Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018099 (gout)
 5,192 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cross-sectional associations between biological, clinical and behavioral factors and serum uric acid (SUA) levels were examined in 2,438 Japanese male office workers aged 20 to 59 years in Osaka, Japan. Stepwise regression analysis for SUA was carried out for all persons and repeated excluding those under medication for hypertension, hyperuricemia or diabetes mellitus. The results were essentially the same without change in the sequence of the seven most important variables. When 150 men under medication were excluded, independent correlates with SUA levels were, in order of relative importance, history of gout, log triglyceride, creatinine, hemoglobin A1c (negative association), body mass index, total protein, alcohol intake, age (negative association), and total cholesterol. 32.7 percent of total variation in SUA was accounted for by these variables combined. Our data suggest that weight and serum lipids control and avoiding excessive drinking may be beneficial in the prevention of hyperuricemia.
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PMID:Serum uric acid: correlation with biological, clinical and behavioral factors in Japanese men. 1033 82

The objective of this prospective study was to determine the prevalence of hyperuricemia and gout in a sample of Saudi individuals and their relationship to certain risk factors, namely, obesity, serum glucose, triglycerides, cholesterol, age, and sex. A total of 487 Saudis (250 males and 237 females) from 14 primary care clinics were interviewed, examined, and investigated. The mean age for the males was 46.89 +/- 17.01 years (range 14-83) and for the females 45.08 +/- 13.67 years (range 21-80). Serum uric acid (SUA) values above 420 micromol/l for males and 360 micromol/l for females were considered to be high. Of the 487 individuals, 41 (8.42%; 20 males and 21 females) had hyperuricemia. The mean SUA was 308.41 +/- 90.64 micromol/l for males and 254.59 +/- 85.79 micromol/l for females. In females, uric acid levels correlated significantly with age, body mass index (BMI), serum creatinine, and the erythrocyte sedimentation rate (ESR), but not with serum cholesterol or triglycerides. In males, uric acid levels only correlated significantly with BMI and serum creatinine. No case of gout was found.
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PMID:Hyperuricemia in Saudi Arabia. 1126 34

Uricase-deficient mice develop uric acid nephropathy, with high mortality rates before weaning. Urate excretion was quantitated and renal function was better defined in this study, to facilitate the use of these mice as a model for evaluating poly(ethylene glycol)-modified recombinant mammalian uricases (PEG-uricase) as a potential therapy for gout and uric acid nephropathy. The uric acid/creatinine ratio in the urine of uricase-deficient mice ranges from 10 to >30; on a weight basis, these mice excrete 20- to 40-fold more urate than do human subjects. These mice consistently develop a severe defect in renal concentrating ability, resulting in an approximately sixfold greater urine volume and a fivefold greater fluid requirement, compared with normal mice. This nephrogenic diabetes insipidus leads to dehydration and death of nursing mice but, with adequate water replacement, high urine flow protects adults from progressive renal damage. Treatment of uricase-deficient mice with PEG-uricase markedly reduced urate levels and, when initiated before weaning, preserved the renal architecture (as evaluated by magnetic resonance micros-copy) and prevented the loss of renal concentrating function. PEG-uricase was far more effective and less immunogenic than unmodified uricase. Retention of uricase in most mammals and its loss in humans and some other primates may reflect the evolution of renal function under different environmental conditions. PEG-uricase could provide an effective therapy for uric acid nephropathy and refractory gout in human patients.
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PMID:Diabetes insipidus in uricase-deficient mice: a model for evaluating therapy with poly(ethylene glycol)-modified uricase. 1131 59

We report a 29 years old woman with a chronic tophaceous gout, whose disease started at the age of 18. On clinical examination, the blood pressure was elevated. The laboratory assessment showed a serum uric acid of 15 mg/dl, a urinary uric acid of 155 mg/24 h, a creatinine clearance of 59 ml/min/1.73 m2 and a uric acid excretion fraction off 1.3% (normal 7 to 12%). The clinical and laboratory features of this patient suggest the diagnosis of a familial juvenile gouty nephropathy.
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PMID:[Familial gout and nephropathy in a young woman. Report of one case]. 1151 Feb 9

