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

Radiographs of two patients with saturnine gout (lead gout) demonstrated radio-opaque material which resembled milk of calcium within several joints. A histochemical examination of knee aspirate of one of the patients revealed a combination of monosodium urate and calcium pyrophosphate dihydrate. Subsequently, the authors suspected that the findings of intra-articular milk of calcium were due to the coexistence of saturnine gout and calcium pyrophosphate dihydrate deposition disease rather than intra-articular calcified tophus.
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PMID:Intra-articular milk of calcium in saturnine gout. 683 19

Arthritis commonly accompanies clinical disturbances of metabolism, while diseases which are primarily articular may cause major general metabolic abnormalities. The relationship between diet, nutrition and joint diseases is complex and varies from simple mechanical factors (as in obesity) to complex metabolic processes. Current knowledge of these processes is extensive in some areas, such as in gout and hyperuricaemia, whereas in others, such as the arthropathy encountered after intestinal bypass surgery, it is very scant indeed. Joint disorders in hyperlipoproteinaemia and diabetes mellitus are varied and the pathogenesis of these articular problems is as yet ill understood. In view of the frequency with which these metabolic problems occur, these disorders offer no opportunities for the clinical study of the processes involved in joint inflammation and damage. In contrast, metabolic abnormalities such as hypergastrinaemia and elevated ionized calcium in rheumatoid arthritis are worthy of study, as they may offer clues to the underlying aetiology of the joint disease. This latter abnormality is suggestive of hyperparathyroidism, a condition which may present with polyarthritis and in which joint changes may be severe, although they are usually obscured by the more obvious bony problems in this disease. An illustrative historical vignette is included.
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PMID:Some metabolic aspects of arthritis. 703 19

Over the past few years periarthritis calcarea - also known as hydroxyapatite rheumatism - has attracted increasing interest. The periarticular calcification hitherto regarded as a secondary finding is today a well-defined disease entity occurring either in localized or generalized form, i.e. around one or more joints respectively. Although the origin of this calcification is now known, various hypothetical causes have been discussed in the literature. In the light of studies on familial clustering and the HL-A constellation, it is now evident that genetic factors have a definite role to play in the etiology of the disease. Even though no metabolic defect has been identified as yet, it is impossible to state with certainty that no metabolic cause is involved. As in gout, periarthritis calcarea is liable to cause attacks of acute pain that last for several days and then disappear. In consequence, the clinical picture is misleadingly similar to that of arthritis. The subsequent disappearance of the periarticular calcium deposits previously shown to be present can be considered a cardinal symptom of the disease. To detect this calcification it is necessary to use the electron microscope, since the crystals are too small to be seen with the light microscope. Periarthritis calcarea undoubtedly ranks as a crystallopathy. Since its origin is unknown, causal therapy such as exists for gout cannot be adopted. Treatment is restricted to purely symptomatic measures.
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PMID:[Periarthritis calcarea]. 705 Dec 77

Turkey poults were fed diets containing oosporein at concentrations of 0, 500, 1,000, and 1,500 micrograms/g from hatching until three weeks of age. Low feed consumption resulted in poor growth rates at every dietary level of oosporein; however, a dose-related increase in water consumption was observed. The most significant effect of dietary oosporein was severe visceral and articular gout, with death ensuing in 24 and 52% of the poults at the 1,000 and 1,500 micrograms/g levels, respectively. Gout and mortality were absent at 0 and 500 micrograms/g. In addition to tissue urate deposition, necropsies revealed dehydration, swollen pale kidneys, hemorrhagic proventriculitis with mucosal necrosis, gizzard enlargement and lining discoloration, an increase in gall bladder size, and focal hepatic necrosis. The relative weights of the kidney, liver, proventriculus, gizzard, and pancreas were increased in a dose-related fashion; spleen and bursa weights were unaffected. Among plasma constituents, uric acid, urea, and the activities of glutamic-oxalacetic transaminase and lactic dehydrogenase were elevated in response to dietary oosporein; albumin, potassium, phosphorus, and calcium were decreased. The toxin had no effect on plasma total protein, sodium, glucose, cholesterol, triglycerides, alkaline phosphatase, or creatine phosphokinase. These data substantiate the original classification of oosporein as a nephrotoxin and etiologic agent of gout in avian species.
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PMID:Oosporein-toxicosis in the turkey poult. 709 45

Chondrocalcinosis is an arthropathy caused by deposits of calcium pyrophosphate-dihydrate microcrystals (CPPD) in the joints and occasionally in the tendons and ligaments. In our region it is almost always seen in its sporadic form in elderly subjects. The patients can be without symptoms or present four different clinical entities: an acute arthritis which can resemble and even be mistaken for an attack of gout or a septic arthritis; an inflammatory polyarthritis suggesting a rheumatoid arthritis; most frequently it appears as a benign polyarthrosis; sometimes it runs a destructive course capable of seriously damaging one or several joints. In certain cases chondrocalcinosis is associated with another metabolic disease. Familial forms have been described in some countries. Factors which induce the formation of the deposits of CPPD in the articular cartilages, fibrocartilages, the synovium and occasionally in the tendons and ligaments remain obscure. In contrast to urate gout, chondrocalcinosis appears to be due to a disturbance of pyrophosphate metabolism localized almost exclusively in the articular region. Its association with polyarthrosis rather frequently leads to destructive arthropathies. No etiological treatment for chondrocalcinosis exists at the present time. Therapy is limited to the administration of nonsteroidal antiinflammatory drugs and physiotherapy.
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PMID:[Chondrocalcinosis]. 711 58

