Chinese Consensus Report on Family-Based Helicobacter pylori Infection Control and Management (2021 Edition).

OBJECTIVE: Helicobacter pylori infection is mostly a family-based infectious disease. To facilitate its prevention and management, a national consensus meeting was held to review current evidence and propose strategies for population-wide and family-based H. pylori infection control and management to reduce the related disease burden. METHODS: Fifty-seven experts from 41 major universities and institutions in 20 provinces/regions of mainland China were invited to review evidence and modify statements using Delphi process and grading of recommendations assessment, development and evaluation system. The consensus level was defined as ≥80% for agreement on the proposed statements. RESULTS: Experts discussed and modified the original 23 statements on family-based H. pylori infection transmission, control and management, and reached consensus on 16 statements. The final report consists of three parts: (1) H. pylori infection and transmission among family members, (2) prevention and management of H. pylori infection in children and elderly people within households, and (3) strategies for prevention and management of H. pylori infection for family members. In addition to the 'test-and-treat' and 'screen-and-treat' strategies, this consensus also introduced a novel third 'family-based H. pylori infection control and management' strategy to prevent its intrafamilial transmission and development of related diseases. CONCLUSION: H. pylori is transmissible from person to person, and among family members. A family-based H. pylori prevention and eradication strategy would be a suitable approach to prevent its intra-familial transmission and related diseases. The notion and practice would be beneficial not only for Chinese residents but also valuable as a reference for other highly infected areas.

[Jinghuaweikang gelatin pearls plus proton pump inhibitor-based triple regimen in the treatment of chronic atrophic gastritis with Helicobacter pylori infection: a multicenter, randomized, controlled clinical study].

OBJECTIVE: To observe the efficacy of Jinghuaweikang gelatin pearls plus proton pump inhibitor (PPI)-based triple regimen in the treatment of chronic atrophic gastritis (CAG) patients with Helicobacter pylori (H.pylori) infection. METHODS: For this multicenter, randomized, controlled clinical study, 90 patients of endoscopically confirmed CAG with positive H.pylori ((13)C or (14)C-urea breath test (UBT) or rapid urease test) were enrolled. There were 46 males and 44 females with an age range of (54 ± 10) years. None of them had H.pylori eradication background. They were randomly divided into 2 groups, Group LACJ (n = 45) received lansoprazole 30 mg+amoxicillin 1000 mg+clarithromycin 500 mg + jinghuaweikang gelatin pearls 240 mg, twice daily, for 10 days (d1-10) plus another 14 days (d11-24) only with jinghuaweikang gelatin pearls 240 mg, twice daily. Group LACB (n = 45) had standard quadruple regimen treatment: lansoprazole 30 mg+amoxicillin 1000 mg+clarithromycin 500 mg+bismuth potassium citrate 220 mg, twice daily for 10 days (d1-10). The status of H.pylori was detected by (13)C-UBT at least 28 days after therapy. RESULTS: The eradication rates in Groups LACJ and LACB were as follows: per-protocol (PP): 70.5% (31/44) and 83.3% (35/42), intention-to-treat (ITT): 68.9% (31/45) and 77.8% (35/45) (both P > 0.05). The symptomatic improvements of bloating in upper abdomen, belching and epigastric pain after treatment in both groups. And those in Group LACJ was higher than those of Group LACB, but no statistical difference existed between two groups (all P > 0.05). CONCLUSIONS: The efficacy of LACJ for the treatment of CAG patients with H.pylori infection is similar to LACB. And the symptomatic improvement of patients is better than LACB.

[Ilaprazole based bismuth-containing quadruple regimen for the first-line treatment of Helicobacter pylori infection: a multicenter, randomized, controlled clinical study].

