Primary hyperuricemia and gout are multifactorial conditions with strong genetic components. recently genome-wide association studies (GWAS) have revealed that several genes are related to primary hyperuricemia and gout which offers a thought for the research into the etiology, disease risk prediction, and prevention and treatment of this disease.

The incidence of hyperuricemia and relevant diseases has been increasing recently since the living improvement and dietary changing. Both patients and doctors do not pay enough attention to this disease, due to the lack of obvious clinical presentations in early stage. This paper comments on the relationship between hyperuricemia and gout, gouty nephropathy, impaired glucose metabolism,and atherosclerotic diseases in order to arouse enough attention to this disease.

Objective To investigate the plasma PAF-AH level in type 1 diabetes patients and the association between the PAF-AH gene polymorphism and type 1 diabetes mellitus. Methods Plasma PAF-AH in115 type 1 diabetes patients and 106 controls were determined by PAF-AH assay kit, and PAF-AH gene G275A genotypes were detected by PCR-RLFP. Results The activity of plasma PAF-AH in the patients with type 1 diabetes was significantly lower than that in the controls. Compared with control group, the frequencies of the GA genotype on G275A polymorphism were significantly higher than that in T1DM group. Conclusion The activity of plasma PAF-AH in the patients with type 1 diabetes was significantly lower than that in normal controls. The G275A polymorphism of PAF-AH gene might be related to type 1 diabetes mellitus.

Objective To investigate the association between -45C→G mutation at promoter of human urate transporter 1 gene and primary hyperuricemia. Methods The allele frequency and genotypo distribution of -45 C→G mutation at promoter of human urate trans-porter 1 gene were determined by PCR-RFLP in 217 patients with primary hyperuricemia and 419 normal controls. Results The frequencies of the G allele and CG genotype at promoter of human urate transporter 1 gene in patients were significantly higher than that in normal controls (P = 0. 031, P = 0.031). The levels of serum uric acid (UA) and triglyceride (TG) in subjects of CG genotype were significantly higher than those in the objects of CC genotype(t=3.058, t=3.699, P=0.002, P<0.001). There were no significant difference in the levels of total cholesterol (TC), fasting plasma glucose (FPG), urea nitrogen (BUN), creatinine (Cr) between the two groups (P>0.05). Conclusion The -45 C→G mutation at promoter of human urate transporter 1 gene may be related to primary hyperuricemia.

Objective To investigate the dynamic changes of serum interleukin (IL)-1β,tumor necrosis factor (TNF)-α,cyclooxygenase (COX)-2 levels in patients with acute gouty arthritis with various severityes and to provide evidence for the course of anti-inflammatory drug used in patients with acute gouty arthritis.Methods Ninety patients with gouty arthritis were randomly selected including sixty acute gouty arthritis patients and thirty gout patients in remission (observation group 3).Sixty acute gouty arthritis patients were divided into severe (observation group 1) and mild (observation group 2) subgroups according to the chief complaints and pain score points (VRS-4 method).All acute gouty arthritis patients were given the same dose and duration of etoricoxib and colchicine (14 days in all).Serum IL-1β,TNF-α,COX-2 levels were detected by enzyme-linked immunosorbent assay (ELISA) after the 1,3,7,10 and 14 days after onset.The 2-tailed independent samples t test was used for the analysis of measurement data.ANOVA were adapted for the comparison between groups.Results The serum levels of IL-1β,TNF-α in the observation group 1,2 were significantly higher than those in the control group in day 1 and 7 (P＜0.01),and almost completely returned to normal at day 10 to 14 day anti-inflammatory therapy.The serum COX-2 levels in observation group 1,2 were significantly higher than those in the control group (P＜0.01) in day 1 to 3,and returned to normal at day 7 to 10 after anti-inflammatory therapy.There were no significant differences between observation group3 and the control group (t=-0.880,-1.201,-0.548; P=0.383,0.235,0.586).② The serum levels of IL-1β,TNF-α were significantly higher in observation group 1 than those in observation group 2 [(24±5) pg/ml and(19±3) pg/ml,(323±84) ng/ml and (234±29) ng/ml; P=0.001,0.002],while there was no significant differences between observation group 2 and the control group (P=0.357).The serum COX-2 levels in observation group 1 were significantly higher than those in observation group 2 at day 7 [(12.9±2.0) pg/ml and (9.1±1.6) pg/ml],while there was no significant difference between observation group 2 and the control group (P=0.941).Conclusion Inflammatory factor can return to normal completely after anti-inflammatory therapy for acute gouty arthritis for 10 to 14 days.This study provides evidence for the course of anti-inflammatory drug used in patients with acute gouty arthritis.

Objective To investigate the plasma PAF-AH level in initialed type 1 diabetes patients and the association between the PAF-AH gene polymorphism and type 1 diabetes mellitus. Methods155 initialed type 1 diabetes patients and 138 controls were selected in this study. Plasma PAF-AH was determined by PAF-AH Assay kit, and the PAE-AH gene G994t genotypes were detected by PCR. ResultsThe activity of plasma PAF-AH in the patients with type 1 diabetes was significantly lower than that in the controls[ (20.64 ± 6.23)nmol/(min · ml) vs (28.56 ± 4. 11)nmol/(min · ml), P ＜0.05). Compared with control group, the frequencies of the GT genotype on G994T polymorphism between type 1 diabetes patients and controls were not significantly different(8.4％ vs 7. 2％, P ＞0. 05). ConclusionThe activity of plasma PAF-AH in the patients with type 1 diabetes was significantly lower than controls. The G994T polymorphism of PAF-AH gene was not related to type 1 diabetes mellitus.

