Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P50583 (asymmetrical)
 12,197 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Microcrystalline arthropathies of the wrist include three main forms of microcrystalline pathology: gout, chondrocalcinosis and apatite calcifications. Gout of the wrist is now rare and may be missed, particularly in its chronic form, occasionally associated with tophi and large, often asymmetrical erosions on the X-rays. Chondrocalcinosis is frequent and easy to diagnose in the wrist and may be responsible for a very typical arthropathy predominantly involving the radiocarpal joint, while the frequency and specificity of scapho-trapezoid involvement are controversial. Apatite deposits in the wrist involve various tendons and ligaments, especially the tendon of flexor carpi ulnaris, but may also be responsible for intra-articular pathology.
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PMID:[Microcrystal deposit arthropathies of the wrist]. 133 92

Radiological gout manifestations are detectable in the early stage, but also especially in the chronic stage of gout. Whereas in the early stage only soft tissue mutations (bursitis inflammation) and light calcium deposits are usually discernible, chronic gout leads to asymmetrical, diverse forms of osseous destruction, favouring smaller joints, but also affecting larger ones, which are caused by the intra-articular and extra-articular deposit of tophus material, corresponding to the progression and degree of severity of the illness. Radiologically-detectable changes in other organs, such as the kidneys, will be addressed. The high number of, and to some extent very characteristic, osseous mutations are compared with those mutations which are very similar to the diagnoses of other syndromes affecting the joints. Specifically, problems in differentiating diagnosis of rheumatoid arthritis, arthritis psoriatica, chondrocalcinosis, and other diseases of the joints will receive special mention. Reference is also made to the extreme diagnostic difficulties resulting from the rare but nevertheless conceivable influence of gout on the spine or sacroiliac joints. The method of magnetic resonance imaging for gout shows a characteristic signal behaviour of the tophus material. It has been determined that, through magnetic resonance tomography, interosseous tophi can be detected earlier and in a more widespread manner than with the aid of native X-ray images, such that an increase in the use of this method is to be expected.
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PMID:[Radiologic findings in gout]. 944 16

Gout is a metabolic disorder in which there is either an increase in production or a decrease in excretion of uric acid leading to hyperuricemia. Long-lasting hyperuricemia causes the deposition of monosodium urate crystals in the joints and soft tissues triggering gouty arthritis and, if not properly treated, the formation of gouty tophi. Characteristic of gout are well-defined, punched-out erosion with overhanging edges, with preservation of the joint space, lack of periarticular osteopenia, asymmetrical involvement, soft tissue nodules, and intraosseous calcifications. On magnetic resonance imaging, tophi usually have low signal intensity on both TI- and T2-weighted images and a variable enhancement pattern.
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PMID:Advanced imaging of gout. 1459 58

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