Gout has been defined as one of the most painful rheumatic diseases. It results from the deposition of crystals of uric acid in connective tissue, joint spaces, or both, and is due to a disorder of uric acid metabolism. It is caused by either an overproduction, or under excretion of uric acid and is manifested by hyperuricemia, acute or chronic recurrent arthritis, and deposits of monosodium urates.

Uric acid serves no physiologic purpose and is the end product of purine metabolism. In lower animals, the enzyme uricase breaks down uric acid to the more soluble allanotoin, thus uric acid does not accumulate. Gout occurs only in humans where there is a miscible pool of uric acid. Under normal conditions, uric acid is dissolved in the blood and passes through the kidney and into the urine for elimination. The amount of cumulated uric acid in men is about 1,200mg and in women, about 600mg. These values are increased several-fold in individuals with gout.

Population studies have shown that serum urate concentrations (and consequently risk of gout) correlates with age, serum creatinine, blood urea nitrogen, male gender, blood pressure, body weight, and alcohol intake. Prevalence increases with age, especially in men. (1) Men are affected by gout approximately 10 times more often than women. Although no genetic marker has been isolated for gout, the familial nature of gout strongly suggests an interaction between genetic and environmental factors. (2)

Hyperuricemia may result when a patient eats too many high-purine foods such as liver, dried beans and peas, anchovies, and gravies. However, dietary purines play an unimportant role in the generation of hyperuricemia in the absence of some derangement in purine metabolism or excretion. Hyperuricemia is not a disease and by itself is not dangerous.

The purines from which uric acid is produced come from three sources: dietary purines, conversion of tissue nucleic acids to purine nucleotides, and de novo synthesis of purine bases. The purines derived from these three sources enter a common metabolic pathway, leading to either the production of nucleic acid or uric acid. Uric acid may accumulate excessively if production exceeds excretion. (3) Several enzyme systems regulate the metabolism of purines, and a partial deficiency of one or more enzymes may be responsible for marked hyperuricemia in otherwise normal individuals. Uric acid may also be overproduced as a consequence of increased breakdown of tissue nucleic acids, as with myeloproliferative and lymphoproliferative disorders.

Uric acid does not accumulate as long as production is balanced with elimination. About two thirds of uric acid is eliminated through the kidneys. The remaining one third is eliminated through the GI tract after enzymatic degradation by colonic bacteria. Almost all the urate in plasma is freely filtered across the glomeruli. Multiple renal tubular transport processes, in addition to the filtered load, determine the concentration of uric acid in the urine. Evidence favors a four-component model including glomerular filtration, tubular reabsorption, tubular secretion, and postsecretory reabsorption. (4) In addition, there appears to be a close linkage between uric acid reabsorption and sodium reabsorption, so there will be an elevated uric acid level in conditions that enhance sodium reabsorption.

There are a number of conditions that affect either uric acid clearance or increase its production. Therefore, a patient with these conditions has a greater risk of developing gout. Some of the conditions associated with hyperuricemia include:


New Zealand Rheumatology Association, 2002.

  • Gout is very common in New Zealand and it is particularly common in Maoris and Pacific Islanders. Some surveys have shown it to be present in up to 10% of adult males.

Mayo Foundation for Medical Education and Research, 1999.

    Gout is a painful problem for over two million Americans. Gout is more common in men than women and is associated with being overweight, overeating, and drinking alcohol excessively.

National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institute of Health, 1999.

  • Gout occurs in approximately 275 out of 100,000 people.
  • Men aged 40 to 50 years are most commonly affected.
  • Gout accounts for about 5% of all arthritis cases.

