Gout
Gout is a recurrent metabolic disorder characterized by the deposition of urate crystals within joint spaces and in the adjacent cartilage and tendons. It is particularly common in the big toe. The onset of symptoms is usually sudden, with an attack often occurring at night. The affected joint becomes hot and painful with varying degrees of swelling. Early attacks, if left untreated, usually resolve spontaneously in three to ten days, but recur with increasing frequency. Chronic arthritis may develop, with deposition of tophi in the joints. Nephrolithiasis with obstructive uropathy may result from precipitation of crystals in the kidneys.
Gout affects more than one million Canadians and Americans. Painful attacks can occur at any age, but the first attack usually occurs between the ages of 40 and 50. Gout is 20 times more common in men than women, however, the number of postmenopausal women with gout is increasing.
CAUSAL FACTORS
Approximately one in four people with gout have a family history of the disease. In some families, the enzyme uricase (which breaks down purines), is missing. A steady diet of purine-rich foods is also associated with the development of gout, as is overeating. Obesity may be an especially important risk factor for gout in men. Children who are obese may have a higher risk for gout in adulthood.
The use of alcohol is associated with gout in younger adults. Binge drinking in particular increases uric acid levels. Alcohol appears to play less of role among elderly patients, especially among women with gout.
Some studies have reported a higher incidence of gout in people with hypothyroidism. There is also some evidence to suggest that can increase uric acid levels, although not to the degree that low thyroid hormones levels do.
Certain drugs reduce the body's ability to remove uric acid. These include diuretics, salicylates, cyclosporine and levodopa. Vitamin B3 (niacin) raises uric acid levels, thereby contributing towards the development of gout in susceptible individuals.
Autoimmune disorders that are associated with excessive breakdown of cells may increase serum purine levels.
TREATMENT MODALITIES
Standard therapy for gout consists of prompt treatment of flare-ups attack with NSAIDs or colchicine. Intrarticular injection of glucocorticoids may sometimes be necessary if response to oral agents is not satisfactory. NSAIDs are also be used prophylactically against recurrent attacks.
Antihyperuricemic therapy is normally instituted to reduce the serum uric acid concentration below its saturation point in extracellular fluid (6.4 mg/dl). Following management of the acute attack and identification of the cause of hyperuricemia, treatment for gout is normally directed at lowering serum uric acid through modification of diet (lowering of purine intake, cessation of alcohol consumption, and/or use of a uricosuric drug or allupurinol to decrease synthesis.)
Many cases of gout respond well to diet revision, but this requires a great deal of motivation and understanding on the part of the patient. Usually, a combination of medication and diet revisions will achieve sound management of symptoms.
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Medications:
Analgesics and Anti-inflammatories
NSAIDs
Nonsteroidal anti-inflammatory drugs (NSAIDs) are a group of drugs commonly used to treat gout because of their analgesic, anti-inflammatory, and antipyretic properties. NSAIDs inhibit the enzymes Cox-1 and Cox-2 (cyclooxygenase), which catalyze arachidonic acid to prostaglandins and leukotrienes. Arachidonic acid is released from membrane phospholipids as a response to inflammatory stimuli. The efficacy of NSAIDs differs from patient to patient. This is likely due to the pharmacokinetic differences among the various NSAIDs.
Through their inhibition of Cox-1 enzyme, NSAIDs can cause stomach irritation, bleeding, fluid retention, and decreased kidney function. Since NSAIDs bind to plasma proteins they may be displaced by or may displace other plasma-bound drugs such as coumadin, methotrexate, digoxin, cyclosporine, oral antidiabetic agents, and sulfa drugs. This interaction can enhance the therapeutic or toxic effects of either drug.
NSAIDs (particularly indomethacin) can interfere with the pharmacologic control of hypertension and cardiac failure in patients who take beta-adrenergic antagonists, angiotensin-converting enzyme inhibitors, or diuretics.
The long-term use of NSAIDs may have a damaging effect on chondrocyte function.
Adverse effects of NSAIDs (which can occur at any time), include renal failure, hepatic dysfunction, bleeding, and gastric ulceration.
