Gastroduodenal pathology in patients with asymptomatic gallbladder stones.

BACKGROUND/AIMS: Gallbladder stones are still a common pathology worldwide, and the number of patients diagnosed without any symptoms is increasing due to the use of ultrasound and imaging tools such as CT and MRI. The aim of this study was to identify gastroduodenal pathologies in patients with diagnosed asymptomatic gallbladder stones, since some cases of epigastric pain may have led to unnecessary cholecystectomies. METHODOLOGY: Gastroscopic investigations were performed in 33 patients diagnosed with asymptomatic gallbladder stones during a gallstone screening program in Chiang Mai, Thailand, and followed-up with yearly ultrasound examinations. The mean age of the patients was 56.6 years, and mean follow-up time was 2.3 years. RESULTS: Our results showed that inflammatory-based gastroduodenal lesions in this group were common (15/33 patients, 45.4%). Lesions included gastric ulcers (1 patient, 3%), duodenal ulcers (5 patients, 15.1%), and gastroduodenal ulcers (2 patients, 6.1%). Almost all of the ulcers were in the healing or scarring stage. Inflammatory-based mucosal changes were also detected in these patients as follows: erosive gastritis (6 patients, 18.2%) and hemorrhagic gastritis (1 patient, 3%). CONCLUSIONS: Inflammatory-based gastroduodenal pathologies such as peptic ulcers and gastritis are common in patients with asymptomatic gallstones. If such patients become symptomatic, meticulous examinations are needed to avoid unnecessary cholecystectomies and resulting complications such as postcholecystectomy syndrome. The theory that gastroduodenal lesions occur after gallbladder removal needs to be re-evaluated given that lesions can be detected before surgery and even before the occurrence of symptoms.

Systematic review and meta-analysis: Helicobacter pylori eradication therapy after simple closure of perforated duodenal ulcer.

BACKGROUND: The most common complications of peptic ulcer are bleeding and perforation. In many regions, definitive acid reduction surgery has given way to simple closure and Helicobacter pylori eradication. AIM: To perform a systematic review and meta-analysis to ask whether this change in practice is in fact justified. MATERIALS AND METHODS: A search on the Cochrane Controlled Trials Register, Medline, and Embase was made for controlled trials of duodenal ulcer perforation patients using simple closure method plus postoperative H. pylori eradication therapy versus simple closure plus antisecretory non-eradication therapy. The long-term results for prevention of ulcer recurrence were compared. RESULTS: The pooled incidence of 1-year ulcer recurrence in H. pylori eradication group was 5.2% [95% confidence interval (CI) of 0.7 and 9.7], which is significantly lower than that of the control group (35.2%) with 95% CI of 0.25 and 0.45. The pooled relative risk was 0.15 with 95% CI of 0.06 and 0.37. CONCLUSIONS: Helicobacter pylori eradication after simple closure of duodenal ulcer perforation gives better result than the operation plus antisecretory non-eradication therapy for prevention of ulcer recurrence. All duodenal ulcer perforation patients should be tested for H. pylori infection, and eradication therapy is required in all infected patients.

Genetic variation in PSCA is associated with susceptibility to diffuse-type gastric cancer.

Gastric cancer is classified into intestinal and diffuse types, the latter including a highly malignant form, linitis plastica. A two-stage genome-wide association study (stage 1: 85,576 SNPs on 188 cases and 752 references; stage 2: 2,753 SNPs on 749 cases and 750 controls) in Japan identified a significant association between an intronic SNP (rs2976392) in PSCA (prostate stem cell antigen) and diffuse-type gastric cancer (allele-specific odds ratio (OR) = 1.62, 95% CI = 1.38-1.89, P = 1.11 x 10(-9)). The association was far less significant in intestinal-type gastric cancer. We found that PSCA is expressed in differentiating gastric epithelial cells, has a cell-proliferation inhibition activity in vitro and is frequently silenced in gastric cancer. Substitution of the C allele with the risk allele T at a SNP in the first exon (rs2294008, which has r(2) = 0.995, D' = 0.999 with rs2976392) reduces transcriptional activity of an upstream fragment of the gene. The same risk allele was also significantly associated with diffuse-type gastric cancer in 457 cases and 390 controls in Korea (allele-specific OR = 1.90, 95% CI = 1.56-2.33, P = 8.01 x 10(-11)). The polymorphism of the PSCA gene, which is possibly involved in regulating gastric epithelial-cell proliferation, influences susceptibility to diffuse-type gastric cancer.

Normalization of pH level and gastric mucosa after eradication of H. pylori in the remnant stomach.

BACKGROUND: The Updated Sydney System (USS) is used to evaluate chronic gastritis and chronic atrophic gastritis (CAG) due to H. pylori infection. Here, we investigated USS scores and gastric juice pH levels in H. pylori infection-positive or -eradicated patients with remnant stomach after surgery. METHODS: Gastric juice pH levels were measured using pH test-tape in 197 patients (112 H. pylori-positive and 85 H. pylori-negative after eradication) who had undergone distal gastrectomy and conventional H. pylori eradication therapy. RESULTS: In H. pylori infection-positive remnant stomach cases, gastric juice pH showed a reverse correlation with pepsinogen I/II ratio, and H. pylori infection-negative patients following eradication showed associations with the degree of atrophy and intestinal metaplasia at both the anastomosis and in the corpus. Further, pH levels in these patients were normalized time depending after the eradication in the remnant stomach. CONCLUSIONS: Eradication therapy for the remnant stomach contributes to the possible improvement of stomach conditions by controlling the pH level of gastric juice. This effect will be protective against the risk of secondary stomach carcinogenesis in the remnant stomach.