OBJECTIVE: To explore the effects of 7-day quadruple regimen as the first-line therapy strategy for Helicobacter pylori(H. pylori)infection and compare the eradication rate of ilaprazole versus esoprazole-based regimen. METHODS: A total of 440 patients with H. pylori infection, who had never received H. pylori eradication treatment, were enrolled from 10 domestic hospitals from October 2010 to July 2011. Diagnosed as chronic gastritis or duodenal ulcer according to their endoscopic examination results, they were randomized into ilaprazole and(or) esoprazole-based bismuth-containing quadruple regimen group with amoxicillin and clarithromycin (n = 110 each). After a 7-day eradication treatment, all patients with duodenal ulcer received PPI (ilaprazole and(or) esoprazole) treatment for 14 days and (13)C urea breath test was performed at least 28 days after the end of therapy. The patients with failed eradication treatment underwent endoscopy examination and biopsy. H. pylori culture and detection of antibiotic-resistant genes were also performed. RESULTS: In gastritis patients, the eradication rate (per-protocol, PP value) were 78.2% (79/101) and 82.0% (82/100) in ilaprazole and esoprazole groups (P = 0.50) while the (intention-to-treat) ITT value of eradication rate were 71.8% (79/110) and 74.5% (82/110) in ilaprazole and esoprazole groups respectively (P = 0.65). And there was no statistical difference (P > 0.05). In duodenal patients, the eradication rate (PP) were 92.1% (93/101) and 91.4% (96/105) in ilaprazole and esoprazole group (P = 0.86) while the ITT value of eradication rate were 84.5% (93/110) and 87.3% (96/110) in ilaprazole and esoprazole groups respectively (P = 0.56). And no significant difference existed between two groups in gastritis and duodenal ulcer patients (P > 0.05). In total, the eradication rate was 80.1% (161/201) (PP) and 73.2% (161/220) (ITT), 91.7% (189/206) (PP) and 85.9% (189/220) (ITT) in chronic gastritis and duodenal ulcer patients respectively. The symptomatic improvements of stomachache, burning, belching and nausea remained almost unchanged. No severe side effect was observed. The point mutations for clarithromycin resistance were detected in all 53 H. pylori strains (100%) isolated from the patients with failed eradication treatment. CONCLUSIONS: The eradication rate of PPI based bismuth-containing quadruple regimen as the first-line treatment is satisfactory in chronic gastritis and duodenal ulcer patients. No significant difference exists between the effects of ilaprazole and esoprazole-based groups. And the treatment failure may be attributed mainly to the clarithromycin resistance of H. pylori.

[Jinghuaweikang capsules combined with triple therapy in the treatment of Helicobacter pylori associated gastritis and duodenal ulcer and analysis of antibiotic resistance: a multicenter, randomized, controlled, clinical study].

