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Query: UMLS:C0018099 (gout)
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Urinary excretion of lead (Pb) was measured in the basal state and following the infusion of EDTA (1g of calcium disodium edetate) in healthy German controls and in patients with chronic renal failure with and without gout. When evaluated with Zeeman-compensated atomic absorption spectroscopy using the L'vov platform and urine pretreated with nitric acid and Triton X-100, the control basal Pb excretion (median 28, range 11-19 nmol Pb/24h) and the postinfusion Pb increment (306, range 131-1,587 nmol/4 days/1.73 m2) were considerably lower than most values reported previously in the literature. Elevated Pb body burden was found in 7 of 8 patients who developed gout in the course of renal failure, but only in 2 of 8 patients who had gout prior to development of renal failure; this confirms that appearance of gout in patients with renal failure points to prior Pb exposure. In 7 of 19 nongouty patients with impaired renal function secondary to known renal diseases, urinary Pb excretion was above the 95th percentile of normal. All these patients had occupational Pb exposure. The high prevalence of elevated Pb body burden in patients with renal failure of known cause may not be coincidental and raises the possibility that Pb adversely affects the course of renal disease.
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PMID:Urinary lead excretion in uremic patients. 308 77

Indices of past lead absorption were measured and compared in patients with chronic renal failure from many causes, including some with chronic lead nephropathy. X-ray fluorescence (XRF) yielded finger bone lead concentrations by a new in vivo method. These correlated significantly with excess urinary lead following calcium di-sodium EDTA (ethylenediamine tetra-acetate) and erythrocyte lead concentration. Discriminant function analysis demonstrated that the patients in the study could be separated into two groups without any reference to the EDTA lead excretion test using the following variables, all of which contributed significantly to the discrimination. In order of importance, these were: a childhood history of acute lead poisoning, a history of gout, a family history of gout and detectable XRF finger bone lead. Although the XRF finger bone lead measurement is convenient and non-invasive, its lack of sensitivity (48%) limits its usefulness as a screening test for chronic lead nephropathy.
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PMID:Chronic lead nephropathy in Queensland: alternative methods of diagnosis. 308 47

The 6 day calcium EDTA lead excretion test was performed on German and Australian subjects with normal and impaired renal function, some of whom had gout, in order to determine if the pattern of results differed between the two countries. The German subjects lived around Heidelberg in an industrialized area where chronic lead nephropathy had not hitherto been thought to exist, while the Australian subjects were all from the State of Queensland where chronic lead nephropathy from the ingestion of lead paint during childhood continues to contribute to morbidity and mortality. Apart from the subjects with normal renal function, the German subjects consistently excreted less lead than the Queensland subjects and a strikingly consistent pattern was found: in both countries, subjects with a history of lead exposure, whether gouty or not, had greater EDTA lead excess values than subjects with gout but no lead exposure, these subjects in turn having greater EDTA lead excess values than subjects with neither gout nor lead exposure. In each country, the highest median EDTA lead excess occurred not in the group with gout and lead exposure, but in the group without gout and with lead exposure.
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PMID:Patterns of lead excretion in patients with gout and chronic renal failure--a comparative German and Australian study. 312 Mar 9

We measured lead and calcium in multiple bone biopsies from 11 cadavers without known excessive past exposure to lead. Paired iliac crest, transiliac and tibial bone biopsies from these cadavers indicated that in bone biopsy specimens the lead/calcium ratio is more reproducible than the absolute lead concentration. There were no significant differences between the lead/calcium ratios from the iliac crest, transiliac, or tibial specimens. Transiliac bone biopsies from 35 patients (13 patients showing symptoms of slight or moderate degree of renal failure, medical history of gout and/or arterial hypertension and 22 lead workers with chelatable lead in excess of 1000 micrograms) indicated that the lead and the lead/calcium ratio in bone biopsies reflect body lead stores as estimated by the EDT A test (r = 0.87 and 0.83, respectively). Chemical and histological studies of transiliac biopsies previously obtained from 153 dialysis patients (from 8 dialysis centers from Belgium, France and Germany) for studies of aluminum-induced bone disease showed that chronic renal failure and dialysis do not cause accumulation of lead in bone and elevated bone lead does not appear to alter trabecular bone histomorphometry. We found that in 5% of the hemodialysis population studied, bone lead concentrations approximated levels found in active lead workers.
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PMID:Bone lead in dialysis patients. 312 11

