Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0948265 (metabolic syndrome)
 24,271 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Gout is a true crystal deposition disease caused by formation of monosodium urate crystals in joints and other tissues. It is a common inflammatory arthritis that has increased in prevalence in recent decades. Gout normally results from the interaction of genetic, constitutional and environmental risk factors. It is more common in men and strongly age related. A major determinant is the degree of elevation of uric acid levels above the saturation point for urate crystal formation, principally caused by inefficient renal urate excretion. Local joint tissue factors may influence the topography and extent of crystal deposition. Recent studies have provided information on dietary risk factors for gout: higher intakes of red meat, fructose and beer are independently associated with increased risk, whereas higher intakes of coffee, low-fat dairy products and vitamin C are associated with lower risk. Several renal urate transporters have been identified including URAT1 and SLC2A9 (GLUT9) and polymorphisms in these genes are associated with an increased risk of hyperuricaemia and gout. Many drugs influence serum uric acid levels through an effect on renal urate transport. Comorbidities, including the metabolic syndrome and impaired renal function are common in gout patients. The usual initial presentation of gout is with rapidly developing acute inflammatory monoarthritis, typically affecting the first MTP joint. If left untreated it may progress with recurrent acute attacks and eventual development of chronic symptoms and joint damage. New knowledge of the modifiable risk factors for gout can be integrated into the management strategy to optimize long-term patient outcomes.
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PMID:New insights into the epidemiology of gout. 1990 32

Gout is a metabolic disease characterized by hyperuricemia and the deposition of monosodium urate (MSU) crystals in the joints and soft tissues, consisting of a self-limited acute phase characterized by recurrent attacks of synovitis and a chronic phase in which inflammatory and structural changes of the joints and periarticular tissues may lead to persistent symptoms. Acute gout is characterized by a sudden monoarthritis of rapid onset, with intense pain, mostly affecting the big toe (50% of initial attacks), the foot, ankle, midtarsal, knee, wrist, finger, and elbow. Acute flares also occur in periarticular structures, including bursae and tendons. The presence of characteristic MSU crystals in the joint fluid, appearing needle-like and showing strong negative birefringence by polarized microscopy, is pivotal to confirm the diagnosis of gout. The time interval separating the first attack from subsequent episodes of acute synovitis may be widely variable, ranging from a few days to several years. During the period between acute attacks the patient is asymptomatic even if MSU deposition may continue to increase silently. The factors that control the rate, location, and degree of ongoing deposition in gouty patients are not well defined. Chronic gout is the natural evolution of untreated hyperuricemia in patients with gouty attacks followed by pain-free intercritical periods. It is characterized by the deposition of solid MSU crystal aggregates in a variety of tissues including joints, bursae and tendons. Tophi can occur in a variety of locations including the helix of the ear, olecranon bursa, and over the interphalangeal joints. Their development is usually related with both the degree and the duration of hyperuricemia. About 20% of patients with gout have urinary tract stones and can develop an interstitial urate nephropathy. There is a strong association between hyperuricaemia and the metabolic syndrome (the constellation of insulin resistance, hypertension, obesity and dyslipidaemia), and gouty patients often have a medical history of kidney disease, diabetes mellitus and signs of vascular illness such as coronary artery disease, heart failure and stroke, resulting with a poor overall quality of life.
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PMID:Clinical features of gout. 2230 30

Gout affects 2.5% of the total UK population and is four times more common in men than women. The peak prevalence and incidence in the UK is in those aged 80-84 years. Gout is associated with comorbidities such as nephrolithiasis, chronic renal impairment, metabolic syndrome, depression and heart disease. It is also associated with increased mortality. Untreated gout can result in disabling irreversible peripheral joint damage and chronic usage-related pain. However, gout is curable. The pathogenic agents that cause gout i.e.urate crystals can be eliminated through a combination of effective patient education and evidence-based, targeted urate-lowering therapy. Gout is caused by the precipitation of monosodium urate crystals in and around a joint. The crystals preferentially form in peripheral, cooler joints and especially in those with osteoarthritis. It is thought that some of these preformed crystals within articular cartilage spill over into the joint space and trigger an acute attack of inflammation. Uric acid is predominantly renally excreted and the common heritable component of gout results from relative inefficiency of urate excretion. Chronic kidney disease, metabolic syndrome and drugs that reduce renal function (e.g. thiazide diuretics, beta-blockers and ACE inhibitors) will all lead to reduced elimination. Patients with chronic gout can present with monoarthritis but more commonly present with asymmetrical polyarthritis or tophi. Joints affected by osteoarthritis are preferentially targeted, the most common sites of involvement are feet, knees, hands and elbows. Diagnosis can be confirmed in primary care by taking a good history and clinical examination. An acute peripheral monoarthritis which reaches its peak within 24 hours and causes 'the worst pain ever experienced' is characteristic of an acute attack. A patient may have co-existing risk factors for gout such as osteoarthritis, obesity, hypertension, renal impairment, diuretic and antihypertensive drug use or increased beer or spirit consumption. A raised serum uric acid can confirm the diagnosis, however, this can be normal in the acute phase. Radiographs are rarely helpful but joint ultrasound may demonstrate deposits in cartilage, the synovium and peri-articular sites.
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PMID:Patients with gout can be cured in primary care. 2560 88