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Kevin Eric Smith
Gout is the most common form of chronic, progressive, inflammatory arthritis. Its prevalence continues to increase worldwide. This condition seems to baffle several fields of medicine who deal with patients suffering with the relentless disease, including podiatrists, chiropractors, rheumatologists, and general practitioners alike.
What is Refractory Gout?
The deposits of MSU, monosodium urate, crystals into the synovial fluid and other tissues take place when the serum uric acid concentration exceeds its solubility. As this progresses, these deposits can occur just about anywhere in the body and lead to chronic pain, bone erosions, tophi, and general joint deformities. This condition can become downright debilitating, and rather difficult to treat.
Treatments for acute Gout flares typically involve dietary adjustments, urate lowering drugs, xanthine oxidase inhibitors, and symptom/pain relieving medications. However, for the 2% of these cases that suffer with Refractory Gout (uncontrolled, chronic and recurring attacks), treatment can be quite challenging. This stage of Gout is rather relentless and often resistant to common management therapies and medications.
Once Gout attacks become chronic, they often become tophaceous, where nodular masses of uric acid are deposited in soft tissue areas of the body. While most tophi is believed to be visible, studies have shown only 25% being detected by a physical exam. Imaging known as DECT, dual-energy computed tomography, has painted a very different picture with the detection of large masses of non-visible tophi all throughout the body, including the organs.
Does this mean that virtually ALL gout is already tophaceous by the time the first attacks occurs? The simple answer is 'yes'. While it may begin small and only microscopically visual, its destructive path can lead to dangerous changes within the body, and eventually show up on the outside of the body, as well.
Gout flares begin with the combination of hyperuricemia and associated chronic inflammation. Uric acid excretion is conducted largely by the kidneys (around 65-75%), with the other 25% or so excreted by the GI tract. Under-excretion of uric acid makes up close to 90% of those that suffer with Hyperuricemia. Only 10% is caused by over-production.
Causes of Hyperuricemia
Under-excreters of urate (~90%)
|Drugs or Dietary Habits
|Low doses of salicylates
||Polycystic kidney disease
||Familial juvenile hyperuricemic nephropathy
||Medullary cystic kidney disease
|Laxative Abuse (alkalosis)
||Toxemia of pregnancy
||Chronic beryllium disease
Overproducers of urate (~10%)
|Drugs or Dietary Habits
||Clinical Disorders Leading to Purine Overproduction
|Diet rich in purines
||Glycogenosis III, V, VII
||Inherited Enzyme Defects
|4-Amino-5-imidazole carboxamide riboside
|Vitamin B12 (patients with pernicious anemia)
||Increased PRPP synthetase
||Glucose-6-phosphatase deficiency (glycogenosis I)