Thiazide diuretics have been in use for over 30 years in the treatment of hypertension. Their action results in a reduction in peripheral resistance without a significant decrease in cardiac output or a major shift in plasma volume. They are as or more effective than any of the other antihypertensive agents when used as monotherapy and can serve as baseline therapy in combination with any of the available adrenergic, converting enzyme-inhibiting agents, or calcium-entry blockers. There is a high degree of patient acceptance; titration to an effective dosage is relatively easy; and cost, relatively low. Although certain undesirable metabolic changes may occur following the use of these agents, most of them are controllable, and there is no evidence to date that they offset the benefits achieved by blood pressure lowering. Asymptomatic elevated uric acids have not been shown to be of great significance. If gout occurs, it can be managed. Alterations in glucose metabolism may occur, and in some patients, it appears that blood glucose levels are elevated over time. This is not a desirable metabolic change, but is one of doubtful prognostic significance. Changes in lipids are generally short-term, and in the major clinical trials, lipid levels have not remained elevated with a continuation of diuretic therapy. Although diuretics produce hypokalemia in a fairly high percentage of patients, this is not generally severe (less than 3.3 mEq per liter) and usually does not produce symptoms. There is no firm evidence that the hypokalemia produced by diuretics predisposes the patient to severe arrhythmias or sudden death, although this point has been emphasized repeatedly in recent publications. Diuretics can usually be given without potassium-maintenance therapy. However, hypokalemia should be prevented in the elderly, in patients with ischemic heart disease, left ventricular hypertrophy and those on digitalis, or with diabetes. We prefer potassium-sparing agents along with a diuretic over supplements to prevent hypokalemia; the number of pills is kept at a reasonable level, and cost is minimized. Physicians should continue to prescribe diuretics as first-step therapy in the majority of patients to maximize therapeutic outcome.
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PMID:Diuretics in the management of hypertension. 330 12

In the past 20 years treatment appears to have had a major impact on all forms of cerebral vascular disease. Morbidity and mortality from strokes have declined nearly 50% in developed countries. Modern imaging techniques, methodology, and biostatistics have identified risk factors and refined clinical trials such that we question all previous studies of stroke management. Control of moderate and severe hypertension has significantly lowered stroke rates. In borderline and mild hypertension the decision to treat is influenced by other stroke risk factors including diabetes mellitus, cigarette smoking, ischaemic heart disease, plasma lipid levels, gout, haematocrit, and body weight. Current data indicate that anticoagulants are of no value, or hazardous, in atherothrombotic strokes; of unknown value in transient ischaemic attacks; of dubious value in evolving strokes; and beneficial in cardiac embolism. The cardiac causes, including mural thrombus, unstable arrhythmias, and mitral valve prolapse should be actively sought. Aspirin, as the prototype anti-platelet agent, holds promise in transient ischemic attacks and minor strokes at both small and moderate dosages. Ticlopine is now being critically evaluated in America. Use of cerebral vasodilators should be abandoned. Enthusiasm in the use of streptokinase and urokinase has been dampened by the conversion of ischemic infarcts into haemorrhagic infarcts. In subarachnoid haemorrhage epsilon-aminocaprioc acid is useful although hazardous, in preventing rebleeding. Certain calcium ion channel blockers are promising in the reduction of vasopasm. Since the November 1985 article in the new England Journal of Medicine on the failure of external-to-internal carotid arterial bypass to reduce the risk of ischemic stroke, the swing is back to conservative management.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Advances in the medical management of cerebral vascular disease. 331 47