Cox-2 Inhibitors
A relatively new sub-class of NSAID, known as Cox-2 inhibitors, work by blocking cyclooxygenase 2 enzyme which is involved in the inflammation pathway. By sparing cyclooxygenase 1 (Cox-1) enzyme, gastrointestinal toxicity is purportedly reduced. Due to their proclaimed reduction of gastro-intestinal side effects, Cox-2 inhibitors have claimed a large marketshare.
Unfortunately, recent studies have indicated that Cox-2 inhibitors can increase the risk of cardiovascular problems including angina, myocardial and cerebral infarction, thrombosis and sudden death, to four times that of traditional NSAIDs. A review of more than 48,000 patients taking rofecoxib revealed that 0.52% of patients taking an inactive placebo pill had a heart attack each year. The annual rate of heart attack was 0.74% for patients taking rofecoxib. One theory for this holds that Cox-1 enzyme plays a role in preventing the clot formation that leads to cardiovascular problems.
The assertion that Cox-2 inhibitors (rofecoxib, celecoxib) do not induce haemorrhage in the upper gastro-intestinal tract, is also under dispute. While studies confirm that Cox-2 inhibitors cause fewer gastro-intestinal events than traditional NSAIDs in the short-term, it is not yet known what the long-term effects of these drugs will have on the gastric mucosa.
*Important News Release September 2004
Vioxx®, the cox-2 inhibitor made by Merck, has been pulled from the market because of severe lethal side effects due to heart attack and stroke.
Acetaminophen
Acetaminophen is often prescribed to relieve mild to moderate pain resulting from gout. The drug possesses analgesic and antipyretic properties, but is not an anti-inflammatory. For this reason, it may usually be safely combined with an anti-inflammatory medication to relieve pain.
Overdosing can cause liver damage that may be severe enough to cause liver failure and death. This damage occurs in a dose-related manner and is the leading cause of rapid onset liver failure in the US, Canada and the UK.
For the average healthy adult, the recommended maximum dose of acetaminophen over a 24-hour period is four grams (4000 mg) or eight extra-strength pills. (Each extra-strength pill contains 500 mg and each regular strength pill contains 325 mg.) A patient who drinks more than two alcoholic beverages per day, however, should not take more than two grams of acetaminophen over 24 hours. For children, the dose is based on weight and age.
A single dose of 7 to 10 grams of acetaminophen (14 to 20 extra-strength tablets) can cause liver injury in the average healthy adult. (This amount is about twice the recommended maximum dose for a 24-hour period.) In children, a single dose of 140 mg/kg body weight of acetaminophen can result in liver injury. However, amounts of acetaminophen as low as 3 to 4 grams in a single dose or 4 to 6 grams over 24 hours, have been reported to cause severe liver injury, sometimes resulting in death. Certain individuals, for example, those who regularly drink alcohol or those with hepatitis C, are more prone than others to developing acetaminophen-induced liver damage.
Cortisone
Cortisone may be injected directly into the joint to relieve severe inflammation and swelling. A cortisone injection can provide almost immediate relief for a tender, swollen or inflamed joint. However, since corticosteroids can degrade cartilage and demineralize the bone, they should only be used rarely. Chronic use of corticosteroids may result in weight gain, hypertension, susceptibility to infection, capillary fragility, acne, excess hair growth, cataracts, glaucoma, diabetes, muscular atrophy, accelerated atherosclerosis, menstrual irregularities, irritability, insomnia and psychosis. Since steroids appear to cause premature death of osteoblasts and slow their replacement; osteoporosis and bone damage are of particular concern. Long-term use may also affect brain cells, causing memory loss. Certain side effects such as hypoglycemia, edema and hypertension can be minimized by treatment.
Substances that may help reduce pain and improve overall health:
URIC ACID ELIMINATORS
Uricosuric medications used to treat inadequate elimination of uric acid include probenecid or sulfinpyrazone. Side effects include of both drugs include nausea, vomiting and diarrhea. The goal of probenecid therapy is to lower serum urate concentrations to about 6 mg/dL. By decreasing concentrations of serum urate, probenecid helps prevent chronic joint changes and tophi formation, reduces the frequency of acute gout attacks, and may improve renal function in patients with gout.
The patient should increase water intake to about 10 x 8 ounce glasses per day when taking uricosuric medications. ASA should also be avoided because it blocks the drug's effects on the kidneys.
