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)

A positive association between hyperuricemia and cardiovascular disease has been reported, but no study has evidenced yet the precise role of serum uric acid in the development of cardiovascular disease. In addition, no epidemiological studies have so far documented a decreased risk of cancer among people with hyperuricemia, even though the antioxidant action of uric acid has recently been stressed to inhibit DNA damage. The present prospective cohort study investigates the relationship between hyperuricemia and health hazards in a Japanese working population. The subjects were 49,413 Japanese male railroad workers, aged 25-60 years at enrollment. Serum uric acid and other baseline data were provided by annual health-survey records from 1975 to 1982. The vital status of the subjects was traced until the end of 1985 for those who remained alive. During an average 5.4-year study period, 984 deaths were recorded. Those with serum uric acid over 8.5 mg/dl showed elevated relative risks (RRs) of death in all causes (RR 1.62, p<0.01), coronary heart disease ( RR 1.52), stroke (RR 2.33, p<0.01), hepatic disease (RR 3.58, p<0.01), and renal failure ( RR 8.52, p<0.01), as compared with those with serum uric acid levels of 5.0-6.4mg/dl. The RR of death in all causes still remains statistically significant when adjusted by age and serum total cholesterol (2.00, p<0.01), age and alcohol intake (1.85, p<0.001), age and smoking (1.69, p<0.001), age and gout treatment (1.61, p<0.05), and also age and BMI (1.50, p< 0.05). On the other hand, the RR of all causes decreased but was still above 1.0 when adjusted by age and blood glucose (1.62), age and systolic blood pressure (1.32), age and GOT (1.23), and also age and history of cardiovascular disease (1.17). These results showed that hyperuricemia has a strong association with the RRs of death in all causes, coronary heart disease, stroke, hepatic disease and renal failure, and indicated that serum uric acid seems to be a considerable risk factor for reduced life expectancy.
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PMID:Does hyperuricemia affect mortality? A prospective cohort study of Japanese male workers. 1121 Jan 10

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

The leaves of Gymnema inodorum (GI) have been known to be effective for some diseases including diabetes mellitus, rheumatic arthritis and gout. The crude saponin mixtures extracted from GI leaves inhibited glucose absorption in the isolated intestinal tract and suppressed the increased blood glucose in rats. In this study, we examined the relationship between chemical structure and pharmacological activity of the four components from GI leave extracts (GiA-1, GiA-2, GiA-5 and GiA-7). These components were the derivatives of (3beta,4alpha,16beta)-16,23,28-trihydroxyolean-12-en-3-yl-beta-D-glucopyranosiduroic acid. GiA-2, GiA-5 and GiA-7 that have suppressive effects on the high K+-induced contraction, an increase in deltaPD and the increased blood glucose level in the glucose tolerance test have -H at the 21st position and -CH2OH at 4beta of aglycon. On the other hand, GiA-1 that does not have any effects on the three parameters mentioned above has -H at the 21st position and -CH3 at 4beta of aglycon. In conclusion, it is suggested that the inhibitory effect of triterpenoids in Gymnema leaves on glucose absorption from the intestinal tract relies on -CH2OH at 4beta.
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PMID:Structure-activity relationships of triterpenoid derivatives extracted from Gymnema inodorum leaves on glucose absorption. 1145 25

Serum uric acid levels are maintained by urate synthesis and excretion. URAT1 (coded by SLC22CA12) was recently proposed to be the major absorptive urate transporter protein in the kidney regulating blood urate levels. Because genetic background is known to affect serum urate levels, we hypothesized that genetic variations in SLC22A12 may predispose humans to hyperuricemia and gout. We investigated rs893006 polymorphism (GG, GT and TT) in SLC22A12 in a total of 326 Japanese subjects. Differences in clinical characteristics among the genotype groups were tested by the analysis of variance (ANOVA). In male subjects, mean serum uric acid levels were significantly different among the three genotypes. Levels in the GG genotype subjects were the highest, followed by those with the GT and TT genotypes. However, no differences between the groups were seen in the distributions of creatinine, Fasting plasma glucose (FPG), HbA(1c), total cholesterol, triglyceride, HDL cholesterol levels or BMI. A single nucleotide polymorphism (SNP) in the urate transporter gene SLC22CA12 was found to be associated with elevated serum uric acid levels among Japanese subjects. This SNP may be an independent genetic marker for predicting hyperuricemia.
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PMID:Association between intronic SNP in urate-anion exchanger gene, SLC22A12, and serum uric acid levels in Japanese. 1692 Jan 56

