Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018099 (gout)
 5,192 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Recent studies have shown elevated inorganic pyrophosphate (PPi) levels in most knee joint fluid supernates from patients with pseudogout (PG) or osteoarthritis (OA) and more modestly elevated levels in some supernates from patients with gout or rheumatoid arthritis (RA) relative to PPi levels found in the venous blood plasma of normal or arthritic subjects. We measured the intraarticular PPi pool and its rate of turnover to better understand the significance of the joint fluid-plasma PPi gradient. Preliminary studies in rabbits showed that (32-P)PPi passed from joint space to blood and vice versa without detectable hydrolysis. Incubation of natural or synthetic calcium pyrophosphate dihydrate (CPPD) microcrystals with synovial fluid in vitro in the presence of (32P)PPi tracer showed no change in PPi specific activity in the supernate over a 19-h period so that exchange of PPi in solution with that in CPPD microcrystals could be ignored. Clearance rates of (32P)PPi and of (33P)Pi, as determined by serially sampling the catheterized knee joints of volunteers with various types of arthritis over a 3-h period, were nearly identical. The (32P)PPi/(32P)Pi was determined in each sample. A mixture of a large excess of cold PPi did not influence the clearance rate of either nuclide. The quantity of PPi turned over per hous was calculated from the pool size as determined by isotope dilution and the turnover rate. The residual joint fluid nuclide was shown to be (32P)PPi. The PPi pool was generally smaller and the rate of turnover was greater in clinically inflamed joints. The mean plus or minus SEM pool size (mu-moles) and turnover rate (percent/hour) in PG knees was 0.23 plus or minus 0.07 and 117 plus or minus 11.9, hydrolysis rate (%/h) to Pi was 27.7 plus or minus 13.2; in OA knees: 0.45 plus or minus 0.26 and 72 plus or minus 9.2, hydrolysis 6.9 plus or minus 0.9; in gouty knees: 0.8 plus or minus 0.41 and 50 plus or minus 11.6, hydrolysis 9.8 plus or minus 2.8; and in RA knees: 0.14 plus or minus 0.14 and 114 plus or minus 35.8, hydrolysis 236 plus or minus 116. PPi turnover (mumoles/hour) correlated with the degree of OA change present in the joint as graded by radiologic criteria irrespective of the clinical diagnosis. Mean PPi turnover in joints with advanced OA was greater than in those with mild or moderate changes (P smaller than 0.001), but the mild and moderate groups showed no significant difference. We conclude that synovial PPi turnover and elevated PPi fluid concentrations are not specific for PG patients, and that these factors alone cannot be the only determinants of CPPD crystal deposition.
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PMID:Inorganic pyrophosphate pool size and turnover rate in arthritic joints. 16 95

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

Articular chondrocalcinosis results from the deposits of calcium pyrophosphate microcrystals in the articular hyalin and fibrocartilages, the synovium and at times the tendons. In our area it is seen most frequently as isolated cases in the elderly and may be asymptomatic. When the affected joints present clinical manifestations, they vary from acute to subacute or chronic recurrent arthritis. A marked articular destruction can be observed in some cases. There is a classical radiological picture: linear opacities are most frequently seen localized in the mid-zone layer of the hyalin cartilage running parallel to but at a certain distance from the bone cortex. A part of our research has shown that in contrast to urate gout, articular chondrocalcinosis results from a metabolic disturbance of the calcium pyrophosphate localized almost exclusively in the same articular structures. Precise information is lacking at the present time to explain why calcium pyrophosphate mycrocrystals accumulate in the cartilage, the synovium and at times at the tendons; nor do we understand the precise role played by the pyrophosphate in bone and cartilage destruction.
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PMID:[Arthropathies due to calcium pyrophosphates]. 23 70

Intrasynovial deposits of monourate crystals in the presence of serum hyperuricaemia, and calcium pyrophosphate dihydrate (CPPD) crystals, are responsible for gout and pseudogout respectively. Identification of these by synovial fluid analysis is described. The clinical features, minimum investigations, history-taking, management and drug regimes of gout and pseudogout are discussed. Periodic review of the patient is stressed. Other intrasynovial crystals are briefly outlined.
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PMID:Crystal induced arthritis: gout and pseudogout. 70 17

Chronic lead nephtropathy, secondary gout (lead-gout) and porphyrinuria may develop after long lasting professional exposure to lead. A printer with giant tophi on his hands and feet excreted a significantly higher amount of lead after infusion of calcium EDTA in comparison with a normal control person. This result indicates an increased mobilization of lead from skeletal deposits. Furthermore, the laboratory findings showed renal insufficency and porphyrinuria up to 1316 mug/l (elevation of total porphyrins with slight or no elevation of delta-amino-levulic acid and porphobilinogene). The clinical triad nephropathy, secondary gout and porphyrinuria seems to be a variant of chronic lead poisoning.
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PMID:[Chronic lead poisoning: Lead gout with giant tophi on the skin, nephrophathy and porphyrinopathy]. 81 45

The diagnosis of gout and pseudogout has traditionally been established by the identification, in synovial fluid, of monosodium urate and calcium pyrophosphate dihydrate crystals with compensated polarizing light microscopy. In this paper the utility of electron microscopy in establishing these diagnosis in two cases, when the conventional means of synovial fluid analysis had failed to do so, is discussed. The application of ultrastructural analysis of synovial fluid increases diagnostic capability in the crystal deposition diseases, and it is recommended for those patients in whom the more usual studies have not established a diagnosis.
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PMID:Crystal deposition disease. Diagnosis by electron microscopy. 87 90

