Monosodium urate crystals

The solubility of uric acid depends on concentration and temperature. At high serum concentrations, lower body temperature causes the precipitation of monosodium urate crystals. Collections of these crystals (called micro tophi) can form in joint spaces in the distal extremities. 

FIGURE 56-1. Synovial fluid containing extracellular and intracellular monosodium urate crystals. (From Reginato AJ. Gout and other crystal arthropathies. In Braunwald E,... 

Aspiration of affected joint fluid is essential for a definitive diagnosis. Joint fluid containing negatively birefrin-gent monosodium urate crystals confirms the diagnosis. Joint fluid has an elevated WBC count with neutrophils predominating. 

Allopurinol is well absorbed with a short half-life of 2 to 3 hours. The half-life of oxypurinol approaches 24 hours, allowing allopurinol to be dosed once daily. Oxypurinol is cleared primarily renally and can accumulate in patients with reduced kidney function. Allopurinol should not be started during an acute gout attack because sudden shifts in serum uric acid levels may precipitate or exacerbate gouty arthritis. Rapid shifts in serum uric acid can change the concentration of monosodium urate crystals in synovial fluid, causing more crystals to precipitate. Thus some clinicians advocate a prophylactic dose of colchicine (0.6 mg/day) during initiation of antihyperuricemic therapy. Acute episodes should be treated appropriately before maintenance treatment is started. 

The term gout describes a disease spectrum including hyperuricemia, recurrent attacks of acute arthritis associated with monosodium urate crystals in leukocytes found in synovial fluid, deposits of monosodium urate crystals in tissues (tophi), interstitial renal disease, and uric acid nephrolithiasis. 

Arthropathies associated with crystals deposition are acute gouty arthritis, chronic gout and chronic tophaceous gout due to monosodium urate crystals. Then there is acute pseudogout and chronic pyrophosphate arthropathy caused by calcium pyrophosphate dehydrate crystals. Acute calcific periarthritis, acute hydroxylapatite arthritis and chronic hydroxyapatite arthritis including Milwaukee-shoulder-knee syndrome are due to basic calcium-phosphate-hydroxyapatite crystals. 

Gouty arthritis is an inflammatory response to the deposition of monosodium urate monohydrate crystals secondary to hyperuricemia. It is called monosodium urate crystal deposition disease. Hyperuricemia is a serum urate concentration > 7 mg% in males and >6 mg% in females. Hyperuricemia results from overproduction (10-15% of individuals) or a renal excretion of urate lower than 400 mg uric acid/24 hours (85-90% of individuals). The urate under-excretors have a urate clearance of <6 ml/min or a urate to creatinine clearance ratio of <6%. The combination of a relative excess of dietary purine consumption together with urate under-excretion is often the basis for hyperuricemia. 

Gout can be diagnosed by the presence of negatively birefringent monosodium urate crystals in aspirated synovial fluid examined by polarized-light microscopy. Here, crystals are within polymorphonuclear leukocytes. 

Gout is a syndrome caused by an inflammatory response to the formation of monosodium urate crystals which develop secondary to hyperuricaemia (Johnstone, 2005). 

Weissman, G. and Rita, G.A., Molecular basis of gouty inflammation Interaction of monosodium urate crystals with lysosomes and liposomes, Nature New Biol., 240, 167, 1972. 

The anti-inflammatory effects of borage seed oil have been demonstrated in animal models. A diet enriched with borage seed oil (23% GLA) was compared to one with safflower oil (<1% GLA) with regard to effects on acute inflammation induced by monosodium urate crystals, subacute or chronic inflammation caused by Freund s adjuvant in a subcutaneous air pouch, or adjuvant-induced arthritis (Tate et al., 1989). Borage seed oil, but not safflower oil, decreased inflammation in all models. In addition, the ratio of DGLA to AA was five times that in the livers of animals fed safflower oil. 

Gout is a hyperuricemic state (>6 mg/dL) that is effectively diagnosed through the detection of monosodium urate crystals in the synovial fluid of the involved joint. 

Lotta Topaigne s gout is caused by depositions of monosodium urate crystals in the joint of her big toe. At a blood pH of 7.4, all of the uric acid has dissociated a proton to form urate, which is not very water-soluble and forms crystals of the Na salt. In the more acidic urine generated by the kidney, the acidic form, uric acid, may precipitate to form kidney stones. 

Gout is a metabolic disease characterized by recurrent episodes of acute arthritis, usually monoarticular, and is associated with abnormal levels of uric acid in the body, particularly the presence of monosodium urate crystals in synovial fluid. Primary gout is a hereditary disease in which hyperuricemia is caused by an error in uric acid metabolism—either overproduction or an inability to excrete uric acid. Secondary gout refers to those cases in which hyperuricemia is caused by an acquired disease or disorder, such as chronic renal disease, lead poisoning, or myeloproliferative disorders. Gout generally occurs in... 

Naked monosodium urate crystals stimulate oxygen radical release by human polymorphonuclear leukocytes. Very recently, two papers dealing with superoxide anion generation by human neutrophils exposed to monosodium urate have been published. From the comparison of the data derived from nitroblue tetrazolium and cytochrome c reduction, it has been suggested that radical production in response to urate crystals is compartmentalized and occurs predominantly in the intracellular space. Microcrystalline sodium urate-induced oxygen consumption and nitroblue tetrazolium reduction were present for at least 15 min after stimulation of the cells. To enhance extracellular radicals neutrophils were converted to secretory non phagocitic cells by use of cytochalasin... 

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