Helicobacter pylori infection, but not genetic polymorphism of CYP2E1, is highly prevalent in gastric cancer patients younger than 40 years.

BACKGROUND: Gastric cancers in young adults are thought to be associated with risk factors that include Helicobacter pylori infection and genetic polymorphism. The objective of this study was to elucidate the roles of these risk factors in patients younger than 40 years by analyzing clinicopathological data and H. pylori infection, and using molecular epidemiologic techniques. METHODS: Clinicopathological features, the presence of H. pylori infection, endoscopic characteristics of gastritis, genetic polymorphism of P4502E1 (CYP2E1), and family history of cancer in patients with gastric cancer treated surgically at Nippon Medical School Hospital from 1991 to 2004 were analyzed, based on our medical database. RESULTS: Gastric cancer in those younger than 40 years was characterized by a predominance of female patients with poorly differentiated adenocarcinoma who had undergone total gastrectomy with extended lymphadenectomy. H. pylori infection had a higher prevalence in patients with gastric cancer than in patients with normal endoscopic results or chronic gastritis, especially in those younger than 40 years (odds ratio, 13.7). Atrophic gastritis, nodular gastritis, and rugal hyperplastic gastritis were observed by endoscopy as H. pylori-associated gastritis. No difference in the incidence of either CYP2E1 genetic polymorphism or a family history of cancer was observed among different age groups. CONCLUSION: Gastric cancer in patients younger than 40 years is closely associated with H. pylori infection, but not with genetic characteristics. Eradication therapy for H. pylori and endoscopic examination of H. pylori-positive young adults may be anticipated to be adopted as a strategy for the prevention and/or early detection of cancer.

Helicobacter pylori infection-negative gastric cancer in Japanese hospital patients: incidence and pathological characteristics.

We used Helicobacter pylori sero-positivity and mucosal atrophy as detected by the serum pepsinogen method to identify H. pylori infection-negative gastric cancer patients with or without atrophy. One hundred and six of 748 (14.2%) primary gastric cancer patients were infection-negative by a serum antibody detection system. Further, 121 (16.2%) of the 748 were negative for gastric mucosal atrophy by the pepsinogen method, of whom 15/748 (2.0%) were H. pylori-negative by pepsinogen I level (>70 ng/mL) and pepsinogen I/II ratio (>3.0). Twenty-seven of 782 (3.6%) gastric cancer patients were H. pylori-negative by antibodies and severe atrophy as determined by pepsinogen I level (<30 ng/mL) and pepsinogen I/II ratio (<2.0). H. pylori-negative gastric cancer patients with severe atrophy likely had a previous infection. These results indicate that the actual number of H. pylori-negative patients is 2.0% at minimum and 10.6% (14.2% minus 3.6%) at maximum in the general Japanese population. Five of 15 (33%) cases displaying neither anti-H. pylori antibodies nor atrophy were intestinal-type and 10 (67%) were diffuse-type adenocarcinomas. Thirteen surgical patients with primary gastric cancer displaying neither antibodies nor mucosal atrophy were further analyzed for pathological and phenotypic characteristics. The mucin phenotype was divided into four gastric, five gastric and intestinal, two intestinal and two null types, independent of histological classification. Intestinal phenotype elements were detected by Cdx2 immunohistochemical methods in nine of 13 (70%) cases examined. We conclude that a small fraction of gastric cancer patients displayed multifactorial carcinogenesis without H. pylori infection, indicating that gastric cancer risk still exists in the absence of H. pylori infection, at an incidence of 2.0% at minimum and 10.6% at maximum in the general Japanese population.

Simple and accurate (13)C-urea breath test for detection of Helicobacter pylori in the remnant stomach after surgery.

BACKGROUND: The efficacy of the (13)C-urea breath test (UBT) for diagnosis of Helicobacter pylori (H. pylori) infection in the remnant stomach after surgery is a matter of controversy. We report a simple and accurate method of (13)C-UBT for diagnosis of H. pylori infection in the remnant stomach after gastrectomy. METHODS: Eighty patients who had undergone gastrectomy with or without subsequent H. pylori eradication therapy were examined a total of 134 times for H. pylori infection by the (13)C-UBT. (13)C-Urea, 10mg per test, was used in powdered form or in the form of film-coated tablets. Breath samples were collected before and 10, 20, and 3 min after ingestion. Mucosal biopsy specimens for bacterial culture and histological examination of the remnant stomach were collected endoscopically after each (13)C-UBT test. RESULTS: Factors that confounded the (13)C-UBT results in the remnant stomach were oral bacteria, posture, and residual food. Lying horizontally on the left side was the best position, and film-coated tablets indicated no necessity for use of mouthwash. The method of anastomosis had no significant effect on the results of the (13)C-UBT. Thirty minutes and a cutoff of 4.5 per thousand were optimal conditions for detection of H. pylori in the remnant stomach. Under these conditions, sensitivity, specificity, and accuracy were 79.4% (27/34 cases), 95.7% (44/46 cases), and 88.8% (71/80 cases), respectively, in ordinary H. pylori diagnosis, and 100% (2/2 cases), 93.3% (14/15 cases), and 94.1% (16/17 cases), respectively, in evaluating eradication at 4 weeks after treatment of H. pylori. CONCLUSIONS: Having the patient lie horizontally on the left side, using a film-coated (13)C-urea tablet without using mouthwash, and measurement at 3 min provided a simple and accurate method of (13)C-urea breath test for detection of H. pylori in the remnant stomach after gastrectomy.

