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Query: UMLS:C0018099 (gout)
 5,192 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Needle-shaped crystals of 75 to 250 A diameter have been identified by transmission electron microscopy in clumps within synovial fluid mononuclear cell vacuoles in a variety of joint diseases. These crystals, similar to those previously associated with calcific periarthritis, were seen in acute undiagnosed arthritis and in exacerbations of osteoarthritis where they may be inducing a synovitis similar to that seen with urate and pyrophosphate crystals in gout and pseudogout. By light microscopy purple staining cytoplasmic inclusions or extracellular globules can suggest the presence of clumps of these crystals. Apatite clumps can also occasionally appear as small birefringent chunks or rods and thus might mimic urate or calcium pyrophosphate. Ultrastructural appearance, electron probe analysis, and X-ray diffraction pattern were those of apatite. Experimental injection of hydroxyapatite crystals into dog knee joints produces inflammation supporting the potential role for these crystals in joint disease.
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PMID:Arthritis associated with apatite crystals. 19 97

Synovial fluids from 106 patients with various types of arthritis were examined for the presence of conversion products of C3 by means of crossed antigen-antibody electrophoresis and for products of factor B by immunoelectrophoresis. C3 conversion was found in all 15 fluids from patients with seropositive rheumatoid arthritis, in 11 of 15 with seronegative rheumatoid arthritis, in the majority with probable and possible rheumatoid arthritis, juvenile rheumatoid arthritis, SLE, pseudogout, gout, Reiter's syndrome, and frequently in other arthritides studied, but in only one of 15 with degenerative arthritis. In 53 synovial fluids a single C3 conversion peak was seen in addition to the native protein and in 18 others two conversion peaks were present. In many synovial fluids showing conversion whole-complement titers and C3 protein concentrations were normal. In both rheumatoid arthritis and crystal synovitis the per cent of C3 conversion, as estimated by planimetry, correlated with synovial fluid leukocyte counts, Factor B conversion was found in 31 fluids and usually occurred in fluids also showing C3 conversion. The findings indicate that in vivo activation of components of the classical and alternative considered mediated by immune complexes. Activation is also commonly present in a wide variety of other inflammatory arthritides and ofter would not be recognized by measuring only concentrations of hemolytic whole complement or C3 by immunodiffusion. The positive association between C3 conversion and synovial fluid polymorphonuclear leukocytes suggests that chemotactic factors generated from complement may be responsible for the attraction of leukocytes into the synovial space in these diseases.
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PMID:Activation of complement components C3 and factor B in synovial fluids. 83 Jul 76

Several points may be stressed. (1)When in doubt, perform joint aspiration and look for crystals of micro-organisms. A joint tap is nearly always indicated. (2)Do not rely on a coincidental elevated serum uric acid level. Question the patient regarding drug therapy and other causes of secondary hyperuricemia. (3)Examine all of the patient, looking for tophi (gout), skin lesions (gonococcal infection, psoriasis), erythema nodosum (allergic reactions, fungal infections), and other clues. (4)Monoarticular rheumatoid arthritis is a rare cause of a single hot joint, but it is much more common that the real rarities (e.g., pigmented willondular synovitis). (5)Anky-losing spondylitis and Reiter's syndrome are common, yet frequently overlooked. (6)Radiologic examination is usually not helpful. (7)Having ruled out infection, crystal synovitis, and hemorrhage, it is sufficient to introduce symptomatic treatment and await the natural development of the joint disease. Follow-up in four to six weeks and simple blood studies often reveal the definitive diagnosis. Most of the time, natural healing processes are effective , and reward the patience of the conservative physician. Blind management must always be avoided.
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PMID:The single hot joint. 97 58

A number of cells, chemotactic factors, and inflammatory mediators are implicated in the complex mechanisms underlying crystal-mediated inflammation. Interleukin-8, released from mononuclear cells that have been exposed to urate and other crystals, is a potent chemotaxin and activator of neutrophils. Experimental and clinical observations suggest that joint movements, local biomechanical factors, and previous joint damage may play a role in influencing the intensity of microcrystalline synovitis and the distribution of articular and periarticular crystal deposits in both calcium pyrophosphate dihydrate crystal deposition disease and gout. There are rare reports of extra-articular calcium pyrophosphate dihydrate crystal deposition in tendons, bursae, dura mater, and ligamentum flavum (with radiculomyelopathy) and of massive "tumoral," tophuslike, periarticular calcium pyrophosphate dihydrate crystal deposits. Synovial fluid levels of ATP, the main substrate for nucleoside triphosphate pyrophosphohydrolase ectoenzyme, which cleaves ATP-releasing inorganic pyrophosphate, are higher in patients with calcium pyrophosphate dihydrate crystal deposition disease than in those with other arthritides, and the levels correlate with inorganic pyrophosphate concentrations. Further reports of acute calcific periarthritis of the first metatarsophalangeal joint (hydroxyapatite pseudopodagra) in young women have been described. The mitogenic response of fibroblasts to stimulation with basic calcium phosphate crystals is accompanied by induction and secretion of collagenase and neutral proteases, implicating a role for the crystals in the pathogenesis of both synovial proliferation and joint damage in chronic basic calcium phosphate crystal-associated arthropathy. Subcutaneous cholesterol crystal deposition with tophus formation is extremely rare and has been described in a patient with scleroderma and calcinosis cutis.
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PMID:Calcium pyrophosphate crystal deposition disease and other crystal deposition diseases. 150 84