OBJECTIVE: To explore the efficacy of Jinghuaweikang capsules plus triple therapy (LACJ) in treatment of Helicobacter pylori (H. pylori) associated gastritis or duodenal ulcer, compare it with bismuth-containing quadruple therapy (LACB) and standard triple therapy (LAC) and analyze the antibiotic sensitivity of gastric mucosal H. pylori strains from the failed patients. METHODS: A total of 565 patients with H. pylori infection were recruited from 11 hospitals from January 2010 to June 2011. There were 336 males and 229 females. They underwent gastroendoscopy examination due to upper gastrointestinal symptoms and had never received H. pylori eradication therapies. Duodenal ulcer patients were divided randomly into LACJ therapy group, LACB therapy group and LAC therapy group while gastritis patients LACJ therapy group and LACB therapy group. Group LAC received lansoprazole 30 mg + amoxicillin 1000 mg + clarithromycin 500 mg, twice a day, for 7 d (d1-7). Group LACJ: LAC therapy plus Jinghuaweikang, 3 capsules, twice a day, for 7 d (d1-7) then Jinghuaweikang, 3 capsules, twice a day, for 14 d (d8-21). Group LACB: LAC plus bismuth potassium citrate 220 mg, twice a day, for 7 d (d1-7) and then bismuth potassium citrate 220 mg, twice a day, for 14 d (d8-21). All duodenal ulcer patients received lansoprazole (30 mg, once a day) for 14 days after the first 7-day of treatment (d 8-21). At least 28 days after the end of treatment, all patients underwent (13)C urea breath test. Gastric mucosa was collected under endoscopy from the failed patients. The detection technique of gene chip was employed to detect antibiotics resistant gene from mucosa. RESULTS: The eradication rates of duodenal ulcer patients in groups LACJ, LACB and LAC were as follows: per-protocol (PP), 80.2% (77/96), 89.9% (89/99) and 72.2% (70/97) (P = 0.007), intention-to-treat (ITT), 78.6% (77/98), 88.1% (89/101) and 70.0% (70/100) (P = 0.007). No statistical differences existed between groups LACJ and LACB or LAC (all P > 0.05). But there were statistical differences between groups LACB and LAC (both P = 0.002). The eradication rates of PP and ITT of chronic gastritis patients in groups LACJ and LACB were as follows: 75.8% (97/128), 74.6% (97/130) vs 83.8% (109/130), 80.1% (109/136) (both P > 0.05). The symptomatic improvements of abdominal pain, burning and acid reflux of duodenal ulcer patients in group LACJ were higher than those in groups LACB and LAC. There were statistical differences between groups LACJ and LAC (all P < 0.05). The symptomatic improvements of bloating and belching for chronic gastritis patients in group LACJ were higher than those of group LACB. But no significant difference existed between two groups (all P > 0.05). Sixty samples of gastric mucosa were collected from the failed patients. The detection rates of antibiotic-resistant gene to clarithromycin and amoxicillin were 60.0% (36/36) and 18.3% (11/60) respectively. CONCLUSIONS: The efficacy of LACJ for the treatment of H. pylori infection patients is similar to LACB and superior to LAC. And the symptomatic improvement of patients is better than the other two regimens. The main cause of treatment failure is antibiotic resistance of H. pylori strains.

[Effect of furazolidone quadruple regimen plus dental plaque removal procedures as rescue treatment of refractory Helicobacter pylori infection].

OBJECTIVE: To observe the effect of furazolidone quadruple regimen plus dental plaque removal procedures as rescue treatment of refractory H. pylori infection. METHODS: A total of 104 patients with H. pylori positive [(13)C-urea breath test (UBT) or rapid urease test positive] failing in previous treatment two or more were enrolled and divided into 2 groups. One group (n = 64) were given quadruple regimen [proton pump inhibitor (PPI) + bismuth + amoxicillin + furazolidone, 10 days] treatment and dental plaque removal treatment. And the others (n = 40) received only quadruple regimen treatment. The status of H. pylori was detected by (13)C-UBT at 4 weeks post-therapy and the eradication rates of two groups were compared. RESULTS: The eradication rate of quadruple regimen + dental treatment group was 85.9% (55/64) while that of the other group 72.5% (29/40) (P = 0.091). CONCLUSION: The PPI + bismuth quadruple regimen plus dental plaque removal procedures as rescue treatment may boost the eradication rate of refractory H. pylori infection patients. And the furazolidone quadruple therapy can be chosen for the treatment of refractory H. pylori infection. Oral H. pylori infection may play a role in the failure of H. pylori infection treatment.

[A multicenter study of Chinese patent medicine wenweishu/yangweishu in the treatment of Helicobacter pylori positive patients with chronic gastritis and peptic ulcer].

