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WHAT IS GOUT
Kevin Eric Smith
Traditional Gout Treatments - Allopurinol
Many with gout continue to suffer because knowledge of effective treatments has been slow to spread to patients and their physicians.
Gout is provoked by an excess of uric acid in the body. This surplus can be precipitated by an increase in production by the body, excessive cellular degeneration, reduced elimination of uric acid via the kidneys and bowels, and/or through an increased intake of purine-rich food selections.
With time, elevated levels of uric acid in the blood will lead to deposits in connective tissue around joints. Eventually, the uric acid may form needle-like crystals in the joints, leading to acute gout attacks. The extreme pain is from the infection and not the crystals themselves. Uric acid may also collect under the skin as tophi or in the urinary tract as kidney stones.
Gout afflicts an estimated 840 out of 100,000 people. Gout and its complications occur more commonly and at a younger age in males.
The definitive diagnosis of gout is dependent on finding uric acid crystals within the joint fluid during an acute attack. Uric acid levels within the blood alone are frequently misleading and may be transiently normal, or even low. Additionally, uric acid levels are often elevated in individuals without gout.
Prescription gout treatment is not typically advised for asymptomatic hyperuricemia (high uric acid levels with no gout attack symptoms). These traditional gout drugs should only be prescribed by informed doctors, in the presence of gout attacks or kidney stones. The undesired side effects associated with these gout drugs, and the damage that they may do to the organs, does not warrant their use based solely on elevated uric acid levels in the blood.
GC® GoutCare, on the other hand, can be used by both gout sufferers and people with high blood levels of uric acid. GC® is safe and only has beneficial side effects from its use, for anyone with or without uric acid problems. In fact, GC® has a positive effect on type two diabetics by aiding to lower their insulin needs. It is even possible to control border line cases in hopes of remaining off insulin altogether.
ALLOPURINOL (Zyloprim -- a prescription drug) inhibits uric acid synthesis and has been linked to skin eruptions, inflammation of the blood vessels, and liver toxicity. Periodic liver enzymes, renal function tests and complete blood counts should be performed in all patients on allopurinol. Alterations in liver enzymes, including transient elevations of serum alkaline phosphatase, AST and ALT, have occurred in some patients. Reversible hepatomegaly, hepatocellular damage (including necrosis), granulomatous changes, hepatitis and jaundice have also occurred.
This report claims that 54 cases, out of 211 people, is "RARE"..... Rare or disturbing? You be the judge:
Allopurinol Hypersensitivity Syndrome
The allopurinol hypersensitivity syndrome (AHS) consists of severe rash, fever, eosinophilia, and hepatitis and renal failure. It is a feared, albeit rare (see below), complication of therapy and is sometimes fatal.
Reported risk factors for AHS include renal impairment and diuretic use. Furthermore, although controversial, some data suggest that a higher dose of allopurinol in patients with renal impairment increases the risk for hypersensitivity. The effect of a creatinine clearance-based initial dosing regimen on risk for hypersensitivity is not well understood.
Stamp and colleagues performed a case/control study in New Zealand to evaluate factors that were associated with the development of AHS.
Fifty-four patients who were treated for gout with allopurinol and developed AHS were identified. These patients were compared with 157 patients with gout who received allopurinol therapy but did not develop AHS.
The median onset of AHS was 30 days after starting allopurinol therapy, and 90% of cases occurred within the first 6 months; 43 cases required hospitalization, and 3 patients (6%) died of AHS.
COLCHICINE (a prescription drug) is used to alleviate attacks. This drug can cause serious side effects and toxicity and even death in high doses.Side Effects: 80% of people who take colchicine in doses that are high enough to be effective develop stomach problems, such as cramping, nausea, diarrhea, or vomiting. Serious side effects of colchicine include bone marrow problems, muscle inflammation, severe anemia, and extremely low white blood counts that can increase the risk of infection developing. Colchicine is usually avoided or the dose adjusted in people who have reduced kidney function.
INDOMETHACIN is a non-steroidal anti-inflammatory drug (NSAID). NSAID's have become the treatment of choice among Doctors and Indomethacin is the most widely used prescription drug for most gout attacks. NSAID's may also have significant toxicity, but if used for the SHORT TERM they are generally well tolerated.
PREDNISONE is being prescribed for gout more and more these days. This immunosuppressive drug, though necessary in some cases, is associated with serious long-term side effects such as cataracts, bone loss, weakening of the immune system, and many others. One of the most serious complications from prednisone is the risk of osteoporosis, which occurs from the bone loss. The most commonly reported side effects are increased acid in the stomach, sodium retention, delayed healing, decreased ability to fight infection, bone and muscle problems, acne, night sweats, increased sugar in the blood, and thrush (yeast growth in the mouth which is a very strong indication of the lack of "friendly" bacteria in the body- sources strongly needed to fight infection). As with many other medications, Prednisone will cover up the disease but it is the underlying problem, the cause of the disease, that must be repaired..