 to 2 g tid of dried powdered root, 4 to 5 ml tid of tincture, or 400 mg tid of dry solid extract during acute attacks.
• Bromelain (Ananas comosus)—proteolytic enzyme (anti-inflammatory) when taken apart from food. Dose is 125 to 250 mg tid during acute attacks.

An experienced homeopath should assess individual constitutional types and severity of disease to select the correct remedy and potency. For acute prescribing use 3 to 5 pellets of a 12X to 30C remedy every one to four hours until acute symptoms resolve.

• Aconite for sudden onset of burning pain, anxiety, restlessness, and attacks that come after a shock or injury
• Belladonna for intense pain that may be throbbing; pain is made worse by any motion and better by pressure; joint is very hot.
• Bryonia for pain made much worse by any kind of motion; pain is better with pressure and with heat.
• Colchicum for pains made worse by motion and changes of weather, especially if there is any nausea associated with the attacks
• Ledum when joints become mottled, purple and swollen; pain is much better with cold applications and is worse from getting overheated.

• Hot and cold compresses—three minutes hot alternated with 30 seconds of cold compresses provide pain relief and increase circulation to the affected joint.
• Bed rest for 24 hours after acute attack. However, prolonged bed rest may exacerbate the condition.

If joint destruction is present, refer patient for orthopedic consultation. Surgical intervention is occasionally needed. There is increased incidence of urolithiasis, with 80% of calculi being uric acid stones, and of hypertension, renal disease, diabetes mellitus, hypertriglyceridemia, and atherosclerosis.

Dietary measures and nutritional supplementation may help prevent attacks and decrease their frequency, thereby decreasing the risk for joint destruction.

• Renal disease or kidney stones are most common, but these develop slowly with no effect on life expectancy.
• Chronic tophaceous arthritis may occur after repeated attacks of acute gout, but only with inadequate treatment.
• Possible nerve or spinal cord impairment

Asymptomatic periods grow shorter as the disease progresses. Marked deformities are possible, but few patients become bedridden. The younger the client at onset, the greater the chance of progressive disease. Destructive arthropathy is rare in those whose first attack is after age 50. Appropriate treatment will suppress attacks and keep uric acid to normal levels.

Because the disease affects mainly men and postmenopausal women, pregnancy is not usually impacted.

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