Gout commonly occurs as an acute arthritis. In a 64-year-old man, gout was associated with a proliferative hemosiderin-laden synovitis. The association of recurrent atraumatic hemarthrosis seems not to have been reported in the literature on gout.
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PMID:Recurrent hemarthrosis associated with gout. 155 50

Recent evidence suggests an important role for kinins in the generation of pain, swelling and the cellular damage associated with inflammatory joint disease. Kinins are considered to be pro-inflammatory peptides for a variety of reasons. They stimulate c fibres in the synovium to cause pain and increase extravasation of fluid to produce swelling. Kinins possess the capacity to release neurotransmitters (substance P, acetylcholine) and a second wave of mediators (interleukin-1, tumour necrosis factor, interleukin-8, prostaglandins, leukotrienes). The steady levels and turnover of kinins is regulated by formation (enzymic action of kininogenases on endogenous substrates called kininogens) and by metabolism (kininases, peptidases that hydrolyse kinins). These components of the kinin system can enter the synovial joint space either by transudation from the plasma or from degranulating neutrophils chemotactically attracted into the synovium from which they migrate into the synovial fluid. If kinins are involved, one would expect neutrophil derived mediators of the system to dominate in rheumatoid arthritis and psoriatic arthritis and plasma derived products to be more important in osteoarthritis and gout. But, the question whether any of the functions attributed to each component of the system can be considered to be a primary factor in the cellular pathology of inflamed joints remains to be established. Future investigations, including therapeutic trials with kinin antagonists and kallikrein inhibitors, will need to address the differential role of the kallikreins and kinins in the different types of synovitis, on symptoms of inflammation and on any remedial effects on the progression of tissue damage within the joint.
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PMID:Kinins--key mediators in inflammatory arthritis? 164 49

Hydrocortisone phonophoresis (HPP) on the affected joints or balneotherapy with iodine bromine baths as well as the complex of these two modalities were used to treat 197 patients with osteoarthrosis. Thirty-one of the patients had secondary arthrosis due to recurrent gout attacks. Monotherapy with HPP proved beneficial in affection of 1-2 joints whereas the baths appeared preferable in polyosteoarthrosis, its association with spinal osteoarthrosis, arterial hypertension. Combined application of HPP and the baths produced more pronounced and stable effect with the best relief recorded in polyosteoarthrosis, its progression, secondary synovitis.
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PMID:[The therapeutic use of iodide-bromide-sodium chloride baths combined with hydrocortisone phonophoresis in patients with osteoarthrosis and gout]. 207 38

Less than 30 years ago, McCarty and others first described a syndrome which presented with gout-like attacks of arthritis but was due to CPPD crystals instead of urate crystals. They termed the condition "pseudogout." It was noted that this was often associated with chondrocalcinosis and it was commonly held that cartilage calcification had to be present if the diagnosis was to be suggested on the basis of the radiographic findings. Subsequently, a clinical and radiographic pattern has emerged in which the diagnosis of CPPD deposition disease can be suggested in the absence of chondrocalcinosis. This condition is termed pyrophosphate arthropathy and is differentiated from degenerative disease by the pattern and distribution of the joint disease. It is important to recognize CPPD deposition disease because of its association with other diseases, such as hemochromatosis and hyperparathyroidism. Although painful periarticular tendinous calcification (peritendinitis calcarea) resulting from the deposition of calcium HA crystals has long been recognized, it has only recently been discovered that intra-articular HA can be associated with an acute inflammatory synovitis. Additionally, patients are now being identified who have CPPD deposition at one anatomic location and HA deposition at another. Differentiation of these various types of crystal-induced arthropathies should lead to more effective therapy in the future.
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PMID:Chondrocalcinosis and other calcifications. 284 68

Calcium pyrophosphate dihydrate crystal deposition disease is a clinical condition characterised by Gout-like synovitis (pseudogout), calcification on and around the joints and an arthropathy that is radiologically similar to osteoarthritis (chronic pyrophosphate arthropathy). Though all these radiological clinical aspects may coexist in the same patient this is often not the case. An examination of the X-ray data on the 68 cases studied which were diagnosed on the basis of the criteria proposed by McCarty, shows that the disease is relatively common especially in the over-fifties. When chronic pyrophosphate arthropathy is the only clinical manifestation of the disease differential diagnosis from the osteoarthrosis so common in the elderly is difficult and depends on the greater severity and progression of the joint damage that may often affect joints not subjected to weight such as the shoulder, unlike what happens in osteoarthritis.
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PMID:[Clinico-radiologic aspects of calcium pyrophosphate dihydrate deposition disease]. 302 32

Nonarticular causes of elbow pain include muscle strains, ligamentous injuries, epicondylitis, olecranon bursitis, and compressive neuropathies. Overuse and trauma commonly cause these conditions. The history and physical examination differentiate them from an intra-articular process such as synovitis. Laboratory analysis of fluid aspirated from a swollen olecranon bursa is necessary to differentiate infection or gout. X-rays are useful in avulsion fracture, osteochondritis dissecans, and epiphyseal separation. Electromyography with nerve conduction velocities can localize the site of nerve entrapment. Treatment, in general, consists of prevention from further overuse, protection by rest and splinting to allow healing, pharmacologic intervention to reduce inflammation, relieve pain and combat infection, and physical therapy to restore motion and function. Surgery may be necessary to repair torn muscle, to release the wrist extensors in refractory lateral epicondylitis, and to decompress an entrapped nerve.
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PMID:Elbow pain. 306 91


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