OBJECTIVETo analyze the relationship between metabolites of polycyclic aromatic hydrocarbons (PAHs) and serum uric acid levels in coke oven workers and to provide new clues to the pathogenic mechanism of PAHs.

METHODSA total of 1302 coke oven workers were divided into four groups, namely control group and low-, intermediate-, and high-dose exposure groups. The concentrations of ambient PAHs at each workplace were determined by high-performance liquid chromatography. The detailed information on the occupational history and health of workers was collected by questionnaire survey and physical examination, and so were their blood and urine samples. Serum uric acid and creatinine levels were measured using a Hitachi 7020 automatic biochemical analyzer. Ten urinary PAH metabolites were detected by gas chromatography-mass spectrometry.

RESULTSSerum uric acid levels were the highest in the high-dose exposure group, followed by the intermediate- and low-dose exposure groups, and were the lowest in the control group. There were significant correlations between serum uric acid levels and the quartiles of 1-hydroxynaphthalene and 1-hydroxyphenanthrene (P < 0.05). After adjustment for PAH metabolite-related relationship, only urinary 1-hydroxyphenanthrene was significantly correlated with serum uric acid levels (P = 0.001). After adjustment for confounding factors and using the 1st quartile of 1-hydroxyphenanthrene as a reference, the odds ratio for hyperuricemia in subjects with the 2nd, 3rd, and 4th quartiles of 1-hydroxyphenanthrene were 1.55, 1.57, and 2.35, respectively.

CONCLUSIONUrinary 1-hydroxyphenanthrene is associated with a dose-response increase in serum uric acid levels in coke oven workers, and exposure to phenanthrene in PAHs may be a risk factor for hyperuricemia.

Adult ; Coke ; Humans ; Male ; Occupational Exposure ; Polycyclic Aromatic Hydrocarbons ; urine ; Uric Acid ; blood

OBJECTIVETo compare therapeutic effects of electroacupuncture (EA) treatment and medication on acute gouty arthritis (AGA), so as to search for a therapeutic method for treatment of gout with renal insufficiency.

METHODSNinety cases of AGA were randomly divided into an EA group, an allopurinol group and a probenecid group, 30 cases in each group. The EA group were treated by EA at Sanyinjiao (SP 6), Fenglong (ST 40), Yinlingquan (SP 9), once a day; the allopurinol group by oral administration of Allopurinol, twice a day, 100 mg each time and the probenecid group by oral administration of Probenecid, twice daily, 0.25 g each time. Contents of blood uric acid (BUA) and urinary uric acid (UUA) in each group were detected.

RESULTSIn all groups, there were significant differences in BUA and UUA levels before and after treatment (P < 0.01). There was no significant difference between the EA group and the allopurinol group in blood uric acid level after treatment (P > 0.05) and there was no significant difference between the EA group and the probenecid group in the urinary innary uric acid level (P > 0.05). Comparison of therapeutic effects among the 3 groups indicated that the mean rank was 56.23 in the EA group, 43.17 in the allopurinol group and 37.10 in the probenecid group, indicating that the therapeutic effect in the EA group was better than that in the allopurinol group, and the allopurinol group was better than that in the probenecid group.

CONCLUSIONEA can reduce the production of uric acid and promote the excretion of uric acid and has a better treatment effect. And there are no harmful effects on renal function. EA is an effective therapeutic method for treatment of gout with renal insufficiency.

Acute Disease ; Adult ; Aged ; Arthritis, Gouty ; metabolism ; therapy ; Electroacupuncture ; Female ; Humans ; Male ; Middle Aged ; Uric Acid ; blood ; urine