After World War II the incidence of urolithiasis increased consistently among the general population in this country. Nearly 25% of all examined renal calculi contain uric acid, sodium acid urate or ammonium acid urate as constituents. There are two peaks in lifespan of occurring urate stones: in the adolescence and in the age between 40 and 60 years. The following conditions are due to the formation of uric acid-containing stones: 1. Gout and primary hyperuricemia; 2. secondary hyperuricemia; 3. idiopathic cases with normal renal excretion of uric acid and normouricemia, but with a higher degree of acidity of the urine than normal considering the total renal excretion of acid products; 4. iatrogenic hyperuricemia during insufficient uricosuric therapy. Up to more than 30% of all the patients with recurrent formation of oxalate stones show a clear association with hyperuricemia, hyperuricosuria and increased renal excretion of calcium. In the presence of sodium urate a considerable promotion of precipitation of crystals consisting of calcium oxalate from a meta-stable solution may occur (so-called epitaxy). Frequently the existence of uric acid stones is without any symptoms. Modern views with regard to prophylactic procedures, diet, general and specific medical management including surgical intervention are presented.
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PMID:[Urate nephrolithiasis. Cause of consequence?]. 95 52

AP isoenzymes were estimated in 292 patients with locomotor diseases and in 124 healthy controls. The diagnostic usefulness of AP determination is increased by estimation of isoenzymes. Investigations were made to study the biological profile of organ specific AP activities: 1. Rheumatoid arthritis and Reiter's syndrome - the total AP and L-AP activities were increased. 2. Ankylosing spondylitis treated by physiotherapy - the total AP, B-AP and I-AP activities were increased. After drug therapy an increase occurred also in L-AP activity while I-AP activity showed no significant change. 3. Progressive OA of hip and knee showed increased levels of total AP and B-AP activities. 4. Degenerative diseases of the spine, chiefly cases of discopathy, showed significantly reduced levels of AP and B-AP activities. 5. In osteoporosis there was an increase in total AP, L-AP, B-AP and I-AP activities. 6. In the active generalised form of Paget's disease, increased levels were found of total AP, B-AP, I-AP and L-AP activities. 7. In neoplastic diseases the isoenzymes can help to reveal metastatic dissemination and thus aid preoperative evaluation. 8. In gout and hyperuricemic syndromes there was a relative increase of B-AP activity and non-significant fall of L-AP activity. Increased levels of L-AP occured in patients with gallbladder disease, after immunosuppressive therapy or after infectious hepatitis. A fall of L-AP levels was found after Corticotrophin and after intraarticular administration of Kenalog. Increased B-AP activities occurred after total hip replacement, in acute or chronic pyelonephritis and in active osteonecrosis and osteoporosis. Anabolic therapy caused a significant fale of B-AP activity to fall significantly. Reduced B-AP levels were also found after antibiotic therapy. Increased I-AP activity was found in cases of osteoporosis, and in secondary amyloidosis; reduced I-AP activity was seen in mucous colitis. The activity of I-AP is assumed to increase as a result of the changed intestinal calcium and phosphorus regulation occurring in association with the enhanced bone tissue metabolism. From this point of view an order of significance is given for the activity of bone pathology in the separate diagnostic groups of locomotor diseases.
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PMID:The clinical significance of serum alkaline phosphatase isoenzymes in locomotor diseases. 105 9

From November 1970 to August 1974 small intestinal bypass was performed in 475 patients for morbid obesity with an operative mortality of 1.6%. Immediate postoperative complications were superficial wound infection (17 patients), pulmonary complications (seven patients), cardiac complications (five patients), wound dehiscence (nine patients), intestinal tract fistula (four patients), and miscellaneous complications (14 patients). Delayed complications included hypokalemia (28%), hypocalcemia (9%), anemia (11%), calcium oxalate urinary calculi (6%), gout (2%), and hepatic failure (1.4%). Fourteen patients died of late complications. Ventral incisional hernia occurred in 3% of the patients; failure to lose sufficient weight in 21%, all but one occurring in patients with end-to-side shunts. Thirteen end-to-side shunts have been converted to end-to-end shunts because of insufficient weight loss. A team concept is important in the handling of the morbidly obese. Small bowel bypass is effective in producing sustained weight reduction in these patients. Careful and continued study of these patients for the rest of their lives is of paramount importance.
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PMID:Metabolic intestinal surgery. Its complications and management. 113 Oct 9

In this report, we describe the development of renal function impairment in a 33-year-old patient with mesangial IgA nephropathy and a history of recent gout. Increased body lead burden was identified with a positive EDTA mobilization test. The patient was treated with 1 g of edetate disodium calcium weekly for 2 months until normalization of urinary lead excretion. Improvement of renal function and proteinuria were noted. It was even more interesting to find that both immunofluorescence and electron microscopy studies of the second biopsy specimen revealed the loss of previous mesangial immune deposits. Our case demonstrated that lead may be a nonspecifically damaging factor related to the deterioration of renal function in patients with preexisting renal disease. Moreover, the disappearance of mesangial immune deposits after chelation therapy has not been previously documented. The pathogenetic basis of this observation is unknown, and its causal relationship with lead requires further elucidation.
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PMID:Disappearance of immune deposits with EDTA chelation therapy in a case of IgA nephropathy. 129 46


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