OBJECTIVE: To evaluate the efficacy of Chinese patent medicine wenweishu /yangweishu in the treatment of Helicobacter pylori (H. pylori) positive patients with chronic gastritis and peptic ulcer. METHODS: A randomized, controlled and multicenter trial was conducted in 642 H. pylori positive patients with chronic gastritis or peptic ulcer. They were randomized to three groups: PCM group (n = 222, pantoprazole 40 mg twice a day, clarithromycin 500 mg twice a day, metronidazole 400 mg twice a day, for 7 days); PCM plus wenweishu group (n = 196); and PCM plus yangweishu group (n = 224). (14)C breath test was performed 4 weeks after therapy. For the patients with gastric ulcer, ulcer healing was determined by endoscopy after therapy. RESULTS: Intention-to-treat H. pylori eradication rate for PCM group, PCM plus wenweishu group, and PCM plus yangweishu group were 57.2% (127/222), 62.2% (122/196), 60.3% (135/224), respectively (P = 0.295, 0.512). Per-protocol H. pylori eradication rates were 62.3% (127/204), 70.1% (122/174), 65.2% (135/207), respectively (P = 0.108, 0.532).Per-protocol analysis gastric ulcer healing rate were 61.9% (13/21) 100.0% (18/18), 86.4% (19/22) respectively. The healing rate in PCM plus wenweishu groups was statistically significantly higher than the rate in PCM group (P = 0.004). The rates of symptom relief in PCM plus wenweishu groups and PCM plus yangweishu were statistically significantly higher than the rate in PCM group (both P < 0.01). Side-effects were rare and comparable between groups. CONCLUSION: Although PCM combined with wenweishu or yangweishu in the treatment of H. pylori positive patients with chronic gastritis and peptic ulcer can not reach a significantly higher eradication rate, it can increase the rates of both gastric ulcer healing and symptom relief.

[Levofloxacin-based triple therapy for first-line Helicobacter pylori eradication treatment: a multi-central, randomized, controlled clinical study].

OBJECTIVE: To compare efficacy and tolerability of 7-day standard triple therapy versus 7-day levofloxacin-based triple therapy in first-line treatment for Helicobacter pylori (H. pylori) infection. METHODS: Three hundred consecutive H.pylori positive patients were randomized to receive: clarithromycin, amoxicillin, lansoprazole (Group A: n = 150); or amoxicillin, levofloxacin, lansoprazole (Group B: n = 150). H. pylori status was rechecked by (13)C-urea breath test 4 weeks after the end of therapy. RESULTS: The eradication rates in intention to treat (ITT) and per protocol (PP) analyses were: Group A, 74.5% (111/149) and 78.2% (111/142); and Group B, 82.4% (122/148) and 83.0%(122/147). Although the eradication rate achieved with levofloxacin-based triple therapy was higher than that with standard therapies in either ITT or PP analysis, but no significantly difference was found between the two triple therapies. The incidence of side effects was similar among groups. CONCLUSIONS: A 7-day levofloxacin-based triple therapy can achieve higher H.pylori eradication rate than standard regimen. The levofloxacin-based regimen can be one effective therapy for the first-line anti-H.pylori treatment.

[Identification of biomarkers for early detection in gastric cancer and its clinical biological significance.].

OBJECTIVE: To systematically understand the cellular and molecular mechanism of gastric cancer (GC) development and to discover early diagnosis and predictive biomarkers, which will be used for early diagnosis and novel treatment targets. METHODS: 70 mer 22 K-oligonucleotide microarrays and bioinformatic analysis were conducted to recognize gene expression profiles in GC and normal appearing tissue (NAT). The control group was collected from non-tumor patients including 20 specimen mixture as a common reference (CR) and 5 individuals as additional control. Our results showed that 837 different expression genes (DEGs) were identified in GC while 570 DEGs were in NATs by Bayesian analysis (P<0.001, Fold change>2.0) as compared respectively with CR. An interesting finding is that we identified 67 over-expressed genes in both GC and NAT tissues, and these gene expression alterations could not be detected by comparison of GC with NATs, which were normally used in routine experiment design. Most of these genes were involved in the control of cell proliferation, metabolism and differentiation. RESULTS: These differential expressed genes were confirmed at mRNA and protein levels in primary tumors using RT-PCR and immunohistochemistry (IHC). The results showed that three genes, EGR1, CYR61 and ADAMTS1 were over expressed in both GC and NATs at mRNA level. These results were consistent with oligo microarray data. Another interesting finding is that these three genes were also over-expressed in intestinal metaplasia (IM) and dysplasia (DYS), which indicated that these three genes might be potential biomakers for early detection of GC. CONCLUSION: Through the systematic analysis of gene expression profiles in GC tissues, NAT and CR normal tissues, we identified a group of genes over-expressed both in GC and precancerous lesions, which might be potential biomarkers for early GC diagnosis.