Purpose: In order to identify the stone risk factors for stone patients with hypertension, we analyzed the stone metabolic studies of stone patients with hypertension and stone patients without hypertension. Materials and Methods: Between January 1998 and December 2005, we analyzed 92 urinary calculi patients with hypertension, and we also 210 urinary calculi patients who had no history of hypertension as a control group. Hypertension was defined as systolic blood pressure >140 mmHg or a diastolic pressure >90mmHg or both, or those patients who were on drug therapy for hypertension. We evaluated such metabolic risk factors as calcium, sodium, potassium, chloride, uric acid, oxalate, phosphorus, the total urine volume and urine citrate level of the 24-hour urine collection, and the uric acid, calcium, phosphorus, cholesterol, triglyceride from the serum. Results: The mean age was 53.2+/-11.2 in the hypertensive group and 48.4+/-14.0 in the normotensive group. There were significant differences between the hypertensive group and the normotensive group for the body mass index (BMI) (28.7+/-0.9kg/m2 vs 25.1+/-1.1kg/m2, respectively), weight (73.2+/-3.2kg vs 67.4+/-2.1kg respectively) and urine calcium (262.4+/-21.7 mg/day vs 205.2+/-22.3mg/day respectively), uric acid (662.7+/-184.3mg/ day vs 578.3+/-179.2 mg/day respectively). Moreover, there were significant differences between the two groups for total cholesterol (198.5+/-47.4mg/dl vs 167.1+/-42.5 mg/dl respectively) and triglyceride (207.5+/-109.5mg/dl vs 160.8+/-107.1 mg/dl respectively). Conclusions: Our results suggest that higher urinary calcium excretion and higher uric acid excretion appear to be the characteristic risk factors in the hypertensive group. Hypercholesterolemia, hypertriglyceridemia and an excessive BMI are also related to stone patients with hypertension.
Blood Pressure ; Body Mass Index ; Calcium ; Cholesterol ; Citric Acid ; Drug Therapy ; Humans ; Hypercholesterolemia ; Hypertension* ; Hypertriglyceridemia ; Phosphorus ; Potassium ; Risk Factors* ; Sodium ; Triglycerides ; Uric Acid ; Urinary Calculi ; Urine Specimen Collection

INTRODUCTIONHyperuricaemia in tumour lysis syndrome (TLS) can cause acute renal failure (ARF), necessitating dialysis. Recombinant urate oxidase (rasburicase) converts uric acid to soluble allantoin, which is excreted easily.

CASE REPORTAn 8-year-old boy with stage 3 Burkitt's lymphoma, TLS was successfully treated with hyper-hydration, diuretics and rasburicase, without dialysis. This is the first paediatric case in Kandang Kerbau Women's & Children's Hospital (KKH) in which rasburicase was used. We review the literature on the effectiveness of urate oxidase in avoiding dialysis in TLS.

TREATMENT AND OUTCOMEOur patient developed rapidly rising serum uric acid (SUA) and progressive renal impairment. Hyper-hydration and rasburicase (0.2mg/kg) were administered. SUA rapidly decreased from 1308 to 437 mmol/L within 12 hours. Urate oxidase has shown better results than allopurinol. There was a need for dialysis in 0.4% to 1.7% of patients with haematological malignancies given rasburicase, compared to 20% in patients given allopurinol.

CONCLUSIONSRasburicase can reverse renal insufficiency. Though expensive, it may be cost-effective by lowering incidence of dialysis, shortening the duration of intensive care and hospitalisation, allowing early chemotherapy.

Burkitt Lymphoma ; complications ; Child ; Humans ; Hyperuricemia ; drug therapy ; Male ; Renal Dialysis ; Singapore ; Treatment Outcome ; Tumor Lysis Syndrome ; physiopathology ; urine ; Urate Oxidase ; metabolism ; pharmacology ; Uric Acid ; analysis ; blood

