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

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

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

The number of crystal or birefringent particles associated with arthritis is increasing, and a uniform taxonomy is needed. The term gout has been proposed as a generic term for these diseases based on historical, clinical, and crystallographic reasons. Calcium pyrophosphate dihydrate gout follows monosodium urate gout in frequency, and its spectrum of clinical manifestations continues to grow. Familial calcium pyrophosphate dihydrate gout was described for the first time in kindreds studied in England and Tunisia; new Jewish and Spanish kindreds were also reported. Type I collagen was shown to nucleate nativelike calcium pyrophosphate dihydrate crystals, and pyrophosphate elaboration was explored in cartilage explants in an attempt to reproduce the in vivo metabolic or endocrine disorders associated with calcium pyrophosphate dihydrate gout. The effect of pyrophosphatase and different cofactors such as magnesium in dissolving calcium pyrophosphate dihydrate crystals was investigated. High-resolution electron microscopy was used to study the interrelation between apatite and other basic calcium phosphate crystals in apatite gout. Raman microscopy was applied for the first time to identify crystals in biologic specimens. A simple and specific technique for basic calcium phosphate crystal identification is necessary to understand the relationship between different calcium phosphate crystals and osteoarthritis. Several reports about children and young patients with primary oxalate gout described the effect of oxalate on eyes, periodontal tissues, and bone. Multicenter studies showed poor results of renal transplantation, but favored combined liver and renal transplantation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Calcium pyrophosphate dihydrate gout and other crystal deposition diseases. 165 74

The authors have established that to higher calciuria in patients with calcium nephrolithiasis correspond higher vales of uric acid serum concentrations and urine excretion than in the controls. In the oral calcium tolerance test a significant correlation was found between the changes in the uric acid urine excretion and those in the diuresis. The following conclusions are put forward. I. In the patients with recurrent calcium nephrolithiasis and hypercalcinosis one should look for active impairment of uric acid metabolism which should be kept in mind when an antirecurrence treatment is planned. 2. The established parallel increase of uricosuria and calciuria in the oral calcium tolerance test means that to patients with recurrent calcium nephrolithiasis and gout a rich calcium diet should not be prescribed since it increases the risk of formation of calcium oxalate stones.
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PMID:[The effect of oral calcium loading on the serum concentrations and urinary excretion of uric acid in patients with recurrent calcium nephrolithiasis and hypercalciuria]. 228 2

The recognition of tissue deposits of crystalline material in a variety of organs, including the kidney, predated the association of crystals and arthritic disease. Because of this, the pathophysiology of crystal formation and its resultant inflammation is based in part on studies of renal stones. A number of disease states involving renal and articular crystallization exist. The most common of these, uric acid precipitation, or gout, and calcium phosphate precipitation were not reviewed in this discussion. This review described a variety of less common disease states involving articular and renal crystal deposition. The renal diseases discussed included both parenchymal or ectopic crystal deposition, as seen in nephrocalcinosis or cystinosis, and ductal crystallization as seen in renal calculus disease. The crystals involved included not only calcium oxalate, but also aluminum, amino acids and proteins (cystine, hemoglobin, cryoglobulins, and immunoglobulins), purine metabolites (xanthine, hypoxanthine), and even lipids and their degradative enzymes (cholesterol, phospholipids, phospholipase, and fatty acids). The simultaneous occurrence of crystals in both kidneys and joints was found in some cases to result from the systemic deposition of an excess of a particular biological compound. However, of more interest, some renal deposits were shown to more selectively reflect the normal or abnormal function of the kidney in its secretory and excretory roles. This is particularly evident in the variety of arthritic states described in end-stage renal disease.
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PMID:Calcium oxalate and other crystals associated with kidney diseases and arthritis. 264 79

We report a case of calcium oxalate arthropathy in a woman undergoing intermittent peritoneal dialysis who was not receiving pharmacologic doses of ascorbic acid. She developed acute arthritis, with calcium oxalate crystals in Heberden's and Bouchard's nodes, a phenomenon previously described in gout. Intermittent peritoneal dialysis may be less efficient than hemodialysis in clearing oxalate, and physicians should now consider calcium oxalate-associated arthritis in patients undergoing peritoneal dialysis who are not receiving large doses of ascorbic acid.
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PMID:Arthritis associated with calcium oxalate crystals in an anephric patient treated with peritoneal dialysis. 340 40