Signs and Symptoms

[span class=alert]The following list does not insure the presence of this health condition. Please see the text and your healthcare professional for more information.[/span]

The attacks of acute gouty arthritis most often affect the first metatarsophalangeal (MTP) joint (great toe) and then, in order of frequency, the insteps, ankles, heels, knees, wrists, fingers and elbows. Attacks most often occur at night, with a patient awakening in excruciating pain. The postulated cause of this is that synovial effusions are thought to occur transiently in weight bearing joints through the day. At night, water may be reabsorbed from the joint space leaving a supersaturated solution of monosodium urate, which precipitates an acute attack of arthritis. Nephrolithiasis occurs in 10-25 percent of patients with gout. (5)

The National Institute of Arthritis and Musculoskeletal and Skin Disorders division of the National Institute of Health (NIH) describes the following four stages of disease progression:

  1. Asymptomatic hyperuricemia - In this stage, a person has elevated levels of uric acid in the blood but no other symptoms. The tendency to develop gout, however, is present. A person at this stage does usually not require treatment.
  2. Acute gout or gouty arthritis - In this stage, hyperuricemia has caused the deposit of uric acid crystals in joint spaces (tophi). This leads to sudden onset of intense pain and swelling in the joints, which may also be warm and tender. An acute attack commonly occurs at night and can be triggered by stressful events, alcohol or drugs, or another acute illness. Early attacks usually subside within 3-10 days, even without treatment, and the next attack may not occur for months or even years. Over time, however, attacks can last longer and occur more frequently.
  3. Interval or intercritical gout - This is the period between acute attacks. In this stage, a person does not have any symptoms and has normal joint function.
  4. Chronic tophaceous gout - This is the most disabling stage of gout and usually develops over a long period, such as 10 years. In this stage, the disease has caused permanent damage to the affected joints and sometimes to the kidneys. With proper treatment, most people do not progress to this advanced stage. (6)


  • Hyperuricemia
  • Presence of uric acid crystals in the joints
  • Arthritis that develops in one day
  • Attacks of arthritis in only one joint, usually the great toe, ankle, or knee
  • A painful joint that is swollen, red, and warm
  • More than one attack of acute arthritis 

Treatment Options


Treatment goals are to ease the pain of an acute attack, prevent recurrent attacks, and avoid formation of new tophi and kidney stones.

Acute attacks of gouty arthritis can be treated by a variety of non-steroidal anti-inflammatory agents or colchicine. Colchicine may be given orally or parenterally. Unless contraindications exist or the patient has renal insufficiency, the usual oral adult dose is 1mg initially, followed by 0.5mg every two hours until the joint symptoms subside, until the patient develops abdominal discomfort or diarrhea, or until a total dose of 8mg has been administered. (7) About 75 to 95 percent of patients with acute gouty arthritis respond favorably to colchicine when ingestion of the drug is begun within 24 to 48 hours of the onset of joint symptoms. (8) The probability of success with the drug diminishes substantially if initiation is delayed longer than 48 hours after the onset of symptoms.

The greatest problem with colchicine is that it causes GI side effects in 50-80 percent of patients before the relief of the attack. Giving the drug parenterally can circumvent the GI side effects. Except in patients with renal insufficiency, the intravenous dose of colchicines is 2mg. If relief is not achieved, an additional 1 mg may be given at 6 and 12 hours until a total dose of 4mg is reached. Colchicine should be diluted with 20ml of normal saline prior to administration to reduce sclerosis of the vein.

Indomethacin is also used to treat acute gouty arthritis. It has been shown to be as effective as colchicine and has fewer GI side effects; thus, it is generally chosen as the preferred treatment. Indomethacin may produce headache and dizziness as a side effect, and, as with all NSAIDS, there is the possibility of gastric ulceration and bleeding; but with short-term therapy, this is unlikely.

A number of other NSAIDS are also effective in treating the inflammation of acute gout. Corticosteroids may also be used to treat acute attacks, but they are primarily reserved for resistant cases or for those with a contraindication to colchicines or NSAIDS. After the first attack of acute gouty arthritis or the passage of the first renal stone, prophylactic therapy should be considered.

Some patients may never have a second attack, or attacks may not occur for as many as 5-10 years. These patients generally had a mild first attack and responded promptly to treatment. Additionally, serum uric acid levels may have only been minimally elevated. For these patients, a wait-and-see attitude is appropriate. However, if the patient experienced a severe attack and/or substantially elevated serum uric acid levels, then prophylactic therapy is recommended. This involves hypouricemic therapy with either a uricosuric drug (probenecid or sulfinpyrazone) or allopurinol. Allopurinol is the drug of choice in patients with a history of uric acid stones or renal insufficiency and in patients known to be overproducers of uric acid.