The aim of the study was to investigate the effects of Siwu decoction on hyperuricemia, kidney inflammation, and dysfunction in hyperuricemic mice. Siwu decoction at 363.8, 727.5, and 1 455 mg·kg(-1) was orally administered to potassium oxonate-induced hyperuricemic mice for 7 days. Serum urate, creatinine, and blood urea nitrogen levels and hepatic xanthine oxidase (XOD) activity were measured. The protein levels of hepatic XOD and renal urate transporter 1 (URAT1), glucose transporter 9 (GLUT9), organic anion transporters 1 (OAT1), ATP-binding cassette subfamily G member 2 (ABCG2), organic cation transporter 1 (OCT1), OCT2, organic cation/carnitine transporter 1 (OCTN1), OCNT2, Nod-like receptor family, pyrin domain containing 3 (NLRP3), apoptosis-associated speck-like protein (ASC), Caspase-1, and interleukin-1β (IL-1β) were determined by Western blotting. Renal histopathology change was obtained following hematoxylin-eosin staining. Our results indicated that Siwu decoction significantly reduced serum urate, creatinine and blood urea nitrogen levels and increased fractional excretion of uric acid in hyperuricemic mice. It effectively reduced hepatic XOD activity and protein levels in this animal model. Furthermore, Siwu decoction down-regulated URAT1 and GLUT9 protein levels, and up-regulated the protein levels of OAT1, ABCG2, OCT1, OCT2, OCTN1, and OCTN2 in the kidney of the hyperuricemic mice. Additionally, Siwu decoction remarkably reduced renal protein levels of NLRP3, ASC, Caspase-1, and IL-1β in the hyperuricemic mice. These results suggested that Siwu decoction exhibited anti-hyperuricemic and anti-inflammatory effects by inhibiting hepatic XOD activity, regulating renal organic ion transporter expression, and suppressing renal NLRP3 inflammasome activation, providing the evidence for its use in the treatment of hyperuricemia and associated kidney inflammation.
Animals ; Blood Urea Nitrogen ; Creatinine ; urine ; Drugs, Chinese Herbal ; administration & dosage ; Humans ; Hyperuricemia ; chemically induced ; drug therapy ; immunology ; urine ; Interleukin-1beta ; genetics ; immunology ; Kidney ; drug effects ; immunology ; Liver ; drug effects ; Male ; Mice ; Organic Anion Transport Protein 1 ; genetics ; immunology ; Sulfuric Acids ; Uric Acid ; urine

OBJECTIVETo study the preventive and therapeutic effects of total saponin of Dioscorea (TSD) on chronic hyperuricemia, and its effect on urate transporter 1 (URAT1) in rats.

METHODNinety male rats were randomly divided into 6 groups: the normal group, the model group, TSD high-, medium- and low-dose (300, 100, 30 mg x kg(-1)) groups and the benzbromarone (10 mg x kg(-1)) group. Potassium oxonate and ethambutol were adopted to establish the chronic hyperuricemia model Since the third week, all the rats were intragastrically administered with drugs for 4 weeks, once a day, in order to determine their uric acid in serum and urine, uric acid excretion and xanthine oxidase (XOD). URAT1 mRNA and URAT1 protein expression in rat renal tubular cells were determined by RT-PCR and immunohistochemistry method respectively.

RESULTSerum uric acid level of the model group increased significantly, while uric acid excretion decreased, with high expressions of renal URAT1 mRNA and URAT1 protein. TSD could dose-dependently reduce the serum uric acid level of chronic hyperuricemia rats, increase the concentration of uric acid and uric acid excretion in urine, and reduce renal URAT1 mRNA and URAT1 protein expression. Its effects were similar with that of benzbromarone, but with no significant effect on XOD and urinary volume of chronic hyperuricemia rats.

CONCLUSIONTSD has an obvious effect of anti-hyperuricemia It may reduce the reabsorption of uric acid by inhibiting the high expression of rat renal URAT1.

Animals ; Anion Transport Proteins ; biosynthesis ; genetics ; metabolism ; Benzbromarone ; pharmacology ; Dioscorea ; chemistry ; Gout Suppressants ; chemistry ; pharmacology ; Hyperuricemia ; blood ; drug therapy ; genetics ; urine ; Kidney Tubules ; drug effects ; metabolism ; Male ; Rats ; Rats, Sprague-Dawley ; Saponins ; chemistry ; pharmacokinetics ; pharmacology ; Uric Acid ; blood ; urine ; Xanthine Oxidase ; metabolism