Objective To study the characteristics and the related risk factors of coronary artery changes in the elderly patients of coronary heart disease complicated with diabetes mellitus. Methods According to WHO diagnostic standards of diabetes, coronary heart disease(CHD) complicated with diabetes mellitus(65 patients) was indicated as CHD+DM group, and the coronary heart disease without diabetes(68 patients) was indicated as CHD group. All patients were examined by coronary angiographic semiquantitative(CAG), and blood pressure, oral glucose tolerance test, level of blood sugar, insulin, lipid, BUN and Cr were measured. The coronary artery changes were analysed by CAG, and the severity of coronary artery stenosis were evaluated by AHA standards. The related risk factors in coronary artery disease were analysed by pluralism straight line statistics. Results The coronary multivessel changes(75 4% vs 38 2%, P

AIM: To study the effect of platelet-activating factor(PAF) on proliferation of cultured rat airway smooth muscle cells(ASMCs).METHODS: The cells were divided into control group and PAF group. The cells in PAF group were subdivided into four small groups by concentrations of PAF 10 -6 , 10 -7 , 10 -8 , 10 -9 mol?L -1 , MTT assay was used not only to investigate the effects of PAF on proliferation of ASMC but also to confirm the optimal concentration. Flow cytometry and immuneohistochemistry for proliferating cell nuclear antigen (PCNA) were also used to analyse its function on proliferation of ASMC.RESULTS: PAF (10 -6 -10 -9 mol?L -1 ) stimulated the cell proliferation and 10 -7 mol?L -1 PAF reached the maximal effect. The cell percentage of the ASMCs of 107 mol?L -1 PAF subgroup at G_ 0/1 phase (68.67%) was much lower than that of control group (85.57%, P

Objective To investigate the role of malondialdehyde(MDA),superoxide dismutase(SOD),and interleukin-1β (IL-1β) played in the pathogenesis of acute gouty arthritis and the treatment efficacy of probucol.Methods Acute gouty arthritis model in rat was established with injection of monosodium urate monohydrate (MSU) into the ankle joint cavity,then the joint swelling index was observed periodically,and MDA,SOD,IL-1β,and white blood cell count in the synovial fluid were determined by 72 h.Results The joint swelling index gradually increased,reaching a peak by 11h,and this finding was most obvious in the model group.The joint swelling index in the group treated with high-dose of probucol was significantly lower than that in the model group by 48 h(P＜0.05).The joint swelling indices in the groups treated with moderate and high doses of probucol were lower than that in the model group by 72 h(P＜0.05).The values of MDA in the moderate and high-dose groups were (14.45±3.11) and (11.54 ±3.10) nmol/ml respectively,being significantly lower than that in the model group[(24.46±4.27) nmol/ml,P＜0.01].The amounts of SOD in the moderate and high-dose groups were (25.56±4.51) and (44.61±4.11)U/ml respectively,being higher than that in the model group[(13.32±2.02) U/ml,P＜0.01].The amount of IL-1β in the high-dose group was lower than that in the model group[(15.41 ± 3.12 vs 19.87±3.99)pg,P＜0.05].The white blood cell counts in the moderate and high-dose groups were (11.08±1.64)×l0~7/L and (7.43±1.52) x 10~7/L,being lower than that in the model group[(14.18±2.30)×10~7/L,P＜0.01].Conclusion The levels of MDA and IL-1β in the synovial fluid were raised,while SOD was significantly decreased in acute gouty arthritis.Moderate and high-doses of probucol can effectively control acute gouty arthritis attack.The efficacy of high-dose probucol was equal to that of colchicines.

Objective To study the association between hURAT1 gene single nucleotide polymorphism(SNP) and primary hyperuricemia(HUA). Methods A total of 215 patients with HUA and 323 healthy subjects were chosen to investigate SNP of hURAT1. Exon 2 to 4 and flanking introns of the hURAT1 gene in patients and control individuals were screened with PCR. The relationship between SNP of hURAT1 gene with HUA was studied with statistical analysis. Results The frequency of AA/AG genotype was significantly increased in HUA patients as compared with that in healthy controls( 11.6% vs 3.7% ,P =3.81 × 10-4). Allele A of hURAT1 intron 3, 11 G ＞A was found significantly higher in the group of HUA patients, being detected in 6.0% of the HUA patients alleles and in 1.9% of the healthy control alleles (P =2.66 × 10-5 ). Those carrying the low frequency AA/AG genotype had a risk effect on the morbidity of HUA and the odds ratio for the HUA patients versus controls was 3.41 with AA/AG genotype versus GG genotype( OR = 3.41,95% CI = 1.67 - 6.95 ). The HT4 haplotype, which carried the intron 3,11A allele, was associated with a significantly increased risk of HUA(69.44% vs 30.56% ,P ＜ 0.001). Conclusion The SNP of 11G ＞A in the intron 3 of hURAT1 gene was apparently associated with HUA, thus suggesting the genetic effect of hURAT1 gene in the pathogenesis of HUA.