Nutritional Supplementation

This category contains no therapies clinically applicable to this disease state.

Herbal Supplementation


Gymnema is a rain forest vine found in Central and Southern India which has a long tradition in the treatment and management of diabetes. The Indian name is Gurmar, which means "sugar destroyer." Its use has been documented in Ayurvedic medical texts for over 2000 years in the treatment of "sweet" urine. Gymnema is gaining popularity with clinicians utilizing natural therapy protocols in the management of diabetes, hyperinsulinemia and impaired glucose tolerance. The leaves of gymnema are thought to increase insulin secretion, and several studies report control of hyperglycemia in moderately diabetic laboratory animals. (9) , (10) A decrease in body weight was also reported. Gymnema reportedly produced blood glucose homeostasis and increased the activity of the enzymes involved in the utilization of glucose by insulin dependent pathways. (11)

Human studies have reported a significant reduction in blood glucose during therapy with gymnema. (12) , (13) A reduction in glycosylated hemoglobin and glycosylated plasma proteins has also been reported, with a reduction in conventional drug dosage. In studies patients with diabetes were able to discontinue conventional drugs and maintain their blood glucose homeostasis with gymnema alone. (14) Researchers suggest that beta cells may be regenerated and/or repaired in Type 2 diabetics on gymnema supplementation. (15) They support their claim by the appearance of increased endogenous insulin levels in the serum of individuals after gymnema supplementation. Other studies report that gymnemic acids suppress the elevation of blood glucose levels by inhibiting glucose uptake in the intestine. (16)

Gymnema has also been reported to selectively suppress the neural responses to sweet taste stimuli. (17) , (18) , (19) Because gymnema leaf powder has an anesthetizing effect on the taste buds which can last for several hours, some researchers feel that gymnema may be a potential agent in weight reduction and sweet cravings. (20) A recent study reports significant serum cholesterol lowering effects of gymnema. (21) Gymnema may potentially be used in athletes to develop a higher ratio of lean muscle mass to body fat. This may be due to the reported increase of insulin output associated with long-term use of gymnema. Increased insulin output and utilization encourages the uptake of amino acids into muscle tissue.


Bromelain is a general name for a family of sulfhydryl proteolytic enzymes obtained from Ananas comosus, the pineapple plant. It is usually classified as either fruit bromelain or stem bromelain depending on its source, with all commercially available bromelain being derived from the stem. These enzymes act on a wide variety of proteins, including food proteins, other enzymes, fibrin and plasminogen, and have been used for years in the food industry as meat tenderizers. (22)

In Europe, a patented tape has been developed containing bromelain that is used clinically for debriding wound eschar. (23) The German Commission E approves the use of bromelain in surgical swelling, particularly of the nasal sinuses. (24) Bromelain is used clinically in conditions such as soft tissue inflammation and arthritis, dyspepsia, and dysmenorrhea, as well as a digestive aid. (25)

Bromelain's primary component is a sulfhydryl proteolytic fraction. (26) Bromelain also contains a peroxidase, acid phosphatase, several protease inhibitors, and organically bound calcium.

Bromelain is used as an anti-inflammatory and analgesic agent in treating the symptoms of arthritis. (27) , (28) The analgesic effects are reportedly due to inhibition of the arachidonic acid pathway of inflammation by selectively decreasing thromboxane generation, changing the ratio of thromboxane/prostacyclin (in favor or prostacyclin), and inhibiting PGE2 in addition to the direct effects on the nociceptors. (29) , (30) , Other reported anti-inflammatory mechanisms of action of bromelain include inhibition of bradykinin at the site of inflammation via depletion of the plasma kallikrein system, and limiting the formation of fibrin by reduction of clotting cascade intermediates. (31) , (32) A few clinical trials in patients with arthritis reported statistical equivalence of pain reduction, whether they were treated with bromelain or diclofenac. (33)

One of bromelain's most common applications is in the treatment of inflammation and soft tissue injuries. It has been reported to speed healing of bruises and hematomas. (34) Treatment with bromelain following blunt injuries to the musculoskeletal system has resulted in a clear reduction in swelling, pain at rest and during movement, and tenderness. (35) Administration of bromelain pre-surgically can reportedly reduce the average number of days for complete disappearance of pain and inflammation. (36) , (37)

Devil's Claw

Historically, devil’s claw tuber has been used as an adjunct therapy for a variety of conditions related to the liver and kidneys. It has also been used to treat lymph toxicity, diabetes, respiratory ailments and arthritic complaints. (38) It reportedly helps with joint mobility and reduces pain and swelling. (39) , (40) The current use of devil’s claw focuses around its anti-inflammatory properties.

Clinical studies have supported that devil’s claw has anti-inflammatory activity, (41) , (42) , (43) although a report has demonstrated negative results. (44) The constituents, harpagoside and beta sitosterol, have been reported to have anti-inflammatory effects. (45) Experiments in laboratory animals have demonstrated the efficacy of devil’s claw in inflammation, with effects comparable to phenylbutazone. (46) The bitter constituents (iridoid glycosides) found in devil’s claw have been reported to be effective in dyspepsia and in regulating bile salts. (47) Devil’s claw is claimed to affect the gallbladder by relaxing smooth muscle, allowing bile to flow more readily. (48) It has been used to treat arthritis, being more suitable for osteoarthritis than rheumatoid arthritis. (49) , (50) The greatest efficacy of devil’s claw in the management of arthritic symptoms is claimed for chronic rather than acute cases. (51)

Acupuncture & Acupressure

Wang Xiao Lin observed the therapeutic effect of acupuncture in the treatment of 36 cases of gouty arthritis with the acupoints of Ahshi-point, Tai Chong (LR 3), and Nei Ting (ST 44). Ahshi-point was pricked first with a three-edged needle to let out a few drops of blood. Then the corresponding point on the healthy hand was pricked. Tai Chong (LR 3) and Nei Ting (ST 44) were punctured. Ahshi-point was punctured with the encircling needling method. These acupoints were stimulated with the reducing method, once every other day. 15 days were considered one therapeutic course of treatment. After one course of treatment, 26 cases were resolved, 9 cases showed considerable improvement, and one case had no effect, with a total effectiveness rate of 97%. (52)

It was reported that 61 cases of gouty arthritis were treated with thermal acupuncture and achieved beneficial therapeutic effects. Zu San Li (ST 36), Gong Sun (SP 4), San Yin Jiao (SP 6), and Ba Feng (EX-LE 10) were punctured and after achieving needling sensations, the needle inserted in Zu San Li (ST 36) was moxibustioned 2 ~ 3 cones for about 30 minutes. Ba Feng (EX-LE 10) was stimulated with the reducing needling method. The treatment was conducted once a day. 7 days constituted one therapeutic course. In the control group, 32 cases of gout were treated with colchicine for 7 consecutive days. The results showed that in the treatment and control groups, 24 and 12 cases were resolved, 26 and 14 cases showed remarkable improvement, 8 and 3 cases showed some improvement, and 3 and 3 cases had no apparent effect, with the effectiveness rates being 95.1% and 90.6% respectively. There was a significant difference between the two groups in their resolve effect (P 0.05), but the resolve rate of the treatment group was significantly superior to that of control group (P< 0.05). (53)

Treatment with blood-letting combined with cupping
In one report, 39 cases of acute gout were treated with blood-letting combined with cupping. After routine sterilization, the affected region was tapped with a plum-blossom needle to cause bleeding, then followed by successive flash cupping for 10 ~ 15 minutes to let out about 10 ~ 15 ml of blood. The treatment was conducted once a day. 3 sessions constituted one course of treatment. The results indicated that the blood-letting treatment was significantly effective in 9 cases, effective in 23 cases, and ineffective in 7 cases. (54)

Traditional Chinese Medicine


Extensive information regarding the treatment of this health condition using Traditional Chinese Medicine is available through the link above.

