Etiology and pathogenesis

 Status hyperuricemia

High uric acid levels may be the result of increased production or decreased uric acid excretion of uric acid by the kidneys. 80% - 90% of patients with primary gout condition decreased uric acid excretion through the kidney tubules despite normal renal function, possibly due to reduced filtration, reabsorption increased or decreased excretion, but the mechanism The most important is still unclear.

High uric acid levels may be secondary to some disease (kidney, bone marrow proliferative diseases, obesity, alcoholism and drug).

Approximately 10% - 20% of patients with primary gout is caused by increased synthesis of purines lead to increased production of uric acid. There are four types of genetic disorders of purine synthesis are: (1) Increase the PRPP synthetase enzyme activity, (2), glucose-6-phosphate deficiency dehydrogenase, (3) lack of enzyme fructose-1-phosphate aldolase, and (4 ) HGPRT deficiency.

  AICD causes increased blood uric

By proposing the transfer cycle promise uric acid, hyperuricemia has many causes. The first is to increase supply through diet, drinking (beer, wine, organ, dog meat, meat Bu ...), too, proposing increased synthesis (genetic disorders ...), and reduced training proposing Too Waste. Or combination of both mechanisms has increased synthesis reduces uric acid excretion in the urine.

Table 1.1: Reasons hyperuricemia and gout

Produces too much uric acid	Primary hyperuricemia: spontaneity, lack of partial or complete enzyme HGPRT; PRPP synthetase enzyme activity increases
Secondary hyperuricemia: diet high in purines; marrow proliferative diseases; haemolysis; psoriasis; Glycogen storage disease type 1, 3, 5.7.
Reducing uric acid excretion	Primary hyperuricemia: spontaneous Secondary hyperuricemia: kidney failure; metabolic acidosis; dehydration; drugs (diuretics, cyclosporine, pyrazinamide, ethambutol, low-dose salicylates); hypertension; kidney disease lead poisoning.
Proliferation and decreased excretion of uric acid	- Alcoholism - 6-phosphatase deficiency Glucose- - 1. phosphat- aldolase deficiency Fructose-

 Deposition process and the formation of uric acid crystals inflammation

at concentrations below 7,0mg / dl (416mmol / l) and pH 7.4, uric acid dissolves almost completely as ion (+) urate. When uric acid levels greater than 7.0 mg / dl, exceed the maximum soluble concentration, urate precipitation of monosodium urate crystal micro (MSU). The favorable conditions for the deposition and precipitation of crystals include low temperatures (in the peripheral joints), decreased intracellular pH, and decreased ability to bind the protein blood urate. There are also other factors such as injury and the concentration of urate in place rapidly due to the mobilization of water from peripheral tissues (while improving leg swelling).

The ability of crystals cause inflammation related to the ability to bind to immunoglobulin and protein, especially complement and lipoproteins. This complex binds to receptors on the surface of macrophages and mast cells, leading to activation and release of cytokines, chemical elements and the active intermediate. The macrophage phagocytosis urate crystals will destroy the lysosome arachidonate liberation, collagenase, oxidative radicals cause joint inflammation

 Stage of the disease

Progress concave classic clinical gout natural evolution through three stages:
Stage I: hyperuricemia asymptomatic (Asymtomatic hyperuricemia)
Stage II: acute gout (acute gouty arthritis) and between exacerbations (Intercritical gout)
Stage III: Still garlic GYT chronic non-performance and particle convergence (chronic and recurrent gout tophaceuos).

Hyperuricemia no symptoms were defined as a still state of the blood acid levels above 7 mg / dl (416 mmol / l) without clinical symptoms of acute gout attacks. There are two types of primary and secondary. Hyperuricemia not usually the primary symptom onset puberty in males and females age rabbit food business. Still hyperuricemia situation lasted for many years (20 years the interior medium) before the onset of an acute gout attack. In the US, the incidence of gout is 4.5% annually; 0.5%; 0.1% respectively in those with blood levels of uric acid are:> 535 mmol / l; 416-529 mmol / l; <416 mmol / l [2].

After an acute gout attack starts and ends phosphate, the second-level course may appear after a few months to several years, between exacerbations absolutely no clinical symptoms. At first, the interval between exacerbations long, but then exacerbations appear more and more, less acute onset over time prolonged inflammation and joint damage much more. Very rarely patients with gout not appear Monday. In a study to be conducted before using medication to reduce blood uric acid found 62% Oily disease onset gout attacks Monday in the first year, 78% of patients with gout appeared Monday in 2 years and 93% second with gout in 10 years [2].

In the period between acute attacks of joint damage was almost no clinical symptoms, but the concave of urate crystal deposition continues. So can find urate crystals in synovial fluid and detection of bone lesions on x-ray.

Finally, after about 5 to 10 years with acute gout episodes, patients progress to chronic gout non-grain bowl. Now that the clinical manifestations, biochemical, X-ray is an expression of urate accumulation in tissues such as cartilage, joints, bursae, tendons DOY, software, kidney, heart ... make up the inflammatory disease multiple joints, destruction and deformity, kidney damage (kidney stones, glomerulonephritis, interstitial nephritis, renal failure) ...