The National High Blood Pressure Education Program has released three Joint National Committee reports and a task force report on the detection, evaluation, and treatment of high blood pressure. Like its predecessors, the 1988 Joint National Committee report was developed using the consensus process; it is based on the latest scientific research and reflects the state of the art regarding hypertension management. This report updates findings of previous reports in several respects: it broadens the step-care approach to provide more flexibility for clinicians; encourages greater patient involvement in the treatment program; emphasizes a consideration of the quality of life in the management of patients; and addresses the cost of care. It also provides more emphasis on control of other risk factors for cardiovascular disease; includes a discussion of the new cholesterol guidelines; recommends a reduction in alcohol consumption; and discusses the use of calcium and fish oil supplementation. This document expands earlier reports on special populations, including blacks and other racial and ethnic minority groups, young and elderly patients, pregnant patients, surgical candidates, and hypertensive patients with cerebrovascular disease, coronary artery disease, left ventricular hypertrophy, congestive heart failure, peripheral vascular disease, renal disease, chronic obstructive pulmonary disease or bronchial asthma, gout, diabetes mellitus, and hyperlipidemia. The report also updates previous drug tables to include new drugs, revised recommended doses of some drugs, and drug interactions. Consideration of step-down therapy after blood pressure has been controlled is suggested. This report is intended as a guide for practicing physicians and other health professionals in their care of hypertensive patients and as a reference for those participating in the many community high blood pressure control programs throughout the country.
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PMID:The 1988 report of the Joint National Committee on Detection, Evaluation, and Treatment of High Blood Pressure. 256

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

Two cases of coexisting septic and crystalline joint disease are reported. In one patient polyarticular septic arthritis occurred simultaneously with gout and pseudogout. In a second patient septic arthritis preceded the appearance of calcium pyrophosphate dihydrate (CPPD) crystals in the joint fluid, supporting an earlier postulate that lysosomal enzymes released during sepsis lead to shedding of crystals from cartilage and synovium into the joint space. This sequence was demonstrated in a rat air pouch model of synovium, in which CPPD crystals embedded in facsimile synovial tissue were released after injection of pyogenic bacteria. Coexisting septic arthritis should always be considered when crystals are identified in inflamed joints, particularly in elderly patients with concurrent infections.
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PMID:Crystal shedding in septic arthritis: case reports and in vivo evidence in an animal model. 346 9

Lead intoxication was recognised as early as 2000 BC and the widespread use of lead has been a cause of endemic chronic plumbism in several societies throughout history. In the twentieth century, lead intoxication is still a common problem. In children it is largely due to ingestion of pica and environmental exposure, whereas adult groups at greatest risk are the industrially exposed: thus, screening of these workers should be undertaken at regular intervals. The clinical features of lead intoxication are nonspecific and often go unrecognised. The early manifestations are largely neuropsychiatric, followed by more significant disturbances of the central and peripheral nervous systems, symptomatic gastrointestinal, musculoskeletal, haematological and endocrine abnormalities. The association of lead poisoning with renal disease is well documented and must be considered, particularly if there is associated hypertension and/or gout. Blood lead concentrations are an unreliable predictor of body lead stores as they are indicative only of recent exposure. Haematological parameters have been used to assess those at risk of toxicity, but although more reliable than blood concentrations, they also fail to predict those patients at risk of toxicity. The recommended assessment for patients with suspected lead intoxication is a calcium disodium edetate chelation test, which is a sensitive marker for assessing body stores and subsequent intoxication. In children the dosage should be 50 mg/kg up to 1000 mg, and in adults 1000 mg administered intravenously or 2000 mg intramuscularly in divided doses 12 hours apart with subsequent 72 hour urinary lead estimations. Lead excretion levels greater than 350 micrograms/72 hours should be considered as suggestive of intoxication, particularly if supported by historical, clinical or biochemical evidence of lead exposure. Treatment of patients with positive chelation tests involves symptomatic treatment and a course of chelation therapy utilising calcium disodium edetate in doses similar to those used for testing, and in the more severely intoxicated patient, the addition of dimercaprol in doses of 75 mg/m2 every 4 hours to a total of 300 mg/m2/day. The safety of these treatment regimens is well documented.
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PMID:Lead intoxication. 354 May 17


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