Diet & Lifestyle

Increase fluids:

Eliminate homogenized milk; it may be a source of xanthine oxidase, which can increase levels of uric acid (55) , (56) potentially leading to an attack of gouty arthritis. Though not specifically related to gout, the physiological activity of xanthine oxidase absorbed from homogenized milk in the diet has been refuted. (57) , (58)

Eliminate alcohol; a case-control study of alcohol consumption and drinking behavior in patients with acute gout: The alcohol intake and drinking behavior of 24 patients who presented with acute gout in a family practice over a 5-year period were compared with these features of a control population matched for sex, age, weight and use of hyperuricemia-inducing diuretics. The average weekly alcohol intake of the group with gout was twice that of the control group (p less than 0.02), and a statistically significant relation was found between alcohol abuse and acute gout (p less than 0.05). About half of the patients with gout drank excessively. Acute gout should be considered a possible clinical sign of alcohol abuse. (59) Other studies have shown an increased risk of gout with alcohol consumption. (60)

Clinical Lab Assessment

Some of the following laboratory testing can provide information necessary for diagnosis and treatment. In addition, the tests listed may also give insight to functional metabolism and functional nutrient status in the body.

Chemistry Profile (Blood)

A multifactorial assessment of chemistry profile values can reveal useful information regarding concurrent disorders and possible nutrient imbalances.

  • Glucose: Blood glucose levels vary in response to food intake, stress, physical exertion, and various disorders. Elevations of serum glucose should lead to confirmatory testing such as fasting insulin, serum phosphorus, magnesium, hemoglobin A1c, and/or fructosamine.
  • Uric Acid: Uric acid is formed as purines are metabolized during formation and degradation of RNA and DNA (also from metabolism of dietary purines). When elevated, uric acid can become deposited in joints and soft tissue and produce an inflammatory response. Rapid cell turnover and inhibited renal excretion can both cause uricemia and may precipitate urate stones. More than 95% of gout patients are hyperuricemic. Normal premenopausal women have serum urate about 1 mg/dl lower than men do. Postmenopausal women have serum urate approximately equal to that of men.
  • Electrolytes: These values are monitored especially when medications are being used. Many diuretics deplete potassium. Low serum potassium (with or without alkalosis) is indication for further renal function study. Diuretics may increase susceptibility or disease intensity in gout. (61)

Thyroid Profile

Thyroid abnormalities are associated with gout. (62) , (63)

Clinical Notes

Quercetin: Allopurinol, which is one of the primary drugs used to treat gout, functions by inhibiting the enzyme xanthine oxidase. (64) Quercetin, which is one of the most widely distributed flavonoids present in fruits and vegetables, possesses antioxidant activity (65) and it is also an inhibitor of xanthine oxidase. (66) This suggests that quercetin might also be helpful in the treatment of gout.


