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

In most patients with primary gout hyperuricaemia results from a renal defect in tubular uric acid secretion. An increased endogenous purine biosynthesis is observed in only 2% of all patients with gout. Secondary hyperuricaemai results either from an increased breakdown of endogenous nucleic acids as in polycythaemia or from a decreased renal excretion of uric acid due to drug treatment, renal insufficiency or metabolic disturbances. Hyperuricaemia may be defined either in statistical terms from epidemiological studies of normal and gouty populations or from physicochemical properties of urate. Monosodium urate and uric acid are soluble in water to the extent of 6.32 mmol/l and 0.39 mmol/l respectively. In human plasma saturation of monosodium urate occurs at a concentration of about 0.42 mmol/l. The solubility of uric acid and urate in urine is more complicated as it is affected by changes in pH and salt concentration. Uricosuric drugs decrease serum uric acid concentration by enhancing the renal excretion of uric acid. Effects and side effects of uricosuric therapy are discussed.
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PMID:Uricosuric therapy and urate solubility in blood and urine. 50 37

De novo purine biosynthesis has been investigated in circulating blood lymphocytes in vitro. N-formyl-glycinamide ribonucleotide (FGAR) has been mesured using 14C-formate incorporation in the presence of azaserine, a metabolic inhibitor blocking the metabolical pathway at the level of FGAR synthesis. Such a synthesis was measured in 20 healthy controls, 24 patients with primary gout (11 on allopurinol therapy) and 26 patients with chronic renal failure and secondary hyperuricemia (8 on allopurinol therapy). Among gouty patients without allopurinol therapy, FGAR synthesis was normal in 5 and increased in the others. FGAR synthesis was decreased in patients with renal failure whatever the therapy. However, FGAR synthesis remained increased in patients with a primary gout complicated with renal insufficiency. The test we propose for de novo purine biosynthesis measurement is simple and of value to analyse the patho-physiology of hyperuricemia and its therapy. The test allows an acurate discrimination between primary and secondary hyperuricemia in the presence of renal insufficiency.
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PMID:[De novo purine biosynthesis. In vitro measurement in hyperuricemia (author's transl)]. 90 38

Benzbromarone, a synthetic benzofurane, was administered in a series of 23 patients with hyperuricaemia: 5 with gout, 8 with secondary forms, 6 with renal insufficiency, 4 undergoing diuresis with etacrinic acid. The drug was also given to 10 subjects with normal values. A surprisingly rapid and constant hypouricamising effect was noted, together with marked hyperuricuria. These changes were more prompt in the controls and relatively late and protracted in the diseased subjects, expecially those with gout. The drug was also active in renal insufficiency. Its effects ceased on suspension. It cannot be seen as a simple hyperuricuric preparation, since it may have some effect on the metabolic pathways that degrade purines to uric acid. The drug is similar to benziodarone. The replacement of iodine by two bromine atoms in its formula, however, ensures its freedom from side-effects.
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PMID:[Benzbromarone in the treatment of hyperuricemias]. 109 64

In addition to uricosuric agents and purine synthesis inhibitors, Urate Oxydase may be used in the treatment of hyperuricaemia. This substance breaks down uric acid to allantoin which is soluble and easily excreted. Use of the medication in 14 cases of major gout with tophi and 9 cases of hyperuricaemia secondary to renal insufficiency showed the good tolerance of the substance and it's clinical and biological effectiveness.
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PMID:[Uricolytic therapy. Value of urate oxidase in the treatment of hyperuricemias]. 109 13

The authors confirm the great rarity of joint complications in patients with Kahler's disease. Among the records of 1953 cases the following complications were the only one found: 2 cases of proved articular amylosis, 2 cases of probable articular amylosis, 3 cases of possible articular amylosis, 20 cases of arthropathy that were impossible to classify, 27 cases of compression of the median nerve in the carpan canal, 6 cases of gouty arthritis, and 3 cases of septic arthritis. The data on symptoms obtained in the course of this enquiry are in conformity with the data in the literature. Articular amylosis often takes on the appearance of a polyarthritic syndrome of progressive installation and extension, involving in particular the hands and the wrists, but sometimes involving in a symmetrical bilateral manner the elbows, the shoulders, and the knees. The affected joints are swollen, stiff, and painful. Local signs of inflammation are, however, often absent. The deformations characteristic of rheumatoid arthritis do not develop. The joints do not show radiological signs for most of the time. In addition, it is not possible to detect the rheumatoid factor in the serum. The arthropathies can also assume an oligo-articular topography. Articular discharges are very frequent: they are usually of a mechanical nature. Whatever the clinical appearance, an exact diagnosis can be established only by means of anatomo-pathological examination of the synovial membrane or of certain para-articular amyloid nodules. Myelomas complicated by amyloid articular deposits are often light chain, with only little increase in the erythrocyte sedimentation rate, discrete hyperproteinaemia, moderate medullary plasmocytosis, and rare or limited radiological lesions. The carpal canal syndrome is either isolated or included within the framework of a polyarthropathy. Compression of the median nerve is due to amyloid infiltration into the synovial sheath of the tendons of the finger flexors, proof of which is not always easy. Gout is rare despite the frequency of hyperuricacidaemia caused by renal insufficiency. Septic arthritis is often caused by renal insufficiency. Septic arthritis is often caused by pneumococci to which those with a myeloma appear particularly suceptible.
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PMID:[Articular complications of Kahler's disease. Results of a survey of 1953 cases of plasmocytic myelomas]. 112 74

