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1.
Chongqing Medicine ; (36): 1643-1644,1647, 2015.
Article in Chinese | WPRIM | ID: wpr-601910

ABSTRACT

Objective To observe the clinical efficacy of glucocorticoidcombined with the eradication of helicobactepylori (HP) in the treatmenof idiopathithrombocytopenipurpura(ITP) and itinfluence on platelecounand cell subset.MethodNinety-foucaseof ITP were randomly divided into two group.The control group(47 cases) wagiven prednisone treatmen, while the observation group(47 cases) wagiven prednisone combined with HP eradication treatmen.The clinical effecand recur-rence rate within 1 yeawere observed ,and the changeof platelecounand cell subsetwere tested .ResultThe total effective rate of the observation group wa89 .36% ,which wasignificantly highethan 70 .21% in the control group ;the 1-yearecurrence rate in the observation group wa36 .17% ,which wasignificantly lowethan 72 .34% in the control group ,the differencebetween the two grouphad statistical significance (P<0 .05) .The platelecounaftetreatmenin the two groupwere significantly in-creased ,platelet-associated antibody(PAIgG) level wasignificantly decreased ,buthe improvemenin the observation group wamore significant(P<0 .05) .The percentage of CD3+CD4+ % increased significantly ,the percentage of CD3+CD8+ % wadecreased significantly ,buthe improvemenin the observation group wamore obviou(P<0 .05) .Conclusion Glucocorticoidcombined with HP eradication treatmenin treating ITP hadefinitely clinical efficacy ,can increase the platelecoun,improve cell subsetimbalance ,and iworthy to be clinically promoted .

2.
Clinical Medicine of China ; (12): 1047-1049, 2010.
Article in Chinese | WPRIM | ID: wpr-386872

ABSTRACT

Objective To investigate whether angiotensin Ⅱ type 1 receptor(AT1R)gene polymorphism is associated with essential hypertension(EH). Methods A total of 200 hypertension patients and 192 normotensive controls were enrolled. The AT1R gene 1166A/C and -810A/T polymorphism were determined by polymerase chain reaction-restriction fragment length polymorphism (PCR-PFLP), and the association between the SNPs and the EH were analyzed statistically. Some biochemical index such as serum glucose (GLU) and total cholesterol (TC),triglyceride (TG), high density lipoprotein (HDL-C) and low density lipoprotein (LDL-C) were also measured. Results There was no significant difference between two groups of 1166A/C polymorphisms of AT1R gene(P > 0.05 ). However, for the -810A/T polymorphism of AT1R gene, -810 AT and TT genotypes frequencies were significantly higher in EH patients than control (P = 0. 004). The -810T allele frequencies were higher in case than in control (22.5% vs. 11.5% ;P =0.000). We also found an association between EH and -810AT and TT genotypes by logistic regression analysis ( P = 0. 003 ), adjusted for other risk factors. The odds ratio was 2.57 (95% CI:1. 37 ~4. 84). Conclusions AT1R -810A/T polymorphism is associated with EH and -810T allele may be a risk factor of hypertension

3.
Clinical Medicine of China ; (12): 1119-1121, 2008.
Article in Chinese | WPRIM | ID: wpr-398076

ABSTRACT

Objective To investigate the effects of Helicohacter pylori infection on plasma lipid levels. Methods HpIgG was measured by ELISA in both 242 patients with coronary heart disease (CHD) and 88 subjects without CHD, and compared between these two groups. Then 242 patients with CHD were divided into HpIgG positive group and HpIgG negative group ,and total cholesterol (TC) ,triglyceride (TG) ,high density lipaprotein (HDL), low density lipoprotein (LDL), apolipoprotein A (ApoA) , apolipoprotein B (ApoB) were analyzed and compared between these two subgroups. Results The rate of seropositivity for HpIgG in CHD patients was significantly higher than that of controls (53.3 % vs. 38.6 %, P < 0.05), and HDL, ApoA level in HplgG seropasitive group was signif-icantly lower than that of HpIgG seronegative one (P < 0.05). However, there was no difference of TC, TC, LDL and ApoB between these two subgroups (P > 0.05). Conclusion Hp infection may be associated with CHD. It may pro-mote the pathogenesis of CHD through lowering serum HDL-C level.

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