The authors studied the combination of hydrochlorothiazide (HCTZ) 50 mg/d plus olmesartan medoxomil (OM) 40 mg/d in stage 2 systolic hypertension during an extension phase of an open-label 12-week dose titration study. Subjects whose blood pressure remained above 120/80 mm Hg (n=105) on OM 40/HCTZ 25 mg/d subsequently received OM 40/HCTZ 50 mg/d for 4 weeks. Increasing HCTZ from 25 mg/d to 50 mg/d decreased systolic blood pressure by 3.6 mm Hg, increased BP control rates (<140/90 mm Hg) from 70.4% to 77.5%, and increased BP normalization rates (<120/80 mm Hg) from 15.4% to 27.8%. The combination was well tolerated. Compared with OM 40 mg/d monotherapy, neither dose of HCTZ affected serum potassium, but both increased serum glucose by about 5%. There was a dose-dependent increase in uric acid but no acute gout attacks. OM 40/HCTZ 50 mg/d is an effective strategy for managing stage 2 systolic hypertension.
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PMID:Titration of HCTZ to 50 mg daily in individuals with stage 2 systolic hypertension pretreated with an angiotensin receptor blocker. 1721 58

The pyrrolizidine alkaloid content of Solanecio gigas (Vatke) C. Jeffrey (Asteraceae), an Ethiopian medicinal plant widely used for the treatment of colic, diarrhea, gout, otitis media, typhoid fever, and noted for its wound dressing and antiabortifacient activities was studied. The flower and leaf extracts contained 0.19% and 0.14% alkaloids (dry weight), respectively. GLC-MS analysis indicated that all the alkaloids in the flowers are pyrrolizidine alkaloids (PAs), whereas the leaves contain other type of alkaloids with PAs occurring in low concentrations. Roughly, 80% and 90% of the total PAs in the flowers and the leaves, respectively, were shown to occur as N-oxides. Eighteen alkaloids were detected in the flower extract with the retronecine type twelve-membered macrocyclic diesters integerrimine, senecionine and usaramine comprising 82% of the total PA content. Analysis of the PA profile of the leaves indicated that it has a simpler pattern than the one observed for the flowers. Only five PAs were detected in the leaves with integerrimine making up about 50% of the total PAs. Quantification of the PA content by GLC showed that the flowers and leaves contain 3321.21 and 84.84 microg per 10 g of dried plant material, respectively. These results indicate that users of this herb are at high risk of poisoning since the most toxic twelve membered macrocyclics of the retronecine type are the dominant PAs in the plant.
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PMID:Identification and quantification of hepatotoxic pyrrolizidine alkaloids in the Ethiopian medicinal plant Solanecio gigas (Asteraceae). 1794 27

High serum uric acid levels elevate pro-inflammatory-state gout crystal arthropathy and place individuals at high risk for cardiovascular morbidity and mortality. Genome-wide scans in the genetically isolated Sardinian population identified variants associated with serum uric acid levels as a quantitative trait. They mapped within GLUT9, a Chromosome 4 glucose transporter gene predominantly expressed in liver and kidney. SNP rs6855911 showed the strongest association (p = 1.84 x 10(-16)), along with eight others (p = 7.75 x 10(-16) to 6.05 x 10(-11)). Individuals homozygous for the rare allele of rs6855911 (minor allele frequency = 0.26) had 0.6 mg/dl less uric acid than those homozygous for the common allele; the results were replicated in an unrelated cohort from Tuscany. Our results suggest that polymorphisms in GLUT9 could affect glucose metabolism and uric acid synthesis and/or renal reabsorption, influencing serum uric acid levels over a wide range of values.
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PMID:The GLUT9 gene is associated with serum uric acid levels in Sardinia and Chianti cohorts. 1799 8