BACKGROUND/AIMS: An association between serum uric acid and cancer risk has been noted over the past few decades. There is ongoing debate about whether hyperuricemia represents an independent risk factor for colorectal neoplasm. We investigated the association between serum uric acid and prevalence of colorectal adenoma considering numerous confounding factors. METHODS: A cross-sectional study was performed with individuals who underwent a routine health check-up examination, including a screening colonoscopy and blood chemistry. The association between serum uric acid and prevalence of colorectal adenoma was estimated from the results of a logistic regression analysis. RESULTS: Of the 1,066 participants, 402 had colorectal adenoma (37.7%). In univariate models, the prevalence of colorectal adenoma was higher in participants in the fourth quartile uric acid level, compared to those in the first quartile uric acid level (OR, 1.67; 95% CI, 1.17-2.42; p=0.004). However, no significant association was detected between serum uric acid and prevalence of colorectal adenoma in multiple logistic regression analysis. A number of metabolic syndrome components exhibited a strong association with the prevalence of colorectal adenoma in the multivariate model (OR, 3.46 for highest vs. lowest; 95% CI, 1.30-9.20; p=0.021). Moreover, serum uric acid was strongly associated with metabolic syndrome-associated variables, including waist circumference, fasting blood glucose, systolic blood pressure, diastolic blood pressure, triglyceride, and high-density lipoprotein. CONCLUSIONS: Uric acid is not an independent risk factor for colorectal adenoma but is a risk indicator for metabolic syndrome-related colorectal adenoma.
Adenoma/*diagnosis/epidemiology/etiology ; Adult ; Asian Continental Ancestry Group ; Blood Glucose/analysis ; Blood Pressure ; Colonoscopy ; Colorectal Neoplasms/*diagnosis/epidemiology/etiology ; Cross-Sectional Studies ; Female ; Humans ; Logistic Models ; Male ; Metabolic Syndrome X/*diagnosis ; Middle Aged ; Odds Ratio ; Prevalence ; Republic of Korea ; Risk Factors ; Triglycerides/blood ; Uric Acid/*blood/urine ; Waist Circumference

The effects of mangiferin on uric acid excretion, kidney function and related renal transporters were investigated in hyperuricemic mice induced by potassium oxonate. Mice were divided into normal control group, and 5 hyperuricemic groups with model control, 50, 100, and 200 mg x kg(-1) mangiferin, and 5 mg x kg(-1) allopurinol. Mice were administered by gavage once daily with 250 mg x kg(-1) potassium oxonate for seven consecutive days to create the model. And 3 doses of mangiferin were orally initiated on the day 1 h after potassium oxonate was given, separately. Serum uric acid, creatinine and urea nitrogon levels, as well as urinary uric acid creatinine levels were measured. Mouse uromodulin (mUMOD) levels in serum, urine and kidney were determined by ELISA method. The mRNA and protein levels of related renal transporters were assayed by RT-PCR and Western blotting methods, respectively. Compared to model group, mangiferin significantly reduced serum uric acid, creatinine and urea nitrogon levels, increased 24 h uric acid and creatinine excretion, and fractional excretion of uric acid in hyperuricemic mice, exhibiting uric acid excretion enhancement and kidney function improvement. Mangiferin was found to down-regulate mRNA and protein levels of urate transporter 1 (mURAT1) and glucose transporter 9 (mGLUT9), as well as up-regulate organic anion transporter 1 (mOAT1) in the kidney of hyperuricemic mice. These findings suggested that mangiferin might enhance uric acid excretion and in turn reduce serum uric acid level through the decrease of uric acid reabsorption and the increase of uric acid secretion in hyperuricemic mice. Moreover, mangiferin remarkably up-regulated expression levels of renal organic cation and carnitine transporters (mOCT1, mOCT2, mOCTN1 and mOCTN2), increased urine mUMOD levels, as well as decreased serum and kidney mUMOD levels in hyperuricemic mice, which might be involved in mangiferin-mediated renal protective action.
Animals ; Blood Urea Nitrogen ; Carrier Proteins ; genetics ; metabolism ; Creatinine ; blood ; Glucose Transport Proteins, Facilitative ; genetics ; metabolism ; Hyperuricemia ; blood ; chemically induced ; physiopathology ; urine ; Kidney ; metabolism ; physiopathology ; Male ; Membrane Proteins ; genetics ; metabolism ; Mice ; Octamer Transcription Factor-1 ; genetics ; metabolism ; Organic Anion Transport Protein 1 ; genetics ; metabolism ; Organic Anion Transporters ; genetics ; metabolism ; Organic Cation Transport Proteins ; genetics ; metabolism ; Organic Cation Transporter 2 ; Oxonic Acid ; Protective Agents ; pharmacology ; RNA, Messenger ; metabolism ; Random Allocation ; Solute Carrier Family 22 Member 5 ; Uric Acid ; blood ; urine ; Uromodulin ; blood ; urine ; Xanthones ; pharmacology