We examined whether the age at onset, gender, arthritic manifestations, and tophus formation in familial gout are different from those in nonfamilial gout, and we also examined the contributory effect of genetic association to the concurrence of hypertriglyceridemia, hypercholesterolemia, type 2 diabetes mellitus (DM), hypertension, obesity, and renal insufficiency with gout in Taiwan. A total of 21,373 gout patients' data from Ho-Ping Gout database were analyzed in this study retrospectively. The clinical and laboratory data were compared between familial and nonfamilial gout. Mean age at onset of gout in familial subjects was significantly 7.5 years lower than that of nonfamilial subjects (40.9 +/- 13.4 v 48.4 +/- 14.2 years, P =.0001), while gender, arthritic severity, and tophus formation were not significantly different between these 2 groups. Familial gout had lower serum triglyceride (TG), total cholesterol (TC), and percentage of hypertension than nonfamilial gout (182.4 +/- 125.3 v 195.9 +/- 135.8 mg/dL, P =.0001; 207.5 +/- 42.5 v 210.4 +/- 48.8 mg/dL, P =.0003; and 19.57% v 22.56%, P <.0001, respectively). Their serum creatinine, body mass index (BMI), and percentage of type 2 DM were not significantly different. Our results demonstrate that familial gout is associated with precocious onset. Furthermore, the contributory effect of genetic association to the concurrence of hyperlipidemia and hypertension with gout is less than that of environmental factors, while the effect of genetic association to the concurrence of obesity, type 2 DM, and renal insufficiency with gout is equivalent to that of environmental factors.
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PMID:Clinical features of familial gout and effects of probable genetic association between gout and its related disorders. 1158 94

A 55-year-old woman was referred to our ward for further evaluation of marked hyperuricaemia and suspected tophi. On physical examination, huge subcutaneous nodules were observed on the knee joints as well as a small nodule on the lateral side of the left sole. Blood chemistry showed marked hyperuricaemia (0.85 mmol/l), hypokalaemia (2.7 mmol/l) and a mild degree of renal insufficiency. Arterial blood gas analysis showed signs of metabolic alkalosis. Daily urinary uric acid excretion on a purine non-restricted diet was 8.9 mmol/day. Uric acid clearance and fractional uric acid clearance were 0.8 ml/min and 2.6%, respectively. Plasma renin activity was 21.8 ng/ml/h, and plasma angiotensin II and aldosterone concentrations were 61 and 121 pg/ml, respectively. However, pressor response to an intravenous administration of angiotensin II was normal. The urinary calcium to creatinine molar ratio was 0.069, and serum magnesium concentration was normal to supranormal. A biopsy of the subcutaneous nodule showed a typical appearance of tophus. Based on these findings, the patient was diagnosed with an atypical case of renal tubular hypokalaemic metabolic alkalosis, with marked hyperuricaemia and tophi as the initial manifestations. So far, only four cases of Bartter's syndrome with gout and/or hyperuricaemia have been described in Japan. This rare case is presented and its mechanism of hyperuricaemia discussed.
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PMID:An atypical case of primary renal tubular hypokalaemic metabolic alkalosis with chronic tophaceous gout. 1164 22

Chronic exposure to high altitude is associated with the development of erythrocytosis, proteinuria, and, in some cases, hyperuricemia. We examined the relationship between high-altitude polycythemia and proteinuria and hyperuricemia in Cerro de Pasco, Peru (altitude, 4,300 m). We studied 25 adult men with hematocrits less than 65% and 27 subjects with excessive erythrocytosis (EE; hematocrit > 65%) living in Cerro de Pasco, Peru and compared them with 28 control subjects living in Lima, Peru (at sea level) and after 48 hours of exposure to high altitude. Serum urate levels were significantly elevated in patients with EE at altitude, and gout occurred in 4 of 27 of these subjects. Urate level strongly correlated with hematocrit (r = 0.71; P < 0.0001). Urate production (24-hour urine urate excretion and urine urate-creatinine ratio) was increased in this group compared with those at sea level. Fractional urate excretion was not increased, and fractional lithium excretion was reduced, in keeping with increased proximal reabsorption of filtrate. Significantly higher blood pressures and decreased renin levels in the EE group were in keeping with increased proximal sodium reabsorption. Serum urate levels correlated with mean blood pressure (r = 0.50; P < 0.0001). Significant proteinuria was more prevalent in the EE group despite normal renal function. Hyperuricemia is common in subjects living at high altitude and associated with EE, hypertension, and proteinuria. The increase in uric acid levels appears to be caused by increased urate generation secondary to systemic hypoxia, although a relative impairment in renal excretion also may contribute.
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PMID:Hyperuricemia, hypertension, and proteinuria associated with high-altitude polycythemia. 1204 23