URIC ACID INHIBITORS
Allopurinol is used for the management of gout when uricosurics cannot be used due to adverse effects, allergy, or inadequate response; when there are visible tophi or evidence of uric acid deposits or stones; or when serum urate concentrations are greater than 8.5 - 9 mg/dL and a family history of tophi and low urate excretion exists.
This long-term medication inhibits xanthine oxidase, the enzyme that catalyzes the conversion the production of uric acid and has very few side effects. The incidence of side effects is higher for people with kidney or liver problems.
The most common adverse effect of allopurinol is a pruritic maculopapular rash. The incidence of rash may be increased in patients with renal insufficiency. In rare instances, a skin rash may be followed by severe hypersensitivity reactions which may sometimes be fatal.
Nutricol®
Nutricol®
Available as the OTC supplement Recovery® in many pharmacies, Nutricol® is proposed to reduce the inflammation that accompanies gout. This may reduce the likelihood of progression and diminish accompanying pain. Nutricol® (Recovery®) is an anti-catabolic agent that works at cellular level to help stabilize joint structures. Biomedica Laboratories, Inc., also believes that this proprietary blending of plant nutrients naturally increases the cells' receptivity to hormones such as insulin which are required to speed the repair of joint tissues.
Recovery® contains the active ingredient Nutricol®, a disease modifying anti-catabolic agent (DMAC), which Biomedica Laboratories is proud to introduce to health care professionals.
Biostructural® Medicine goes beyond simply addressing symptoms; it is a cell structure-oriented health that addresses the pathogenic factors of degenerative and inflammatory conditions.
Nutricol® (Recovery®) may be safely combined with other arthritis medications or taken on its own to help counter pain and inflammation. It does not produce unpleasant side effects. Since this product works to modify the body's responses, it may take up to six weeks for your patients to experience relief, with most people noticing benefits within a month.
The ultimate goal of Recovery® is to reduce the formation of uric acid deposits and increase the flushing of existing deposits.
Recovery® is proposed to decrease catabolism of cells induced by uric acid deposits. Research into the possible ability of Recovery® to reduce the formation of urate crystals in ongoing.
When used as directed, Recovery® with Nutricol® is proposed to:
- Reinforce membrane and matrix structures by increasing aldimine reducible cross-linking of collagen fibers; this acts to reinforce the strength and elasticity of connective tissue structures such as cartilage, synovium, ligaments, tendons, fascia, bone, blood vessel walls and the dermis of the skin (26,27)
- Neutralize reactive oxygen species (ROS) and catabolic enzymes before they can negatively impact cellular and extracellular structure and function; this results in increased membrane receptivity to growth factors such as insulin, somatomedins and thyroxin that are required for anabolic repair and cellular maintenance (4,10,13,28-30,35,49)
- Decrease catabolism of membrane and matrix collagen and glycosaminoglycan (GAG) structures via decreasing the pathological production of catabolic enzymes and other biochemicals such as collagenase, elastase, hyaluronidase, tumor necrosis factor, nitric oxide synthase and xanthine oxidase*; these biochemicals are released from immune, microbial and damaged cells and cause further damage to connective and epithelial tissue structures, resulting in joint pain, inflammation, capillary fragility and other soft-tissue damage (4,25,31-35)
- Stabilize cellular membranes, preventing the release of compounds that promote inflammation such as histamine, serine proteases, prostaglandins and leukotrienes by non-competitively inhibiting the release of associated inflammatory enzymes such as cyclo-oxygenase, lipoxygenase and phosphodiesterase (33,36)
- Increase the stability and production of protective epithelial mucosal surfaces in the digestive, respiratory and genitourinary tract to decrease the absorption of antigens (environmental compounds that may initiate immune or non-immune mediated inflammation, spasm and damage within blood vessels) (37-40)
Biostructural® Medicine goes beyond simply addressing symptoms and focuses on the degenerative process and optimal healing.
Nutricol® (Recovery®) may be safely combined with other medications or taken on its own to help counter inflammation and improve the quality and rate of healing.
Information for Doctors: Print an 5-page detailed information package that provides the following:
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Click here to view feedback from health professionals and users about the results noted from Recovery® with Nutricol®.