[Genotypic homogeneity and susceptibility to clarithromycin for clarithromycin-resistant Helicobacter pylori strains].

OBJECTIVE: To investigate the mixed infection of clarithromycin susceptibility and genotype of Helicobacter pylori resistant strains. METHODS: Ten single colonies were picked randomly from each of 16 resistant strains. Genomic DNA was prepared from single colony isolates and their parental clarithromycin-resistant strains by the hexadecyltrimethylammonium bromide (CTAB)-phenol extraction method. Susceptibilities of single colony isolates to clarithromycin were determined by agar dilution and mutations in clarithromycin-resistant isolates identified by polymerase chain reaction and restrictions analysis. Genotypes of 16 resistant strains and their single colony isolates were tested by the fingerprinting patterns of random amplified polymorphic DNA (RAPD). RESULTS: All single colony isolates derived from 16 resistant strains were also resistant to clarithromycin and had the A2143G point mutation in 23 S rRNA gene. The RAPD fingerprints of single colony isolates derived from the same patient were identical to each other and to the RAPD fingerprint of the corresponding parental isolate. CONCLUSION: Neither mixed susceptibility nor mixed genotype was found in clarithromycin resistant strains.

[Establishment of Mongolian gerbil model of long-term Helicobacter pylori infection].

OBJECTIVE: To establish a model of long-term infection with Helicobacter pylori (Hp) in Mongolian gerbil (Meriones unguiculatus), and to investigate if Hp combined with N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) has a synergistic effect to induce gastric mucosa injury. To investigate pathological changes of gastric mucosa during long-term Hp infection in Mongolian gerbil model. METHODS: 90 healthy male Mongolian gerbils were randomly divided into 4 groups: Hp group (n = 24) undergoing gastric perfusion of Hp suspension of the line NCTC11637 in brain-heart infusion (BHI) 10(8)-10(9) CFU/ml once a day for 10 days and then gastric perfusion of 1 ml normal saline (NS) once a day for 10 days since the 4th week after Hp perfusion, Hp + MNNG group (n = 24) undergoing gastric perfusion of Hp solution once a day for 10 days and then MNNG 1 ml (2 mg/ml) once a day for 10 days, MNNG group (n = 20) undergoing gastric perfusion of BHI once a day for 10 days and then gastric perfusion of MNNC once a day for 10 day since the 4th week after BHI perfusion, and control group (n = 22) undergoing gastric perfusion of BHI once a day for 10 days and then gastric perfusion of NS again once a day for 10 day since the 4th week after the BHI perfusion. 4 and 8 weeks 1 gerbil from the control group and 2 gerbils from the Hp and Hp + MNNG groups each were killed to observe the pathological changes and Hp colonization by liquid-based urease test and Warthin-Starry silver staining. 20 and 40 weeks after the Hp inoculation 10 gerbils from each group were killed to observe the pathology of the gastric mucosa. RESULTS: (1) A Mongolian gerbil model of long-term Hp infection was successfully established. (2) Hp induced the process progressing from normal gastric mucosa --> chronic atrophic gastritis --> intestinal metaplasia --> dysplasia. Until 40 weeks after Hp infection, the gastric mucosa of the control group remained normal. Twenty weeks after Hp infection 3 gerbils in the Hp group and 1 gerbil in the Hp + MNNC group showed glandular atrophy and intestinal metaplasia respectively, and 40 weeks after infection, glandular atrophy, intestinal metaplasia, and dysplasia at different degrees in the gastric mucosa were seen in the three experimental groups. The pathological changes of the Hp + MNNG group were the most severe. The incidence rates of precancerous lesions of the Hp + MNNG group were significantly higher than those of the other groups, but no gastric carcinoma was found in the experimental animals. CONCLUSION: Hp colonizes stably in the glandular gastric mucosa of Mongolian gerbils. The histological changes after infection are similar to those of the Hp infected human being. Hp and MNNG both cause the injury of gastric mucosa. With synergistic effect, the two pathogenic agents attack the gastric mucosa, they cause more severe injury.

Interaction or relationship between Helicobacter pylori and non-steroidal anti-inflammatory drugs in upper gastrointestinal diseases.

According to a meta-analysis, H pylori and non-steroidal anti-inflammatory drugs (NSAID) independently and significantly increase the risk of gastroduodenal ulcer and ulcer bleeding. Their coincidence is frequent, demonstration of a possible relationship and consequent attitude is of important implications. But unfortunately, no consensus has been approved in the past years and their interactions are still controversial. H pylori and NSAID are known to share a number of pathogenic mechanisms, but there is no evidence for the significant synergic action between these two risk factors. Their relationship is independent, additive, synergistic or antagonistic without considering the influence of other factors because studies on this subject are different in almost all aspects of their methodology, including the definition of a NSAID user as well as the types, doses, duration and their indications for NSAID use, as well as their end-points, definition of dyspepsia and regimes used for eradication of H pylori. These might contribute to the conflicting results and opinions. H pylori infection in humans does not act synergistically with NSAID on ulcer healing, and there is no need to eradicate it. This notion is supported by the finding that the eradication of H pylori does not affect NSAID-induced gastropathy treated with omeprazole and that H pylori infection induces a strong cyclooxygenase-2 (COX-2) expression resulting in excessive biosynthesis of gastroprotective prostaglandin which in turn counteracts NSAID-induced gastropathy and heals the existing ulcer. Other investigators claimed that H pylori infection acts synergistically with NSAID on ulcer development, and H pylori should be eradicated, particularly at the start of long-term NSAID therapy. Eradication of H pylori prior to NSAID treatment does not appear to accelerate ulcer healing or to prevent recurrent ulcers in NSAID users. However, some recommendations can be drawn from the results of clinical trails.

[Influence of resistance of Helicobacter pylori to antibiotics on the Helicobacter pylori eradication regimens].

OBJECTIVE: To investigate the influence of resistance of Helicobacter pylori (H. pylori) to antibiotics on the efficacy of lansoprazole triple therapy for H. pylori eradication. METHODS: 157 patients, 102 males and 55 females, aged 42.7 (18 - 70), with upper abdominal symptoms, 59 with chronic gastritis and 98 with peptic ulcer, underwent gastroendoscopy 157 H. pylori strains were isolated from the gastric biopsy specimens of these patients and cultured. Minimal inhibitory concentrations of 3 antibiotics (metronidazole and clarithromycin) were determined by E-test. The 157 patients were treated by triple therapies, including lansoprazole, metronidazole, and clarithromycin for 7 days. Reexamination was done at least 4 weeks after the therapy. RESULTS: The resistance rates of H. pylori to metronidazole and clarithromycin were 45.9% (72/157) and 18.5% (29/157) respectively. The reexamination showed an eradication rate of H. pylori of 61.8% (97/157). The eradication rates of the metronidazole-sensitive and resistant strains were 89.4% (76/85) and 29.2% (21/72) respectively (P < 0.01), and the eradication rates of the clarithromycin-sensitive and resistant strains were 72.7% (93/128) and 16.0% (4/29) respectively (P < 0.01). Presence of a gastroduodenal ulcer, age and gender did not differ significantly between the eradicated and non-eradicated groups (all P > 0.05). CONCLUSION: Resistance of H. pylori to antibiotics is the most important cause of the failure of H. pylori eradication.

[Preventive effects of teprenone on gastric mucosal lesions induced by Helicobacter pylori in mice].

OBJECTIVE: To determine the preventive effect of teprenone on gastric mucosal injury induced with Helicobacter pylori concentrated culture supernatant (CCS) in Balb/c mice. METHODS: Gastric mucosa lesions were induced with intragastrical administration of Helicobacter pylori CCS. Sixty Balb/c mice were divided into control group, injury group, sucralfate protective group and teprenone protective group. Mice of two protective groups were pretreated with sucralfate or teprenone respectively before induction of gastric mucosa lesions. Mucosal changes were assessed by microscopic examination, quantitative histology and electron microscopy. RESULTS: Histologic and ultrastructural lesions in protective groups were less severe than those in injury group. Epithelial damage scoring (EDS) of teprenone protective group (1.68 +/- 0.69) and sucralfate protective group (1.72 +/- 0.73) were significantly decreased than injury group (2.47 +/- 0.58, P < 0.05). CONCLUSION: Teprenone as well as sucralfate reduces gastric mucosal lesions induced by Helicobacter pylori CCS in mice.

[Relations of transforming growth factor-beta1 expression to differentiation and prognosis of advanced gastric cancer].

OBJECTIVE: To clarify the correlation of transforming growth factor-beta1 (TGF-beta1) expression with the differentiation and prognosis of advanced gastric cancer (GC). METHODS: Whole genome expression chip hybridization, was used to detect the expression of TGF-beta1 and TGF-betaR1 in 20 specimens of intestinal-type GC and para-cancer tissues. RT-PCR and immunohistochemistry (IHC) analysis were used to detect the mRNA and protein expression of TGF-beta1 and TGF-betaR1 in 30 specimens of intestinal-type GC tissue and para-cancer tissues. The mixture of gastric mucosa tissues from 20 non-tumor patients was used as common reference. RESULTS: The expression level of TGF-beta1 and TGF-betaR-1 genes was higher in the GC tissues than in the para-cancer tissues. However, the expression of Smad gene family was not significantly different between the GC tissues and para-tumor normal tissues. TGF-beta1 gene expression and TGF-betaR1 gene expression were higher in the GC tissues. RT-PCR showed that both TGF-beta1 and TGF-betaR-1 genes were highly expressed in the mRNA level in 21 of the 30 CC patients IHC showed that TGF-beta1 protein was expressed mainly in the cytoplasm. 32 of the 90 specimens of GC tissue were highly positive in TGF-beta1 protein (64%), in comparison with the positive rate of 5% (1/20) in the para-cancer normal tissues. The TGF-beta1 protein expression rate of the highly and moderately differentiated GC tissues was 59% (59%, 23/39), significantly higher than that of the lowly differentiated GC tissues (18%, 9/51, P < 0.01). IHC showed that the TGF-beta R-I rate was 57% (42/74) in the well differentiated specimens, particularly 68% (26/38) in the highly differentiated specimens, and was 44% in the poorly differentiated GC (6/20, P < 0.05). Log rank test showed that the prognosis of the patients positive in TGF-beta1 was significantly better than those negative in TGF-beta1 (P = 0.0058). However, the survival rate did not differ significantly according to TGF-beta R-I expression (P = 0.8453). CONCLUSION: TGF-beta1 expression is significantly correlated with the differentiation degree of GC. Moreover, positive expression of TGF-beta1 is a favorable prognostic factor in advanced GC. Expression of TGF-beta1 may be an important preoperative prognostic variable for advanced GC.

[The epidemiology of Helicobacter pylori resistance to antibiotics in Beijing].

OBJECTIVE: To investigate the prevalence of Helicobacter pylori (H. pylori) resistance to metronidazole, clarithromycin and amoxicillin in Beijing. METHODS: H. pylori strains were cultured from the gastric biopsy samples obtained from 159 patients with upper abdominal symptoms by gastroendoscopy. Minimal inhibitory concentrations of antibiotics were determined by E-test method. RESULTS: The resistance rates of H. pylori to metronidazole and clarithromycin in Beijing were 36.0% (18/50) and 10.0% (5/50) in 1999-2000, 43.1% (47/109) and 18.3% (20/109) in 2001-2002, respectively. H. pylori resistance to both metronidazole and clarithromycin were 10.0% (5/50) in 1999-2000 and 14.7% (16/109) in 2001-2002. Only one strain was found resistant to amoxicillin in 49 patients. CONCLUSION: The resistance rates of H. pylori to metronidazole and clarithromycin were increased in Beijing in recent years. The strains resistant to amoxicillin were rare.