A 77-year-old man was in good health until he complained of fatigue 3 weeks before presentation. Two weeks before admission, he developed gradually worsening shortness of breath. One week before admission, he developed a cough that initially was nonproductive but later was associated with hemoptysis.His past medical history was remarkable for a history of colon cancer (Dukes' stage III), for which he underwent a hemicolectomy and treatment with adjuvant chemotherapy in 1993. He had a myocardial infarction in 1986 and underwent coronary artery bypass surgery in 1999. He also had a history of hypertension, type 2 diabetes, and gout. He smoked in the past but had stopped more than 30 years ago.He was initially evaluated by his primary care physician, who noted that he complained of diaphoresis but denied fevers, chills, or contact with others who were ill. His physical examination was remarkable for bilateral crackles that were more pronounced on the right. A chest radiograph demonstrated bilateral pulmonary infiltrates (Figure 1). He was treated with amoxicillin. The next day, however, his physician noted that his dyspnea had worsened and that his oxygen saturation on room air was poor. He was therefore admitted for further evaluation. The amoxicillin was discontinued, and he was treated with levofloxacin, followed by ceftriaxone and azithromycin as his pulmonary status continued to deteriorate. He received intravenous diuretic agents, which failed to improve his respiratory status. During the initial phase of hospitalization, he was anemic, with a hematocrit of 21.3%. His serum creatinine level, which had been 1.0 mg/dL in 1999, was now 2.5 mg/dL. Urinalysis was remarkable for the presence of numerous red blood cells. His oxygen requirement increased, and he eventually required a 100% nonrebreather mask. A computed tomographic scan of the chest demonstrated prominent alveolar opacities throughout the right upper, middle, and lower lobes, with similar opacities in the left upper and left lower lobes (Figure 2). An echocardiogram showed an ejection fraction of 50%, as well as mild mitral regurgitation. Serologies were remarkable for an antinuclear antibody titer of 1:320 and a P-antineutrophil cytoplasmic antibody (P-ANCA) titer of greater than 1:320. C-ANCA was negative. Anti-glomerular basement membrane and anti-human immunodeficiency virus antibodies were undetectable.
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PMID:Cases from the medical grand rounds of the Osler Medical Service at Johns Hopkins University. 1207 15

Hyperuricemia, unlike clinical gout, is extremely common in renal transplant patients. The high prevalence of hyperuricemia is related to prolonged exposure to cyclosporine rather than to its dose or serum concentration. Serum creatinine levels do not show significant correlation with hyperuricemia, behaving more like a surrogate marker for cyclosporine dose and trough level. The low incidence of gout in renal transplant patients, despite the hyperuricemia, may be related to the prolonged immunosuppression effect.
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PMID:Hyperuricemia and gout in renal transplant recipients. 1216 3

CD27 is expressed on lymphocytes, but also on renal tubules. On the damaged renal tubules, CD27 is cleaved into soluble CD27 (sCD27) and cytoplasmic tail CD27. Renal tubule apoptosis is induced by the CD27 ligand, Siva, binding to the truncated tail CD27. Theoretically, serum sCD27 should be a marker of renal tubule apoptosis. Serum sCD27 levels were measured by ELISA in 274 patients at University Hospital School of Medicine, Japan. Among 73 males and 63 females with high plasma creatinine levels, 68 (93%) males and 51 (81%) females showed high serum sCD27 values (>or=500 U/ml). In the 42 males with plasma creatinine levels of 1.18-5.00 mg/dl and the 55 females with plasma creatinine levels of 0.83-4.65 mg/dl, the correlation coefficients between plasma creatinine and sCD27 were 0.605 and 0.469, respectively. SCD27 was a more sensitive marker of renal tubule apoptosis than plasma creatinine. Of 138 patients with normal plasma creatinine, 42 showed high serum sCD27 levels (>or=500 U/ml). Among the 42 patients, 19 patients had high blood urea nitrogen and 11 patients showed plasma creatinine elevations 3-11 days later. Nine patients with hemolysis and 39 patients with aneurysms had clearly higher sCD27 levels of 1633+/-483 U/ml and 905+/-437 U/ml, respectively, than normal values of 215+/-57 U/ml ( n=27) ( P value >or=0.001). Vasodilators, hypotensors, diuretics, and drugs for gout, arrhythmia, thrombosis, and diabetes were prescribed in 40%, 37%, 33%, 13%, 8%, 8%, and 5% of the 78 patients analyzed with high sCD27 levels (>or=500 U/ml). In total, 59 (76%) patients were prescribed at least one of the drugs. In conclusion, serum sCD27 was a more sensitive indicator of renal tubule apoptosis than plasma creatinine, especially during the early stage of apoptosis. Tubule apoptosis with high serum sCD27 levels was found in patients with glomerular vascular injuries.
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PMID:High levels of serum soluble CD27 correlated with renal dysfunction. 1262 11


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