Characterized by tender, red, hot, swollen joints, and recurring attacks of acute inflammatory arthritis, Gout affects the metatarsal phalangeal joint at the base of the big toe in fifty percent of all cases, where it is then known as podagra, or uric acid arthropathy. Gout produces joint pains that can last up to four hours at a time, as well as during the night due to lower body temperatures then. Gout may manifest as kidney stones, urate nephropathy, renal insufficiency, hyperuricosuria, uric acid tophis, high fevers, fatigue, chronic arthritis, bone erosions, and high levels of uric acid in the blood, heels, fingers, wrists, and knees.
Gout is caused by crystallized elevated levels of uric acid deposited in tissues, joints, tendons, and the blood that may result from alcohol consumption (especially beer), insulin resistence, genetics, hypertension, obesity, diuretics, renal insufficiencies, diets, underexcretion of uric acid salts, overproduction of urate, fructose sweetened drinks, seafood, red meat, physical traumas, surgeries, Familial Juvenile Hyperuricemic Nephropathy, super activity of the Tamm-Horsfall mucoprotein, the phosphoribosyl pyco phosphate synthetase protein, medullary cystic kidney disease, the Lesch-Nyhan Syndrome, the Kelley-Seegmiller Syndrome, Juvenile Gout, deficiencies in the hypoxanthine-guanine phosphosibosyl transferase enzyme, aspirin, niacin, Vitamin B3, Cyclosporine and Tacrolimus that are used in post-allogeneic organ transplants, and Hydrochlorothiazide that prevents the kidneys from retaining water and to treat hypertension.
The diagnosis of Gout can be readily made once monosodium urate crystals have been identified in a tophis found in bones, cartilage, joints, the kidneys, nasal cartilages, and other locations throughout the body, or in the synovial fluid of inflamed joints under polarized light microscopes, Other diagnostic tools for determining Gout include the Classic feature of hyperuricemia, through elevated white blood cell counts, renal malfunctions, in electrolytes, by erythrocyte sedimentation rates of red blood cells, by the Biernacki Reaction Test, and by Synovial Fluid Gram Stains for bacterial organism classifications.
Options available for treating Gout include nonsteroidal anti-inflammatory medications, the first-line treatment for Gout, ibuprofen, Indomethacin that prevents prostaglandis lipids from developing, reduces fevers, swelling, pain, and stiffness, protein pump inhibitors, Calchicine, however, its side effects may limit its use, glucocorticoids that regulate glucose metabolism, Pegloticase IV injections administered every other week, Allopurinol that blocks uric acid production, Febuxostat that prevents xanthine oxidase enzyme activities in purine metabolism, Probenecid that increases uric acid excrement, hypourecemic medicines, decreasing meat and seafood intakes, increasing Vitamin C consumption, avoiding obesity, and limiting alcohol and fructose.
A disorder of purine metabolism, combined with losses of uricase that breaks down uric acid, Gout may be triggered by rapid changes in uric acid levels, acidosis, increased levels of acid in the blood, extracellular matrix proteins, articular hydration, collagens, proteogylcans, chondroitin sulfate, chemotherapies, Allopurinol, traumas, and a variety of surgeries.
Acute Gout typically subsides in about seven days, however, without treatment as many as sixty percent of patients with the ailment will develop a second attack within a year’s time, and all Gout sufferers are at a higher risk for diabetes, hypertension, renal diseases, Reaven’s Syndrome, Insulin Resistance Syndrome, Cadiometabolic Syndrome, destruction of joint surfaces, Chronic Gout, kidney stones, chronic renal dysfunctions, and tophis in the Achilles tendons, helix of the ear, and over the olecranon bones of the forearms behind the elbows.
This Article was compiled from several websites that provide much more information about Gout including: