鸡关节炎型葡萄球菌病的感染门试验

通过多种途径实验感染，评定了分离自关节炎型病鸡病变关节的金黄色葡萄球菌对组织的亲嗜性以及病型与感染门的关系。关节内注射感染引起了典型的关节炎疾病；静脉注射感染除引起脓血症外，尚出现急性化脓性关节炎；皮下或肌肉注射感染均能致局部皮肤坏死、出血和蜂窝组织炎，但一般不致关节炎；气管内、气囊内或嗉囊内感染仅引起局部轻度炎症或不能致病。因而推论，关节炎型葡萄球菌病很可能仅由特定菌株经关节伤口感染才能引起。

恶性组织细胞病误诊为肝硬化肺门感染1例

患者男，35岁，于1987年10月以纳差、乏力、全身皮肤黄染入院，患者于2月前无诱因出现不规则发热、纳差、全身乏力、厌油，恶心，并于1月前出现咳嗽、咳痰，经某医院给予抗炎、对症治疗无效，继出现腹胀、全身皮肤黄染来我院就诊。

7例肺结核合并超鞭毛虫感染的诊断和治疗分析

目的探讨肺结核合并超鞭毛虫感染的临床诊断和治疗。方法对7例肺结核合并超鞭毛虫感染患者的临床和影像表现、实验室检查和治疗进行分析。结果患者以咳嗽和发热为主要症状,正规抗结核治疗后多仍有发热和明显盗汗,支气管肺泡灌洗液沉渣涂片镜检有助于提高超鞭毛虫检出率,甲硝唑治疗效果良好,可进一步恢复患者体温并消除盗汗。结论深圳地区肺结核患者合并超鞭毛虫感染临床并不少见,提高认识及时诊断治疗预后良好。

胸腰椎疾患后路内固定术后感染的诊治及临床分析

目的 探讨胸腰椎疾患后路内固定术后感染的原因及治疗措施。方法 分析 16例胸腰椎疾患后路内固定术后感染的原因 ,行内固定物取出、病灶清除、灌洗引流、抗感染治疗。结果 16例平均随访 4 5年 ,所有患者疼痛消失 ,切口愈合良好。结论 胸腰椎疾患后路内固定术后感染为初次手术时手术污染所致 ,微创及严格的无菌操作是预防该并发症的根本措施。确诊后行病灶清除、灌洗引流术 ,疗效满意。

三联皮试对小儿肺门结核的鉴别价值

用三联皮试辅助鉴别20例小儿反复结核性与非结核性肺门感染，结果说明特殊性强，准确性高．

The Effect of Helicobacter Pylori Infection on Expression of hMSH2, hMLH1 and p53 in Gastric Carcinogenesis

Objective： To detect the expression of hMSH2, hMLH1 and p53 in gastric epithelial cells with and without Helicobactcr pylori （H. pylori） infection and investigate the relationship between H. pylori infection and these genes in gastric carcinogenesis. Methods： H. pylori infection was detected by rapid urease tests. Expression of hMSH2, hMLHland p53 in gastric cancer （GC） tissue, its adjacent mucosa, gastritic mucosa and normal mucosa was assessed by immunohistochemistry SP method. Results： Positive expression rate of hMSH2 in GC tissue （62.7%） was higher than those in adjacent mucosa （29.4%）, gastritic mucosa （32.4%） and normal mucosa （30.0%） （P〈0.001）. Positive rate of hMSH2 in poorly differentiated adenocarcinoma （76.4%） was higher than those in other carcinomas （54.3%, 53.1%） （P〈0.05）. Positive expression rate of hMLH1 in GC tissue （64.3%） mucosa （82.4%） and normal mucosa （80.0%） was lower than those in adjacent mucosa （84.4%）, gastritic （P〈0.01）. Positive rate of hMLH1 in mucoid carcinoma （43.7%） was lower than those in other carcinomas （78.2%, 64.7%） （P〈0.01）. Positive expression rate of p53 in GC tissue （51.9%） was higher than those in adjacent mucosa （3.1%）, gastritic mucosa （0.0%） and normal mucosa （0.0%） （P〈0.001）. Positive rate of p53 in well differentiated adenocarcinoma （32.6%） was lower than those in other carcinomas （58.8%, 68.7%） （P〈0.01）. Positive rates of hMSH2 and hMLH1 in GC with H. pylori infection were lower than those without the infection, respectively （P〈0.05）. Positive rate of p53 in GC with H. pylori infection （61.4%） was higher than that without the infection （40.6%） （P〈0.05）. Conclusion： Gastric carcinogenesis may be associated with abnormal expression of hMSH2, hMLH1 and p53; H. pylori infection affecting expression of these genes may be one of its carcinogenic mechanisms.

Comparison of sequential and 7-,10-,14-d triple therapy for Helicobacter pylori infection

AIM:To compare the effectiveness of sequential therapy for Helicobacter pylori(H.pylori) infection with that of triple therapy of varying durations.METHODS:The 460 patients enrolled in this study had H.pylori-associated gastritis or a gastric or duodenal ulcer.After screening,H.pylori-infected patients were randomly assigned to receive either conventional triple therapy for 7,10 or 14 d,or a new 10-d sequential therapy.Each of the 4 treatment groups included 115 patients.The outcomes of eradication therapy were assessed 4 wk after treatment by the urea breath test and histology.RESULTS:The overall eradication rate was 81.0%,and eradication rates were 75.7% for 7-d conventional triple therapy,81.9% for 10-d conventional triple therapy,84.4% for 14-d conventional triple therapy,and 82.0% for 10-d sequential therapy.Neither intention-to-treat analysis nor per protocol analysis showed significant differences in eradication rates using sequential therapy or the standard triple therapy(P = 0.416 and P = 0.405,respectively).CONCLUSION:There are no significant differences between 10-d sequential eradication therapy for H.pylori and any duration of standard triple treatment in Korean patients.

H pylori:Treatment for the patient only or the whole family?

AIM： To compare the effects of treatment of H pyloriinfected individuals with the effects of treatment of individuals as well as all Hpylori-infected family members.METHODS： H pylori-positive patients with similar demographic specifications were prospectively randomized with respect to treatment, with a triple regimen of either patients and all Hpylori-positive family members living together （group Ⅰ ） or patients only （group Ⅱ）. Nine months after treatment, all patients were assessed for H pylori positivity.RESULTS： There were 70 H pylori-positive patients in each group; patients in groups Ⅰ and Ⅱ lived with 175 and 190 Hpylori-positive relatives, respectively. Age, sex and Hpylori positivity rate were similar in both groups of relatives. Nine months after 14 d standard triple therapy, Hpylori positivity was 7.1% in group I patients and 38.6% in group 11 patients [P 〈 0.01, OR = 8.61 95% confidence interval （CI）： 2.91-22.84].CONCLUSION： The present results indicate bad environmental hygienic conditions and close intra-familial relationships are important in H pylori contamination. These findings indicate all family members of H pyloripositive individuals should be assessed for H pylori positivity, particularly in developing countries where H pylori prevalence is high; they also suggest patients, their spouses and all H pyloN-positive family members of H pylori-positive individuals should be treated for H pylori infection.

Influence of Helicobacter pylori infection on ghrelin levels in children

AIM:To compare ghrelin levels in plasma and gastric mucosa before and after Helicobacter pylori(H.pylori) treatment in children with H.pylori-associated functional dyspepsia.METHODS:Children with H.pylori-associated functional dyspepsia were enrolled in this study.H.pylori infection was confirmed by positive bacterial culture results.All of the children received triple H.pylori eradication therapy(a 2 wk course of omeprazole,amoxicillin,and clarithromycin).The children were divided into two groups based on the success of the H.pylori treatment:group 1(eradicated)-patients who had a negative 13C-urea breath test 2 mo after the end of therapy;and group 2(non-eradicated)-patients who had a positive 13C-urea breath test.Plasma ghrelin,gastric ghrelin mRNA,and the body mass index were evaluated in both groups before and after the H.pylori treatment.The plasma ghrelin levels were measured by a radioimmunoassay.The expression of gastric ghrelin mRNA was determined by real-time reverse transcription polymerase chain reaction.RESULTS:A total of 50 children with H.pylori-associated functional dyspepsia were treated with triple H.pylori eradication therapy.The mean age of the children was 5.52 ± 0.83 years,and there were 28 males and 22 females.Among the 50 H.pylori-positive children,30 successfully achieved eradication,and 20 did not.The mean plasma ghrelin levels of group 1 were 22.17 ± 1.73 ng/L and 26.59 ± 2.05 ng/L before and after the treatment,respectively,which was a significant increase(P = 0.001).However,the mean plasma ghrelin level of group 2 before and after the H.pylori treatment was 21.34 ± 2.40 ng/L and 22.24 ± 2.10 ng/L(P = 0.785).The plasma ghrelin levels increased substantially after treatment in group 1 but showed only minor changes in group 2.Similarly,the gastric ghrelin mRNA expression in group 1 before treatment was 2.84 ± 0.08.After treatment,the level was 3.11 ± 0.65,which was significantly different(P = 0.023).The gastric ghrelin mRNA expression in group 2 did not change significantly during the treatment(2.82 ± 0.44 vs 2.79 ± 0.31,P = 0.875).The plasma ghrelin and gastric ghrelin mRNA levels in group 1 increased substantially after the treatment but did not do so in group 2.In addition,the body mass index the two groups did not differ significantly 2 mo before and after the H.pylori treatment.CONCLUSION:H.pylori eradication increases the plasma and tissue ghrelin levels in children with H.pylori-associated functional dyspepsia.

Frequencies of the expression of main protein antigens from Helicobacter pylori isolates and production of specific serum antibodies in infected patients

AIM: To investigate the frequencies of the expression of main protein antigens of Helicobacter pylori (H py/ori) isolates, such as UreB, VacA, CagA1, HpaA, NapA, FlaA and FlaB and the production of specific antibodies in sera from H pylori-infected patients, and to understand the correlations among the different clinical types of chronic gastritis and peptic ulcer and the infection and virulence of H pylori. METHODS: H pylori strains in biopsy specimens from 157 patients with chronic gastritis and peptic ulcer were isolated and serum samples from the patients were also collected. The target recombinant proteins rUreB, rVacA, rCagAl, rHpaA, rNapA, rFlaA and rFlaB expressed by the prokaryotic expression systems constructed in our previous studies were collected through Ni-NTA affinity chromatography. Rabbit antisera against rUreB, rVacA, rCagAl, rHpaA, rNapA, rFlaA and rFlaB were prepared by using routine subcutaneous immunization. By using ultrasonic lysates of the isolates as coated antigens, and the self-prepared rabbit antisera as the first antibodies and commercial HRP-labeling sheep anti-rabbit IgG as the second antibody, expression frequencies of the seven antigens in the isolates were detected by ELISA. Another ELISA was established to detect antibodies against the seven antigens in sera of the patients by using the corresponding recombinant proteins as coated antigens, and the sera as the first antibody and HRP-labeling sheep anti-human IgG as the second antibody respectively. Correlations among the different clinical types of chronic gastritis and peptic ulcer and the infection and virulence of H pylori were statistically analysed. RESULTS: In the 125 isolates of H pylori, the positive rates of UreB, VacA, CagAl, HpaA, NapA, FlaA and FlaB were 100%, 65.6%, 92.8%, 100%, 93.6%, 100% and 99.2% respectively. In the 125 serum samples from the H pylori infected patients, the positive rates of antibodies against recombinant UreB, VacA, CagA1, HpaA, NapA, FIaA and FlaB were 100%, 42.4%, 89.6%, 81.6%, 93.6%, 98.4% and 92.8% respectively. H pylori strains were isolated from 79.6% (125/157) of the biopsy specimens, but no close correlations among the H pylori infection frequencies and different types of chronic gastritis and peptic ulcer could be found (P>0.05, x2 = 0.01-0.87). The VacA positive rate (82.40%) in the strains isolated from the specimens of patients with peptic ulcer and the anti-VacA positive rate (54.3%) in the sera from the patients were significantly higher than those (51.5%, 32.3%) from the patients with chronic gastritis (P<0.01, x2= 13.19; P<0.05, x2= 6.13). When analysis was performed in the different types of chronic gastritis, the VacA in the strains isolated from the specimems of patients with active gastritis showed a higher expression frequency (90.0%) than those from superficial (47.9%) and atrophic gastritis (30.0%) (P<0.05, x2 = 5.93; P<0.01,x2 = 7.50). While analysis was carried out in the strains isolated from the specimens with superficial (93.8%) and active gastritis (100%), NapA showed a higher expression frequency compared to that from atrophic gastritis (60.0%) (P<0.01, x2 = 8.88; P<0.05, X2=5.00). CONCLUSION: The types of chronic gastritis and peptic ulcer and their severity are not associated with H pylori infection frequency but closely related to the infection frequency of different virulent H pylori strains. The optimal antigens for developing vaccine and diagnostic kit are UreB, FlaA, HpaA, FlaB, NapA and CagAl, but not VacA.

Trends in the eradication rates of Helicobacter pylori infection for eleven years

AIM:To evaluate the trends in the eradication rate of Helicobacter pylori(H.pylori) over the past 11 years in a single center.METHODS:This retrospective study covered the period from January 2000 to December 2010.We evaluated 5746 patients diagnosed with gastric ulcers(GU),duodenal ulcers(DU),GU + DU,or nonpeptic ulcers associated with an H.pylori infection.We treated them annually with the 2 wk standard first-line triple regimen,proton pump inhibitor(PPI) + amoxicilin + clarithromycin(PAC;PPI,clarithromycin 500 mg,and amoxicillin 1 g,all twice a day).The follow-up test was performed at least 4 wk after the completion of the 2 wk standard H.pylori eradication using the PAC regimen.We also assessed the eradication rates of 1 wk second-line therapy with a quadruple standard regimen(PPI b.i.d.,tripotassium dicitrate bismuthate 300 mg q.i.d.,metronidazole 500 mg t.i.d.,and tetracycline 500 mg q.i.d.) after the failure of the first-line therapy.Statistical analysis was performed with 95%CI for the differences in the annual eradication rates.RESULTS:A total of 5746 patients [2333 males(58.8%),1636 females(41.2%);mean age of males vs females 51.31 ± 13.1 years vs 52.76 ± 13.6 years,P < 0.05,total mean age 51.9 ± 13.3 years(mean ± SD)] were investigated.Among these patients,1674 patients were excluded:35 patients refused treatment;18 patients ceased H.pylori eradication due to side effects;1211 patients had inappropriate indications for H.pylori eradication,having undergone stomach cancer operation or chemotherapy;and 410 patients did not undergo the follow-up.We also excluded 103 patients who wanted to stop eradication treatment after only 1 wk due to poor compliance or the side effects mentioned above.Finally,we evaluated the annual eradication success rates in a total of 3969 patients who received 2 wk first-line PAC therapy.The endoscopic and clinical findings in patients who received the 2 wk PAC were as follows:gastric ulcer in 855(21.5%);duodenal ulcer in 878(22.1%);gastric and duodenal ulcer in 124(3.1%),erosive,atrophic gastritis and functional dyspepsia in 2055(51.8%);and other findings(e.g.,MALToma,patients who wanted to receive the therapy even though they had no abnormal endoscopic finding) in 57(0.5%).The overall eradication rate of the 2 wk standard firstline triple regimen was 86.5%.The annual eradication rates from 2000 to 2010 were 86.7%,85.4%,86.5%,83.3%,89.9%,90.5%,88.4%,84.5%,89.1%,85.8%,and 88.3%,sequentially(P = 0.06).No definite evidence of a significant change in the eradication rate was seen during the past eleven years.The eradication rates of second-line therapy were 88.9%,82.4%,85%,83.9%,77.3%,85.7%,84.4%,87.3%,83.3%,88.9%,and 84%(P = 0.77).The overall eradication rate of 1 wk quadruple second-line therapy was 84.7%.There was no significant difference in the eradication rate according to the H.pylori associated diseases.CONCLUSION:This study showed that there was no trend change in the H.pylori eradication rate over the most recent 11 years in our institution.

Polymorphism of -765G > C COX-2 is a risk factor for gastric adenocarcinoma and peptic ulcer disease in addition to H pylori infection:A study from northern India

AIM: To investigate -765G > C COX-2 polymorphism and H pylori infection in patients with gastric adenocarcinoma, peptic ulcer disease (PUD) and non- ulcer dyspepsia (NUD). METHODS: We enrolled 348 adult patients (62 gastric adenocarcinoma, 45 PUD and 241 NUD) undergoing upper gastrointestinal endoscopy at two referral centers between September, 2002 and May, 2007. H pylori infection was diagnosed when any of the four tests (RUT, culture, histopathology and PCR) were positive. Genotyping for -765G > C polymorphism of COX-2 was performed by PCR-RFLP analysis. RESULTS: Frequency of C carrier had significantassociation with gastric adenocarcinoma as compared to NUD [77.4% vs 29%, P < 0.001, odds ratio (OR) 8.20; 95% confidence interval (95% CI), 4.08-16.47] and PUD (77.4% vs 31.1%, P < 0.001; OR 8.04; 95% CI, 3.25-19.90). Risk of gastric adenocarcinoma was significantly higher in patients having C carrier with (OR 7.83; 95% CI 3.09-19.85) and without H pylori infection (OR 7.06; 95% CI, 2.61-19.09). Patients with C carrier and H pylori infection had significant risk for the development of PUD (P < 0.001; OR 5.65; 95% CI, 2.07-15.34). CONCLUSION: -765G > C COX-2 polymorphism with or without H pylori could be a marker for genetic susceptibility to gastric adenocarcinoma. COX-2 polymorphism in presence of H pylori infection might be useful in predicting the risk of PUD.

Gastric carcinoid in a patient infected with Helicobacter pylori:A new entity?

There are four types of gastric carcinoid tumors, classified according to their histology and malignant potential. Only a few cases of carcinoid tumors in patients infected with Helicobacter pylori （H. pylor/） have been reported so far. We report a patient infected with H. pylori presenting with a small solitary gastric carcinoid tumor with very low proliferative rate and normal gas- trin levels. The tumor was endoscopically removed and the patient received an eradication therapy against H. pylori. No signs of metastatic disease have been found so far during more than 3 year of follow-up. Infection with H. pylori may cause chronic gastritis with normal or elevated gastrin levels, leading to the develop- ment of gastric carcinoids by mechanisms unrelated to gastrin. Enterochromaffin-like cell tumors related to a chronic H. pylori infection may be considered as a distinct type of gastric carcinoid tumors.

Effects of Helicobacterpyloriinfection on gastric emptying rate in patients with non-ulcer dyspepsia

AIM:The pathogenesis of delayed gastric emptying in patients with non-ulcer dyspepsia(NUD)remains unclear. We aimed to examine whether gastric emptying rate in NUD patients was associated with Helicobacter pylori(Hpylori) infection and whether it was affected by eradication of the infection. METHODS:Gastric emptying rate of a mixed solid-liquid meal was assessed by the paracetamol absorption method in NUD patients and asymptomatic controls(n=17).Hpylori status was assessed by serology and biopsy urease test. H pylori-positive NUD patients(n=23)received 10-day triple eradication therapy.Hpyloristatus was re-assessed by biopsy urease test four weeks later,and if eradication was confirmed,gastric emptying rate was re-evaluated. RESULTS:Thirty-three NUD patients and 17 controls were evaluated.NUD patients had significantly delayed gastric emptying compared with controls.The mean maximum plasma paracetamol concentration divided by body mass (Cmax/BM)was 0.173 and 0.224 mg/L.kg respectively (P=0.02),the mean area under plasma paracetamol concentration-time curve divided by body mass(AUC/BM) was 18.42 and 24.39 mg.min/L.kg respectively(P=0.01). Gastric emptying rate did not differ significantly between H pylori-positive and H pylori-negative NUD patients.The mean Cmax/BM was 0.172 and 0.177 mg/L·kg respectively (P=0.58),the mean AUC/BM was 18.43 and 18.38 mg·min/ L·kg respectively(P=0.91).Among 14 NUD patients who were initially H pylori-positive,confirmed eradication of the infection did not significantly alter gastric emptying rate. The mean Cmax/BM was 0.171 and 0.160 mg/L.kg before and after Hp eradication,respectively(P=0.64),the mean AUC/BM was 17.41 and 18.02 mg.min/L.kg before and after eradication,respectively(P=0.93). CONCLUSION:Although gastric emptying is delayed in NUD patients compared with controls,gastric emptying rate is not associated with H pylori status nor it is affected by eradication of the infection.

Improvement in symptoms after H_2-receptor antagonist-based therapy for eradication of H pylori infection

AIM: To investigate the therapeutic effects of triple therapy combining lafutidine with clarithromycin and amoxicillin on H pylori infection and the resolution of gastroesophageal symptoms after eradication. METHODS: We conducted a randomized, multicenter, open-label controlled trial to compare the effective-ness of a triple therapy of lafutidine, clarithromycin, and amoxicillin (lafutidine group) with that of a triple therapy of lansoprazole, clarithromycin, and amoxicillin (lansopra- zole group) in patients with H pylori infection. The study group comprised 22 patients with gastric ulcers and 18 patients with duodenal ulcers who had H pylori infection. RESULTS: H pylori eradication rates were similar in the lafutidine group (14/20, 70%) and the lansoprazole group (14/20, 70%). Gastroesophageal reflux and ab-dominal symptoms improved after eradication therapy in both groups, whereas abdominal discomfort, diarrhea, and constipation were unchanged. H pylori status had no apparent effect on improvement of gastroesophageal reflux or abdominal symptoms after treatment. Adverse events were similar in both groups. CONCLUSION: The triple therapy including lafutidine is equivalent to triple therapy including lansoprazole in terms of H pylori eradication rates and improvement in gastroesophageal reflux and abdominal symptoms.These results are attributed to the fact that lafutidine has strong, continuous antisecretory activity, unaffected by CYP2C19 polymorphisms.

Alteration of sister chromatid exchange frequencies in gastric cancer and chronic atrophic gastritis patients with and without H pylori infection

AIM: To determine, by counting sister chromatid exchange (SCE) frequencies, whether genetic impairment and DNA damage have an effect on the pathogenesis of gastric cancer (GC). METHODS: Analysis of SCE is a cytogenetic technique used to show DNA damage as a result of an exchange of DNA fragments between sister chromatids. We analyzed SCE frequency in 24 patients with GC, 26 patients with chronic atrophic gastritis (CAG), and 15 normal controls. The presence of H pylori was confirmed by urease test, toluidine-blue stain and hematoxylin-eosin stain. RESULTS: SCE was significantly increased in H pylori- negative GC patients, and in H pylori-negative CAG patients compared with controls (7.41 ± 1.36 and 6.92 ± 1.20, respectively, vs 5.54 ± 0.8, P < 0.001). There was no difference in the SCE frequency between H pylori- negative GC patients and H pylori-negative CAG patients (P > 0.05). On other hand, the SCE frequencies in H pylori-positive GC patients were higher than those in H pylori-positive CAG patients (9.20 ± 0.94 vs 7.93 ± 0.81, P < 0.01). Furthermore, H pylori-positive GC patients had a higher SCE frequency than H pylori- negative GC patients (9.20 ± 0.94 vs 7.41 ± 1.36, P < 0.001). Similarly, a significant difference was detected between H pylori-positive CAG patients and H pylori-negative CAG patients (7.93 ± 0.81 vs 6.92 ± 1.20, P < 0.05). CONCLUSION: We suggest the increased SCE in patients reflects a genomic instability that may be operative in gastric carcinogenesis.

Helicobacter pylori-infected animal models are extremely suitable for the investigation of gastric carcinogenesis

Although various animal models have been developed to clarify gastric carcinogenesis, apparent mechanism of gastric cancer was not clarified in recent years. Since the recognition of the pathogenicity of Helocobacter pylori（H pylori）, several animal models with H pylori infection have been developed to confirm the association between Hpylori and gastric cancer. Nonhuman primate and rodent models were suitable for this study. Japanese monkey model revealed atrophic gastritis and p53 mutation after long-term infection of Hpylori. Mongolian gerbil model showed the development of gastric carcinoma with H pylori infection alone, as well as with combination of chemical carcinogens, such as N-methyl- N-nitrosourea and N-methyl-N-nitro-N＇-nitrosoguanidine. The histopathological changes of these animal models after H pylori inoculation are closely similar to those in human beings with Hpylori infection. Eradication therapy attenuated the development of gastric cancer in Hpylori- infected Mongolian gerbil. Although several features of animal models differ from those seen in human beings, these experimental models provide a starting point for further studies to clarify the mechanism of gastric carcinogenesis as a result of Hpylon infection and assist the planning of eradication therapy to prevent gastric carcinoma.

Latest insights into the effects of Helicobacter pylori infection on gastric carcinogenesis

There appears to be the strong association between Helicobacter pylori （H pylori） and gastric cancer. We reviewed the latest evidences about the effects of H pylori infection on gastric carcinogenesis, classified into epidemiology, dynamics of gastric mucosal changes, DNA damages, virulence factors, host factors, and source of gastric malignancy. Through the considerable progress made in research into virulence factors resulting from differences between Hpylori strains, such as cagA positivity, as well as into host factors, such as gene polymorphisms, a diverse spectrum of H pyloriassociated diseases, including gastric cancer, is beginning to lend itself to elucidation. The impact of the novel hypothesis advanced by Houghton et al proposing bonemarrow derived stem cells （BMDC） as a potential source of gastric malignancy on evolving research remains to be seen with interest. Further progress in research into H pylori eradication as a viable prophylaxis of gastric cancer, as well as into the mechanisms of gastric carcinogenesis, is to be eagerly awaited for the current year and beyond.

Retinol-binding protein, acute phase reactants and Helicobacter pylori infection in patients with gastric adenocarcinoma

AIM： To determine the serum levels of c-reactive protein （CRP）, transferrin （TRF）, a2-macroglobulin （A2M）, ceruloplasmin （CER）, al-acid glycoprotein （AAG）, prealbumin （P-ALB） and retinol-binding protein （RBP） in gastric carcinoma patients and to explore their possible correlation with underlying Helicobacter pylori （H pylon） infection. METHODS： We measured the serum levels of CRP, TRF, A2M, CER, AAG, P-ALB, and RBP in 153 preoperative patients （93 males; mean age： 63.1±11.3 years） with non-cardia gastric adenocarcinoma and 19 healthy subjects. RESULTS： The levels of CRP, CER, RBP, and AAG in cancer patients were significantly higher than those in healthy controls （P〈0.0001）, while no difference was found regarding the TRF, P-ALB, and A2M levels. Cancer patients with H py/ori infection had significantly lower RBP values compared to non-infected ones （P〈0.0001） and also higher values of CRP and AAG （P = 0.09 andP = 0.08, respectively）. CONCLUSION： High serum levels of CRP, CER and AAG in cancer patients do not seem to be related to H pylori infection. Retinol-binding protein seems to discriminate between infected and non-infected patients with gastric carcinoma. Further studies are needed to explore if it is directly involved in the pathogenesis of the disease or is merely an epiphenomenon.

H pylori and host interactions that influence pathogenesis

H py/ori is probably the most prevalent human pathogen worldwide. Since it was initially suggested in 1983 by Marshall and Warren to be implicated in gastritis and peptic ulcer disease, H pylori has also been implicated in gastric carcinoma and was classified as a class I carcinogen. In the last two decades, a noteworthy body of research has revealed the multiple processes that this gram negative bacterium activates to cause gastroduodenal disease in humans. Most infections are acquired early in life and may persist for the life of the individual. While infected individuals mount an inflammatory response that becomes chronic, along with a detectable adaptive immune response, these responses are ineffective in clearing the infection. Hpylori has unique features that allow it to reside within the harsh conditions of the gastric environment, and also to evade the host immune response. In this review, we discuss the various virulence factors expressed by this bacterium and how they interact with the host epithelium to influence pathogenesis.