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

Frequency of gout in French Polynesia has induced us to define a type of "hyperuricemia Polynesian" from a population of patients admitted in a general Medicine Ward. Each admitted patient gets immediately a blood check-up. A figure higher than 70 mg/l in male and 60 mg/l in female is considered as pathological. In such a case, uricemia and uraturia are tested every 24 h for three days and we consider the mean value of these three tests. On the other side, some admitted patients non-hyperuricemic, are examined according to the same protocol. So, we have two groups: 31 hyperuricemics and 20 non-hyperuricemics, secondarily grouped according to age, sex, ethnic. We did not consider some secondary causes of hyperuricemia (chronic renal insufficiency diuretic treatment, psoriasis etc.). 1. Within the hyperuricemic population, mean uricemia is 85.35 mg/l versus 52.65 mg/l in the second sample. In the hyperuricemic group (21 males and 10 females) 48% are gouty and 13% of them are females. Articular manifestations are acute arthritis, affecting mainly inferior limbs, ankles, knees). We did not notice any significant divergence between uricemia and uraturia of gouty and non gouty people. Within the group of gouty people, percentage of individual hyper excretion is 53% (uraturia greater than 600 mg/24 h) with no significant divergence with the non-gouty group: Nephrolithiasis is rare (3%). There is no significant divergence between urinary pH of gouty and non-gouty people. Associated metabolic troubles are: diabetes (26%) high triglyceridemia (43%) three syndromes associated together (hyperuricemia + diabetes + hypertriglyceridemia) in 19.5%, total cholesterol is normal (2.07 g/l) but a low cholesterol (0.30 g/l).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Study of hyperuricemia in Tahiti. 31 cases hospitalized at the Territorial Hospital Center in Papeete (Tahiti)]. 160 55

We describe 3 patients with painful intraarticular knee effusions composed of a viscous milky white suspension of monosodium urate crystals, in the absence of any cellular component. Two patients presented with acute bilateral knee pain. One patient presented with unilateral knee pain of gradual onset. All 3 patients had a history of ethanol abuse. Two patients had a history of gout. Two patients had chronic renal insufficiency, hypertension, and congestive heart failure. One patient had alcoholic cirrhosis. Two patients' pain responded to colchicine. One patient's discomfort was relieved only by repeated arthrocentesis. We conclude that intraarticular free urate can cause painful joints in the absence of an apparent inflammatory response.
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PMID:Intraarticular noninflammatory free urate suspension (urate milk) in 3 patients with painful joints. 235 87

Among 196 patients with primary gout examined in hospital or earlier stable or transient hyperuricemia was noted in 160 (81.6%). These patients were entered into the study group. The control group included 36 persons in whom the level of blood uric acid did not exceed normal values. The familial pattern of disease was established in the patients of the study group. Urolithic, proteinuric and hypertensive types of nephropathy as well as chronic renal insufficiency were more frequently observed in hyperuricemia patients. Alongside with severe tubular, interstitial and vascular changes, glomeruli in the form of mesangioproliferative or mesangiocapillary glomerulonephritis were regularly involved in the pathological process. In the rest of the patients vascular lesions were less marked and less frequent, renal glomerular changes reminded the picture of mesangioproliferative glomerulonephritis only; urolithiasis in them took a more favorable course. Thus, a high level of blood uric acid is one of the risk factors of renal affection in gout determining in many ways prognosis of disease.
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PMID:[Hyperuricemia as a risk factor of nephropathy in gout]. 336 19

The authors observed 10 patients from 4 families with hereditarily determined gout and detected some specific features in its course. The familial disease was sex-unrelated, its first signs manifested themselves early acquiring a subsequent severe course; purine metabolic derangement was of a metabolic type, a urolithic form of nephropathy was seldom observed. A morphological picture was characterized by a glomerular lesion looking like focal segmental mesangiocapillary or mesangioproliferative glomerulonephritis with noticeable changes in the tubules, stroma and vessels causing early renal insufficiency. Pathogenetic therapy with uricodepressants made it possible to improve the course of nephropathy. The authors described a pedigree of 3 generations of a family in which gout developed in its 10 out of 17 members, in 6 with chronic renal insufficiency.
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PMID:[Familial gout]. 396 78

Until the past decades, end stage renal disease was considered a major cause of death among patients with gout. Modern long-term follow up studies of renal function however have indicated that hyperuricemia and gout rarely result in kidney damage unless other renal diseases supervene. Subsequently, the use of the EDTA lead mobilization test confirmed that gout in the presence of chronic renal failure is a useful marker of chronic lead intoxication. Chelation treatment with EDTA can slow the progression of renal insufficiency, without apparent damage associated with the use of the chelating agent. Since chronic lead intoxication may remain clinically concealed for years, a high index of suspicion is warranted. Occult lead intoxication should be sought actively in gouty patients with chronic renal insufficiency of unknown etiology.
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PMID:[Gout nephropathy--ghost or reality?]. 1549 17

Two of our patients experienced myotoxicity associated with colchicine administration. The first was a 54-year-old woman who was receiving dialysis and came to the emergency department with progressive generalized weakness and vomiting. She recently had taken colchicine for the treatment of gout. Physical examination revealed proximal muscle weakness and tenderness on palpation. Her creatine kinase (CK), alanine aminotransferase (ALT), and aspartate aminotransferase (AST) levels were elevated at 7185, 563, and 541 U/L, respectively. Drug-induced myopathy was suspected and colchicine was discontinued. The patient was discharged after symptom resolution 1 week later. The second patient was an 83-year-old woman with chronic renal insufficiency who came to the hospital with anorexia, diarrhea, and inability to get out of bed due to progressive weakness. Her colchicine dosage recently had been increased for gout management. Physical examination revealed generalized muscle weakness and tenderness on palpation. Her CK, ALT, and AST levels were elevated at 1797, 147, and 172 U/L, respectively. Electromyographic results were consistent with colchicine myopathy. The patient was discharged with minimal residual muscle weakness 1 week after discontinuation of colchicine. A literature search identified 82 documented cases of colchicine-induced myotoxicity. Most patients had a history of proximal weakness and pain with elevated CK, ALT, and AST levels. Onset of symptoms generally occurred days to weeks after initial administration of colchicine at the usual dosage in patients with renal impairment or a change in underlying disease state in those receiving long-term therapy. Muscle toxicity was not necessarily accompanied by gastrointestinal symptoms. Concomitantly administered drugs often were cyclosporine or corticosteroids. Diagnosis may be confirmed by electromyography or muscle biopsy. Colchicine-induced myotoxicity is a rare adverse effect but is well described in the literature. Clinicians should recognize that renal impairment is the primary risk factor for development of colchicine-induced myotoxicity, and that dosage adjustment or alternative therapy may be required.
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PMID:Colchicine myotoxicity: case reports and literature review. 1558 44

We report a 66-year-old Chinese man with chronic renal insufficiency (creatinine 1.7 mg/dL) and gout suffering from slurred speech and right hemiplegia for 3 days. Acute cerebral infarction was confirmed by computed tomography. Conscious disturbance occurred on the tenth hospital day without significant changes on imaging study when compared with a previous scan. Hypercalcemia (total calcium 14.1 mg/dL) and acute exacerbation of chronic renal failure (serum creatinine 2.5 mg/dL) were noticed. Hypercalciuria (FECa 3.2%), and low serum levels of intact parathyroid hormone and 1,25(OH)2D3 suggested nonparathyroidal hypercalcemia. An extensive workup failed to identify any etiology of hypercalcemia. Hypercalcemia and renal failure were temporarily ameliorated after aggressive volume expansion and loop diuretic treatment but recurred 2 weeks later. Immobilization hypercalcemia was considered after the exclusion of other discernible causes and was successfully treated with rehabilitative exercises and bisphosphonates without further recurrence during a 2-year follow-up. Clinical alertness to immobilization as a possible cause of hypercalcemia may avoid unnecessary and invasive examinations, life-threatening complications and annoying recurrences.
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PMID:An unrecognized cause of recurrent hypercalcemia: immobilization. 1663 46

Analysis of clinical-roentgen-laboratory features of the course of hereditarily determined gout in 74 patients is represented. It is exhibited that hereditarily induced gout begins at the young age and is accompanied by the acute disturbance of purine exchange resulting in serious relapsing course of the articular (with availability of radiological attributes of osteal destruction) and the renal syndromes (urate nephrolithiasis, immune complex glomerulonephritis, tubulointerstitional nephritis) as well as in the early occurrence and rapidly progressing chronic renal insufficiency. The disease is accompanied by high frequency of the cardiovascular pathologies negatively influencing the mean lifetime of patients.
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PMID:[Genetically determined gout: characteristics of the course]. 1693 56

Many patients with rheumatic diseases have their management complicated by renal problems. Renal failure modifies the metabolism of many drugs, especially by retention. Questions often arise about the effects of renal failure on the handling of drugs commonly used in rheumatology. For which drugs must we be especially concerned about increased toxicity? Patients on chronic dialysis may also need a variety of drugs for rheumatic disease. How are our drugs dialyzed, and which of these can be safety used and how best to use them?Decisions about dosing of rheumatic drugs are often required for the patients with chronic renal insufficiency or on long-term dialysis, although many drugs have not been formally studied in these settings. Patients with renal insufficiency are excluded from most drug trials. Data for some of these drugs have to be extrapolated based on the information available about the pharmacokinetics of the drug.This review addresses dosing of commonly used drugs in rheumatology in patients with chronic renal insufficiency or failure. It is compiled from a MEDLINE search of papers dealing with renal handling of antirheumatic drugs and suggestions for dose adjustments for these drugs. Drugs reviewed include commonly used disease-modifying antirheumatic drugs (DMARDS), drugs used for treatment of gout, commonly used nonsteroidal antnflammatory drugs (NSAIDS) and the newer COX-2 inhibitors.
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PMID:Dosing of antirheumatic drugs in renal disease and dialysis. 1704 8

Percutaneous radiofrequency thermal ablation (RFA) is considered an effective technique for providing local control in the majority of Hepatocellular carcinoma (HCC) patients. Although RFA is generally well tolerated, recent studies have reported complications associated with RFA. We describe a case of acute gouty arthritis in a 71-year-old man with chronic renal failure who was treated with RFA for a HCC lesion and who had hepatitis B-associated cirrhosis and mild renal insufficiency. Regular surveillance of the patient detected a 3.5 cm HCC lesion. Because the patient had declined surgery, RFA was chosen for therapy. On the third post-procedural day, the laboratory results showed increases in his uric acid and potassium levels, which were compatible with a tumor lysis syndrome. On the 6th post-procedural day, the patient complained of new right knee pain. Subsequent joint aspiration revealed monosodium urate monohydrate crystals. We made the diagnosis of acute gouty arthritis arising from tumor lysis and liver infarction caused by HCC ablation, which was aggravated by acute renal insufficiency. After adequate hydration and administration of oral colchicines, the patient's right knee pain subsided and the uric acid serum level returned to normal. This is the first described case of acute gouty arthritis after RFA for a HCC lesion in a patient with underlying chronic renal insufficiency. To avoid hyperuricemia and an acute attack of gout after RFA therapy for HCC, early identification of patients at risk is warranted, such as those with a large tumor, rapid tumor growth, and renal insufficiency, and preventative measures should be considered.
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PMID:A case of gouty arthritis following percutaneous radiofrequency ablation for hepatocellular carcinoma. 2013 29


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