Recently, calcium oxalate crystals have been identified in the synovial fluid of patients with arthritis and end-stage renal failure. We describe 4 patients who, during the course of long-term hemodialysis, developed calcium oxalate crystal deposits in the synovium and skin. Clinical manifestations included podagra, tenosynovitis, olecranon bursitis, and acute and chronic synovitis of the large joints that were associated with chondrocalcinosis or subchondral bone erosions. Diffuse involvement of the hand, with chondrocalcinosis of the finger joints, miliary calcified deposits in the skin, and artery calcifications, was observed in 3 patients. The fourth patient had erosive arthropathy. Oxalosis secondary to end-stage renal failure in patients treated with long-term hemodialysis can present with articular manifestations that resemble those of gout, pseudogout, and apatite deposition disease. Other characteristic features of the synovitis associated with oxalosis secondary to end-stage renal disease were: predominant involvement of the hand, mild inflammatory changes in the synovial fluid and synovium, and poor response to administration of nonsteroidal antiinflammatory agents.
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PMID:Arthropathy and cutaneous calcinosis in hemodialysis oxalosis. 377 44

Morphologic characteristics of granulomatous inflammation in the heart and pericardium are discussed. In rheumatic fever, two types of myocardial lesion are present--a nonspecific myocarditis and a specific lesion characterized by granulomas known as Aschoff's nodules. The latter undergo a cycle of development and resolution; in their mature stage, they contain Aschoff's cells which are uni- or multinucleated histiocytes with a serrated nuclear chromatin bar. Ultrastructural studies do not suggest a relationship between these cells and cardiac or smooth muscle cells. In metabolic disorders, granulomas occur in Farber's disease (lipogranulomatosis), gout (in which tophi are associated with calcific deposits and with a foreign body cellular reaction), the various syndromes of oxalosis (in which oxalate deposits also lead to a foreign body reaction), and in chronic granulomatous disease of childhood. Foreign body giant-cells can also be found in association with calcification of necrotic myocytes and in the syndromes of "cholesterol pericarditis." Well-developed granulomas occur in sarcoidosis, giant cell myocarditis, as a reaction to foreign bodies and devices implanted within the cardiovascular system, and in certain diseased caused by infective agents (tuberculosis, fungal and parasitic disorders). Infiltration of the heart by nongranulomatous masses of histiocytes can occur in Whipple's disease, Niemann-Pick disease, the hyperlipoproteinemias, Gaucher's disease, and in proliferative disorders of the mononuclear phagocyte system (juvenile xanthogranuloma, Chester-Erdheim syndrome, and malignant histiocytosis).
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PMID:Granulomatous inflammation of the heart. 391 77

The responses of cultured rabbit synovial fibroblasts to amorphous and microcrystalline calcium oxalate were compared with responses to MSUM. Like urate crystals, crystalline calcium oxalate (but not amorphous oxalate) caused marked stimulation of secretion of latent collagenase and PGE2 after 3 days of culture without significant change in cell protein or gross cellular morphology. Collagenase rose from undetectable levels in control cultures to 32.4 +/- 6.0 and 27.4 +/- 7.9 U/mg of cell protein for crystalline calcium oxalate and MSUM, respectively. PGE2 rose from a control level of 0.24 +/- 0.14 to 19.47 +/- 5.15 and 23 +/- 4.84 micrograms/mg of cell protein for crystalline calcium oxalate and sodium urate compared to 1.22 +/- 0.48 microgram for amorphous calcium oxalate. Although the crystalline species studied caused LDH in the media to increase threefold, this was minimal. Cell stimulation by amorphous oxalate and the crystals did not correlate with membranolytic potential as measured with an erythrocyte lysis assay. Stimulation of resident synovial cells by crystalline calcium oxalate and sodium urate may contribute to the chronic inflammation and destruction of joint tissues that occurs in oxalosis and gout.
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PMID:Stimulation of synovial fibroblasts by calcium oxalate and monosodium urate monohydrate. A mechanism of connective tissue degradation in oxalosis and gout. 629 14

Immune triggered granulocyte (PMN)-endothelial interactions have been implicated in the pathogenesis of vascular diseases. While hyperuricemia and gout are associated with an increased risk of atherogenesis, we studied the modulation by monosodium-urate (MSU) crystals of PMN-endothelial interactions in vitro. The relationship between calcium oxalate (COX) crystals - implicated in the vasculitis of primary oxalosis - and immunologically mediated endothelial injury was also explored. Both MSU- and COX-crystal treated sera stimulate PMN to adhere to and induce significant 51Cr-release from endothelial cells in vitro. Platelets significantly increase crystal-triggered PMN endothelial cell adherence and 51Cr-release. This platelet augmenting effect depends on the release of platelet constituents (e.g. serotonin). Microcrystalline material present in vessel walls, thus may cause C-activation and may trigger PMN and platelets to damage endothelium in vitro and in vivo. These findings may have relevance to the understanding of the accelerated atherogenesis of hyperuricemia and the fulminant vasculitis of oxalosis or ethylene glycol poisoning.
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PMID:Mechanisms of vascular damage in gout and oxalosis: crystal induced, granulocyte mediated, endothelial injury. 663 34


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