Serum uric acid concentrations are correlated with gout and clinical entities such as cardiovascular disease and diabetes. In the genome-wide association study KORA (Kooperative Gesundheitsforschung in der Region Augsburg) F3 500K (n = 1,644), the most significant SNPs associated with uric acid concentrations mapped within introns 4 and 6 of SLC2A9, a gene encoding a putative hexose transporter (effects: -0.23 to -0.36 mg/dl per copy of the minor allele). We replicated these findings in three independent samples from Germany (KORA S4 and SHIP (Study of Health in Pomerania)) and Austria (SAPHIR; Salzburg Atherosclerosis Prevention Program in Subjects at High Individual Risk), with P values ranging from 1.2 x 10(-8) to 1.0 x 10(-32). Analysis of whole blood RNA expression profiles from a KORA F3 500K subgroup (n = 117) showed a significant association between the SLC2A9 isoform 2 and urate concentrations. The SLC2A9 genotypes also showed significant association with self-reported gout. The proportion of the variance of serum uric acid concentrations explained by genotypes was about 1.2% in men and 6% in women, and the percentage accounted for by expression levels was 3.5% in men and 15% in women.
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PMID:SLC2A9 influences uric acid concentrations with pronounced sex-specific effects. 1832 56

The aim of the study was to compare BMI with waist circumference (WC), waist-to-hip ratio (WHR), and waist-to-stature ratio (WSR) as a predictor of diabetes incidence. A total of 1,841 men and 2,104 women of Mauritian Indian and Mauritian Creole ethnicity, aged 25-74 years, free of diabetes, hypertension, cardiovascular disease, and gout were seen at baseline in 1987 or 1992, and follow-up in 1992 and/or 1998. At all time points, participants underwent a 2 h 75 g oral glucose tolerance test. Hazard ratios for diabetes incidence were estimated applying an interval-censored survival analysis using age as timescale. Six hundred and twenty-eight individuals developed diabetes during the follow-up period. Multivariable adjusted hazard ratios for diabetes incidence corresponding to a 1 s.d. increase in baseline BMI, WC, WHR, and WSR for Mauritian Indians were 1.49 (1.31-1.71), 1.58 (1.38-1.81), 1.54 (1.37-1.72), and 1.61 (1.41-1.84) in men and 1.33 (1.17-1.51), 1.35 (1.19-1.53), 1.39 (1.24-1.55), and 1.38 (1.21-1.57) in women, respectively; and for Mauritian Creoles they were 1.86 (1.51-2.30), 2.07 (1.68-2.56), 1.92 (1.62-2.26), and 2.17 (1.76-2.69) in men and 1.29 (1.06-1.55), 1.27 (1.04-1.55), 1.24 (1.04-1.48), and 1.27 (1.04-1.55) in women. Paired homogeneity tests showed that there was no difference between BMI and each of the central obesity indicators (all P > 0.05). The relation of BMI with the development of diabetes was as strong as that for indicators of central obesity in this study population.
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PMID:BMI compared with central obesity indicators as a predictor of diabetes incidence in Mauritius. 1900 66

Studies in both healthy and diabetic subjects demonstrated that fructose produced a smaller postprandial rise in plasma glucose and serum insulin than other common carbohydrates. Substitution of dietary fructose for other carbohydrates produced a 13% reduction in mean plasma glucose in a study of type 1 and type 2 diabetic subjects. However, there is concern that fructose may aggravate lipemia. In 1 study, day-long plasma triglycerides in healthy men were 32% greater while they consumed a high-fructose diet than while they consumed a high-glucose diet. There is also concern that fructose may be a factor contributing to the growing worldwide prevalence of obesity. Fructose stimulates insulin secretion less than does glucose and glucose-containing carbohydrates. Because insulin increases leptin release, lower circulating insulin and leptin after fructose ingestion might inhibit appetite less than consumption of other carbohydrates and lead to increased energy intake. However, there is no convincing experimental evidence that dietary fructose actually does increase energy intake. There is also no evidence that fructose accelerates protein glycation. High fructose intake has been associated with increased risk of gout in men and increased risk of kidney stones. Dietary fructose appears to have adverse effects on postprandial serum triglycerides, so adding fructose in large amounts to the diet is undesirable. Glucose may be a suitable replacement sugar. The fructose that occurs naturally in fruits and vegetables provides only a modest amount of dietary fructose and should not be of concern.
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PMID:Dietary fructose and metabolic syndrome and diabetes. 1940 23


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