  1. Kelley WN, Worthman RL. Gout and hyperuricemia. In: Kelley WN, Harris EP, Ruddy S, Sledge CB, eds. Textbook of Rheumatology. Philadelphia: Saunders; 1997:1313-1351.
  2. Hawkins DW, Rahn DW. Gout and Hyperuricemia. In: DiPiro JT, et al, eds. Pharmacotherapy, A Pathophysiologic Approach, 4th ed. Stamford, CT: Appleton & Lange; 1999.
  3. Hawkins DW, Rahn DW. Gout and Hyperuricemia. In: DiPiro JT, et al, eds. Pharmacotherapy, A Pathophysiologic Approach, 4th ed. Stamford, CT: Appleton & Lange; 1999.
  4. Levinson DJ, Becker MA. Clinical gout and the pathogenesis of hyperuricemia. In: Koopman WJ, ed. Arthritis and Allied Conditions, 13th ed. Baltimore: Williams & Wilkins; 1997:2041-2071.
  5. Yu T. Nephrolithiasis in patients with gout. Postgrad Med. 1978;63:164-170.
  6. National Institute of Arthritis and Musculoskeletal and Skin Diseases fact sheet: Questions and Answers about Gout. Jan1999.
  7. View Abstract: Emmerson BT. The management of gout. N Engl J Med. 1996;334:445-451.
  8. View Abstract: Tan N, Lertratanalcul Y, Barr WG. Acute gouty arthritis. Postgrad Med. 1993;94:73-78.
  9. Srivastava Y, et al. Hypoglycemic and Life-prolonging Properties of Gymnema sylvestre Leaf Extract in Diabetic Rats. Isr J Med Sci. Jun1985;21(6):540-42.
  10. View Abstract: Okabayashi Y, et al. Effect of Gymnema sylvestre, R.Br. On Glucose Homeostasis in Rats. Diabetes Res Clin Pract. May1990;9(2):143-48.
  11. View Abstract: Shanmugasundaram KR, et al. Enzyme Changes and Glucose Utilization in Diabetic Rabbits: The Effect of Gymnema sylvestre, R.Br. J Ethnopharmacol. Mar1983;7(2):205-34.
  12. View Abstract: Baskaran K, et al. Antidiabetic Effect of a Leaf Extract from Gymnema Sylvestre in Non-insulin-dependent Diabetes Mellitus Patients. J Ethnopharmacol. Oct1990;30(3):295-300.
  13. View Abstract: Shanmugasundaram ER, et al. Use of Gymnema sylvestre Leaf Extract in the Control of Blood Glucose in Insulin-dependent Diabetes Mellitus. J Ethnopharmacol. Oct1990;30(3):281-94.
  14. View Abstract: Shanmugasundaram ER, et al. Use of Gymnema sylvestre Leaf Extract in the Control of Blood Glucose in Insulin-dependent Diabetes Mellitus. J Ethnopharmacol. Oct1990;30(3):281-94.
  15. View Abstract: Shanmugasundaram ER, et al. Possible Regeneration of the Islets of Langerhans in Streptozotocin-Diabetic Rats Given Gymnema sylvestre Leaf Extracts. J Ethnopharmacol. Oct1990;30(3):265-79.
  16. View Abstract: Shimizu K, et al. Suppression of Glucose Absorption by Extracts From the Leaves of Gymnema inodorum. J Vet Med Sci. Sep1997;59(9):753-57.
  17. View Abstract: Kamei K, et al. Amino Acid Sequence of Sweet-taste-suppressing Peptide (Gurmarin) from the Leaves of Gymnema sylvestre. J Biochem (Tokyo). Jan1992;111(1):109-12.
  18. View Abstract: Imoto T, et al. A Novel Peptide Isolated from the Leaves of Gymnema sylvestre - I. Characterization and Its Suppressive Effect on the Neural Responses to Sweet Taste Stimuli in the Rat. Comp Biochem Physiol A. 1991;100(2):309-14.
  19. View Abstract: Kurihara Y. Characteristics of Anti-sweet Substances, Sweet Proteins, and Sweetness-inducing Proteins. Crit Rev Food Sci Nutr. 1992;32(3):231-52.
  20. View Abstract: Brala PM, et al. Effects of Sweetness Perception and Caloric Value of a Preload on Short Term Intake. Physiol Behav. Jan1983;30(1):1-9.
  21. View Abstract: Preuss HG, et al. Comparative Effects of Chromium, Vanadium and Gymnema sylvestre on Sugar-Induced Blood Pressure Elevations in SHR. J Am Coll Nutr. Apr1998;17(2):116-23.