The effects of low-mineral content water (Adelholzener Primus-Quelle) in 62 patients were studied of which 14 were hypertonic. Changes of blood sodium, potassium, chloride and bicarbonate were not observed in either group. In the hypertonic patients, blood pressure decreased from a mean systolic value of 168 to 140 mmHg and mean distolic pressure from 105 to 88 mmHg. Observations to date suggest the following indications for a low-mineral content water diet: 1. hypertension, 2. renal insufficiency in stages of compensated and decompensated retention, especially in cases with high serum potassium levels, 3. in the initial therapy of diabetes, gout and obesity; patients with a high water demand should be treated with low-mineral content water until the optimal intake of electrolytes is established.
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PMID:[Effects of water with a low mineral content on serum electrolytes and blood pressure]. 122 36

The development of tophi in the absence of prior episodes of gouty arthritis is unusual. We present six such cases and review 26 previously published cases. These patients differ from those with typical gout in that they were older, more likely to be women, and usually had predominant or exclusive finger involvement. Most had renal insufficiency and many were receiving an anti-inflammatory or diuretic. Although several possibilities for the lack of gouty arthritis in the presence of tophi exist, usually no clear explanation is found.
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PMID:Tophi as the initial manifestation of gout. Report of six cases and review of the literature. 155 51

Polyarticular gout may be misdiagnosed in the elderly. This reflects the confusing clinical presentation of "diuretic gout" in the elderly, characterized by polyarticular onset, subacute symptoms, hand involvement, and early development of tophi. A misdiagnosis of rheumatoid arthritis can lead to poor treatment of gout, failure to recognize underlying renal insufficiency, and associated cardiac risks. Hyperuricemia may reflect systemic ATP depletion in acutely ill patients and thus represents a predictor for mortality. Medical treatment of polyarticular gout in elderly patients with compromised cardiac and renal function requires recognition of the clinical profile and consideration of the increased toxicity from standard therapies.
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PMID:Misdiagnosis of rheumatoid arthritis in an elderly woman with gout. 201 May 92

We reviewed the clinical features and uric acid metabolism in 37 female patients with gout. In 32 female patients (86%), gout was diagnosed after menopause. Among the five premenopausal patients, four had renal insufficiency and one had superactivity of phosphoribosylpyrophosphate synthetase. More than 50% of the female patients had osteoarthritis, hypertension, or renal insufficiency or were treated with diuretics. Comparison with 220 male patients with gout showed that female patients developed gout significantly later, more frequently had associated diseases, and more often were receiving diuretics, whereas significantly more male than female patients had alcoholism. The articular features of gout were similar in both groups. However, the prevalence of tophi was higher and its localization different in female than in male patients. Female patients with gout had a higher mean serum urate concentration and a lower mean urinary uric acid excretion than did male patients with gout. These differences were significant and independent of the effects of age, renal insufficiency, alcoholism, or previous diuretic intake. Renal underexcretion of uric acid appears to be more severe in female than in male patients with gout.
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PMID:Female gout. Clinical spectrum and uric acid metabolism. 201 55

The prevalence of gout in the United States has been rising steadily for the past two decades. Hyperuricemia is considered a necessary but not sufficient precondition for gout. Known risk factors for gout include male sex, hypertension, renal insufficiency, obesity/weight gain, diuretic use, lead exposure, and family history. The association of gout and hyperuricemia with coronary artery disease is controversial. Current evidence from the Framingham Study suggests that gout is in fact an independent risk factor for CHD. These data suggest that patients with gout should be screened for modifiable risk factors for CHD, and that early intervention in such patients may be worthwhile. Finally, the effect of AHU as risk factor for CHD remains unclear but is probably a weak one.
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PMID:Gout and hyperuricemia. 221 57


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