105 consecutive patients who presented to a rheumatologist because of joint disease and who also had evidence of deposition of calcium pyrophosphate dihydrate (CPD) were studied clinically and radiologically. There were 76 women (mean age 73) and 29 men (mean age 62). Of only 18 patients below the age of 60 at presentation 12 were men. The majority of the younger male group suffered from acute attacks of synovitis, and had no clinical or radiological evidence of joint damage. In contrast the older female group had widespread destructive changes. Associated joint disease included generalised osteoarthritis (45), rheumatoid arthritis (8), joint hypermobility (13), previous knee surgery (8), and gout 92). Sixteen patients had received long-term steroid therapy. Severe destructive joint changes were seen in 16 patients. The radiological features in those with rheumatoid arthritis by ARA criteria were atypical. The relationship between CPD deposition and arthritis is discussed in the light of these findings.
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PMID:Pyrophosphate arthropathy: a clinical and radiological study of 105 cases. 711 20

The articular chondrocalcinosis--conditioned by the formation of crystals of calcium pyrophosphate dihydrate in the joint cartilage--increasingly gains clinical interest. The symptomatology is multivariant: mono-, oligo- and polyarticular with simultaneous localisation in the discs. Characteristic, but not proving, is the calcification demonstrated in the X-ray picture. Apart from the familial forms increasingly are observed spontaneous, solitary cases in persons older than 50 years (in 3% of all postmortem examinations). The chondrocalcinosis gains differential-diagnostic importance as to primary osteoarthroses, attacks of gout, rheumatoid arthritis and other diseases of bones and joints. It appears symptomatically in hyperparathyroidism and hemochromatosis. The present paper gives as survey on the modern state of knowledge concerning clinic, heredity, diagnostics and pathogenesis.
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PMID:[Polymorphism of articular chondrocalcinosis]. 713 87

Of 264 patients with urolithiasis those with pure uric acid or urate stones were compared to those with other types of calculi for differences in epidemiologic factors and uric acid, calcium and phosphate metabolism. Patients with uric acid stones were predominantly older men. These patients had comparatively lower incomes and spent less money on food but consumed more alcohol. The urinary pH was lower than in the other groups. The absence of abnormally elevated serum uric acid levels and elevated 24-hour urinary uric acid excretion suggests this variety of uric acid lithiasis to be idiopathic in nature. This finding is supported by the results of standardized oral purine loading, which showed no post-loading differences in serum levels and revealed urinary concentrations in 12 patients with pure uric acid stones and 10 normal subjects. However, there is evidence to suggest that this condition may be a precursor of primary gout. Hereditary mechanisms are absent and the relapse rate is the same as in patients with other stones. Therefore, our results suggest the existence of an idiopathic variety of uric acid lithiasis that, at least in central Europe, occurs more frequently than previously assumed. The condition is not inherited, alcohol consumption is a major etiologic factor and there is no evidence of a causative role of abnormalities in purine metabolism.
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PMID:Idiopathic uric acid lithiasis: epidemiologic and metabolic aspects. 715 74

Forty-nine patients with gout, many with hypertension and/or renal calculi, were given hydrochlorothiazide, furosemide, or ticrynafen. Diuresis and increased clearances of sodium (Na), potassium (K), chloride (Cl), and calcium (Ca) occurred after a single dose of hydrochlorothiazide, 100 mg, or furosemide, 40 mg, orally. There was very slight change in urate and phosphorus clearances. With prolonged use of hydrochloride or furosemide, diuresis and increased electrolyte excretion disappeared. Urate and Ca excretion fell with hydrochlorothiazide. With long-term use of furosemide, urate excretion was suppressed, but Ca excretion was sustained. Ticrynafen produced diuresis and increased clearances of Na, K, and Cl. Calcium excretion was increased after a single dose and minimally decreased after long-term use. Most striking was the severe and rather sustained uricosuria. Though ticrynafen is an effective uricosuric, natriuretic, and antihypertensive agent, its hepatotoxicity and nephrotoxicity mitigate against its clinical use.
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PMID:Effects of diuretics on urate and calcium excretion. 723 11

Introduction of new uricosuric diuretics will be accompanied by the unknown risk factors associated with the use of any new drug, as demonstrated by reports of hepatic toxicity associated with ticrynafen. In addition to unexpected reactions, there are potential risks related to induction of uricosuria, which are serious and have been reported to occur. More importantly, the risk of developing clinical gout or coronary heart disease due to mild asymptomatic hyperuricaemia appears minimal, so indications for the use of uricosuric diuretics are limited. If a uricosuric diuretic is thought necessary (and is available), it would seem prudent to measure the daily excretion rate of uric acid to identify those patients with hyperuricaemia related to overproduction of uric acid. A uricosuric diuretic should be avoided in those patients, as well as in patients with uric acid stones, and possibly in those with calcium stones. A uricosuric diuretic might be useful for patients with hypertension who also have hyperuricaemia due to a low excretion of uric acid.
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PMID:The risks of asymptomatic hyperuricaemia and the use of uricosuric diuretics. 726 49


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