  22. View Abstract: Monograph: Bromelain. Altern Med Rev. Aug1998;3(4):302-5.
  23. View Abstract: Houck JC, et al. Isolation of an effective debriding agent from the stems of pineapple plants. Int J Tissue React. 1983;5(2):125-34.
  24. Blumenthal M, et al, eds. Herbal Medicine: Expanded Commission E Monographs. MA: Integrative Medicine Communications Newton; 2000:33-35.
  25. View Abstract: Monograph: Bromelain. Altern Med Rev. Aug1998;3(4):302-5.
  26. Kelly G. Bromelain: A literature review and discussion of its therapeutic uses. Alt Med Rev. Nov1996;1(4).
  27. View Abstract: Taussig SJ, et al. Bromelain, the enzyme complex of pineapple (Ananas comosus) and its clinical application. An update. J Ethnopharmacol. Feb1988;22(2):191-203.
  28. View Abstract: Rovenska E, et al. Enzyme and combination therapy with cyclosporin A in the rat developing adjuvant arthritis. Int J Tissue React. 1999;21(4):105-11.
  29. View Abstract: Taussig SJ, et al. Bromelain, the enzyme complex of pineapple (Ananas comosus) and its clinical application. An update. J Ethnopharmacol. Feb1988;22(2):191-203.
  30. View Abstract: Felton GE. Fibrinolytic and antithrombotic action of bromelain may eliminate thrombosis in heart patients. Med Hypotheses. Nov1980;6(11):1123-33.
  31. View Abstract: Kumakura S, Yamashita M, Tsurufuji S. Effect of bromelain on kaolin-induced inflammation in rats. Eur J Pharmacol. 1988;150:295-301.
  32. View Abstract: Uchida Y, Katori M. Independent consumption of high and low molecular weight kininogens in vivo. Adv Exp Med Biol. 1986;198:113-118.
  33. View Abstract: Klein G, et al. Reducing pain by oral enzyme therapy in rheumatic diseases. Wien Med Wochenschr. 1999;149(21-22):577-80.
  34. Blonstein JL. Control of swelling in boxing injuries. Practitioner. 1969;203(214):206.
  35. View Abstract: Masson M. Bromelain in blunt injuries of the locomotor system. A study of observed applications in general practice. Fortschr Med. 1995;113:303-306.
  36. Tassman GC, Zafran JN, Zayon GM. A double-blind crossover study of a plant proteolytic enzyme in oral surgery. J Dent Med. 1965;20:51-54.
  37. Tassman GC, Zafran JN, Zayon GM. Evaluation of a plant proteolytic enzyme for the control of inflammation and pain. J Dent Med. 1964;19:73-77.
  38. Bradley P, ed. British Herbal Compendium. Bournemouth: British Herbal Medicine Association; 1992:78-80.
  39. Newall CA, et al. Herbal Medicines: A Guide for Health Care Professionals. London: The Pharmaceutical Press; 1996:98-100.
  40. View Abstract: Baghdikian B, et al. An Analytical Study, Anti-inflammatory and Analgesic Effects of Harpagophytum procumbens and Harpagophytum zeyheri. Planta Med. 1997;63(2):171-76.
  41. Erdos A, et al. Contribution to the Pharmacology and Toxicology of Different Extracts as Well as the Harpagosid from Harpagophytum procumbens DC. Planta Medica. 1978;34:97.
  42. View Abstract: Chrubasik S, et al. Effectiveness of Harpagophytum Extract WS 1531 in the Treatment of Exacerbation of Low Back Pain: A Randomized, Placebo-controlled, Double-blind Study. Eur J Anaesthesiol. Feb1999;16(2):118-29.
  43. View Abstract: Lanhers MC, et al. Anti-inflammatory and Analgesic Effects of an Aqueous Extract of Harpagophytum procumbens. Planta Medica. 1992;58(2):117-23.
  44. View Abstract: Whitehouse LW, et al. Devil's Claw (Harpagophytum procumbens): No Evidence for Anti-inflammatory Activity in the Treatment of Arthritic Disease. Can Med Assoc J. Aug1983;129(3):249-51.
  45. Grahame R, et al. Devil's Claw (Harpagophytum procumbens): Pharmacological and Clinical Studies. Ann Rheum Dis. 1981;40(6):632.
