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Background:Chronic atrophic gastritis(CAG)is a common disease of digestive system and is a precancerous lesion of the intestinal type gastric cancer. Serum pepsinogens(PGs)and gastrin 17(G17)are biological markers of gastric mucosal lesions,which have a prominent role in diagnosis of CAG and screening of early gastric cancer. Aims:To study the correlation of serum PGs and G17 with age in patients with CAG. Methods:A total of 582 CAG patients admitted from Jan. 2016 to Sep. 2017 at the Baoding First Central Hospital were enrolled. The levels of serum PGⅠ,PGⅡ and G17 were determined by ELISA,and the PGⅠ/ PGⅡ ratio(PGR)was calculated. The correlations of these indices with the clinical data of CAG patients were analyzed. Results:The levels of serum PGⅠ and PGⅡ were increased with age(P<0.01),and the levels of PGR and G17 were decreased with age(P <0.05). Spearman rank correlation coefficient analysis showed that the levels of PGⅠ and PGⅡ were positively correlated with age(rs=0.374,P<0.01;rs=0.559, P<0.01),and the levels of PGR and G17 were negatively correlated with age(rs= -0.649,P<0.01;rs= -0.141, P<0.05). Conclusions:The levels of serum PGⅠ,PGⅡand G17 in patients with CAG were correlated with age. When serum PGs and G17 are used as serological indicators for diagnosis of CAG and screening of early gastric cancer,the impact of age on these indices should be taken into account.
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Objective To investigate the effect and recurrence of the esomeprazole combined with trimebutine on treatment for non-erosive reflux disease(NERD).Methods One hundred and twenty-five cases of patients with NERD were randomly divided into the treatment group (n =62) and the control group (n =63).Patients in treatment group were received the esomeprazole 20 mg,twice a day and trimebutine 0.2 g,3 times a day,in control group were received the esomeprazole 20 mg,twice a day and mosapride 5 mg,3 times a day.After 8 weeks treatment,6 months follow-up was conducted and the effects and recurrence were evaluated.Results The clinical curative rates at 4th and 8th weeks treatment in treatment group were 75.8％ (47/62) and 95.2％ (59/62),higher than that of control group (57.1％ (36/63),x2 =4.879,P =0.027 ; 84.1％ (53/63),x2 =4.083,P =0.043).The GERDQ curative rates at 4th and 8th weeks treatment in treatment group were 72.6％ (45/62),93.5％ (58/62) respectively,significantly higher than that of the control group (52.4％ (33/ 63),x2 =5.434,P =0.020 ; 79.4％ (50/63),x2 =5.350,P =0.021).The recurrence rates of 6 months followup were 77.4％ (48/62) in the treatment group and 81.0％ (51/63) in the control group,there was no significant difference between the two groups (P =0.627).Conclusion Esomeprazole combined with trimebutine is safe and effective treatment on non-erosive reflux disease,and the recurrence rates was lower than that in the control group.
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Objective To explore the effect of the intestinal ischemia/reperfusion injury on paracrine patterns of BM-MSCs in order to provide evidence for BMSCs repair.Methods BMSCs were isolated,cultured,characterized,and stained.The rat intestine ischemia/reperfusion model (IRI) was established.Intestinal epithelial mucosal extracts were obtained either from IRI rat or normal rat.Those two type extracts were added into the culture medium,and BM-MSCs were cultured with the two conditioned medium respectively.The culture medium was collected at 0 h and 24 h after culturing with intestinal epithelial mucosal extracts.The levels of TGF-ot,VEGF,FGF and IGF-1 in the medium were assayed by ELISA.Results The contents of all the growth factors detected in cultured medium with intestinal extracts from IRI rats were significantly higher than in regular rats (P ＜ 0.05).The levels of TGF-α,VEGF in culture medium containing IRI epithelium extracts were significantly higher than that in the medium containing normal intestinal epithelium extracts (P ＜ 0.05)Conclusion BM-MSCs can secret TGF-α,VEGF,FGF,and IGF-1 in the presence of intestinal extracts from IRI rat in the culture.These factors might stimulate the differentiation and proliferation of intestinal epithelial cells through paracrine mechanism.