  46. Eichler O, et al. Antiphlogistic, Analgesic and Spasmolytic Effect of Harpagoside, a Glycoside from the Root of Harpagophytum procumbens DC. Arzneim-Forsch/Drug Res. Jan1970;20(1):107-09.
  47. Newall CA, et al. Herbal Medicines: A Guide for Health Care Professionals. London: The Pharmaceutical Press; 1996:98-100.
  48. View Abstract: Occhiuto F, et al. A Drug Used in Traditional Medicine: Harpagophytum procumbens DC. IV. Effects on Some Isolated Muscle Preparations. J Ethnopharmacology. 1985;13:201-08.
  49. Grahame R, et al. Devil's Claw (Harpagophytum procumbens): Pharmacological and Clinical Studies. Ann Rheum Dis. 1981;40(6):632.
  50. View Abstract: Lanhers MC, et al. Anti-inflammatory and Analgesic Effects of an Aqueous Extract of Harpagophytum procumbens. Planta Medica. 1992;58(2):117-23.
  51. Newall CA, et al. Herbal Medicines: A Guide for Health Care Professionals. London: The Pharmaceutical Press; 1996:98-100.
  52. Wang Xiao Lin. Treating 36 cases of gouty arthritis with acupuncture. Journal of Hunan College of TCM. 1999;19(2): 60.
  53. Yang Jin Hong, et al. Treating 48 cases of gout inducted arthritis with combination of acupuncture and external application of herbs. China Journal of Acupuncture. 2000;20(7):395-396.
  54. Chen Lei. Treating 39 cases of acute gout with blood-letting puncturing and cupping method. Shanghai Journal of Acupuncture. 1999;18(5):30.
  55. View Abstract: Bhavadasan MK. Free and membrane-bound xanthine oxidase in bovine milk during cooling and heating. J Dairy Sci. Mar1980;63(3):362-7.
  56. View Abstract: Eger BT, Okamoto K, Enroth C, Sato M, Nishino T, Pai EF, Nishino T. Purification, crystallization and preliminary X-ray diffraction studies of xanthine dehydrogenase and xanthine oxidase isolated from bovine milk. Acta Crystallogr D Biol Crystallogr. Dec2000;56(Pt12):1656-8.
  57. View Abstract: McCarthy RD, Long CA. Bovine milk intake and xanthine oxidase activity in blood serum. J Dairy Sci. Jun1976;59(6):1059-62.
  58. View Abstract: Mangino ME, Brunner JR. Homogenized milk: is it really the culprit in dietary-induced atherosclerosis? J Dairy Sci. Aug1976;59(8):1511-2.
  59. View Abstract: Sharpe CR. A case-control study of alcohol consumption and drinking behavior in patients with acute gout. Can Med Assoc J. Sep1984;131(6):563-7.
  60. View Abstract: Choi HK, et al. Alcohol intake and incidence of gout in men; a prospective study. Lancet. Apr 2004;363:1277-81.
  61. View Abstract: Waller PC, Ramsay LE. Predicting acute gout in diuretic-treated hypertensive patients. J Hum Hypertens. Dec1989;3(6):457-61.
  62. View Abstract: Erickson AR, Enzenauer RJ, Nordstrom DM, Merenich JA. The prevalence of hypothyroidism in gout. Am J Med. Sep1994;97(3):231-4.
  63. Berkow R, Talbott JH. Merck Manual, 13th ed. 1977:1339.
  64. Product Brochure. Bedminster, NJ: Faro Pharmaceuticals Inc; Feb1999:07921.
  65. View Abstract: Morand C, et al. Plasma metabolites of quercetin and their antioxidant properties. Am J Physiol. Jul1998;275(1 Pt 2):R212-9.
  66. View Abstract: Nagao A, et al. Inhibition of xanthine oxidase by flavonoids. Biosci Biotechnol Biochem. Oct1999;63(10):1787-90.
diabetic ketoacidosis obesity myeloproliferative disorders
sarcoidosis renal dysfunction congestive heart failure
lactic acidosis Down’s syndrome lymphoproliferative disorders
starvation psoriasis glycogen storage disease type 1
pernicious anemia hypothyroidism acromegaly
hypoparathyroidism acute alcoholism hyperparathyroidism
chronic hemolytic anemia