Helicobacter pylori infection in combination with the serum pepsinogen I/II ratio and interleukin-1beta-511 polymorphisms are independent risk factors for gastric cancer in Thais.

BACKGROUND: Thailand has the lowest incidence of gastric cancer in the world. Helicobacter pylori infection, a low serum pepsinogen I/II ratio, and interleukin (IL)-1beta-511 polymorphisms are suspected to be risk factors for gastric cancer. METHODS: A total of 167 Thais, comprising 56 cancer patients and 111 volunteers without cancer, underwent an esophagogastroduodenoscopic examination and three fixed-point biopsies; a cancer tissue biopsy was also done, and blood samples were collected. The subjects without cancer were divided into normal subjects and chronic gastritis patients. IL-1beta-511 polymorphisms were analyzed by polymerase chain reaction-restriction fragment length polymorphism, and the serum levels of pepsinogen I and II were determined by a radioimmunoassay. Helicobacter pylori IgG antibody and tissue pathology were tested in all groups. RESULTS: The pepsinogen I/II ratio was significantly lower in the gastric cancer group than in the normal and chronic gastritis groups [odds ratio (OR), 2.3; 95% confidence interval (CI), 1.10-4.80; P = 0.025]. Gastric cancer patients were positive for the H. pylori IgG antibody more frequently than negative (OR, 2.946; 95% CI, 1.4-6.39; P = 0.005). However, only 15 (27%) cancer patients were both positive for H. pylori IgG antibody and had low serum pepsinogen I/II. The C/C genotype was found more frequently in the gastric cancer group than in the group with a normal gastric mucosa (OR, 0.64; 95% CI, 0.50-0.81; P = 0.014). CONCLUSIONS: A low serum pepsinogen I/II ratio combined with positivity for H. pylori IgG, and a IL-1beta-511 C/C genotype may be independent risk factors for gastric cancer in Thais.

Interleukin-8, cyclo-oxygenase-2, and trefoil factor family 1 gene expression and their association with Helicobacter pylori infection in the remnant stomach.

PURPOSE: The risk factors for secondary stomach carcinogenesis after distal gastrectomy have not been evaluated in detail. METHODS: Using gastrointestinal endoscopy, we examined 112 patients who had undergone gastrectomy. Biopsy specimens were taken from the stoma and the upper corpus mucosa in the remnant stomach to examine the associations among Helicobacter pylori (H.pylori) infection, bile reflux, and the expressions of interleukin-8 (IL-8), cyclo-oxygenase-2 (COX-2), and trefoil factor family 1 (TFF1) genes in the stomach mucosa. RESULTS: The IL-8 levels in the corpus mucosa were significantly higher in the H.pylori-positive patients than in the H.pylori-negative patients (P = 0.015). The IL-8 levels were significantly higher in the stomal mucosa than in the corpus mucosa in the H.pylori-positive patients (P = 0.047). The COX-2 levels in the corpus mucosa tended to be higher in the H.pylori-positive patients, but these levels were not significantly different in the stoma mucosa. The COX-2 levels in the corpus were significantly higher after Billroth II (BII) anastomosis than after Billroth I (BI) anastomosis (P = 0.041). TFF1 expression in the stoma was higher in the H.pylori-positive patients than in the H.pylori-negative patients, but the difference was not significant. CONCLUSIONS: Both H.pylori infection and bile reflux increased IL-8 levels after BI anastomosis. Furthermore, COX-2 levels were higher after BII than after BI anastomosis. These indicators will become useful not only as biomarkers to predict the degree of inflammation in the stomach mucosa, but also as surrogate biomarkers to predict the risk of secondary stomach carcinogenesis in the remnant stomach mucosa.

Identification of Helicobacter pylori and the cagA genotype in gastric biopsies using highly sensitive real-time PCR as a new diagnostic tool.

The CagA protein is one of the virulence factors of Helicobacter pylori, and two major subtypes of CagA have been observed, the Western and East Asian type. CagA is injected from the bacteria into gastric epithelial cells, undergoes tyrosine phosphorylation, and binds to Src homology 2 domain-containing protein-tyrosine phosphatase SHP-2. The East Asian type CagA binds to SHP-2 more strongly than the Western type CagA. Here, we tried to distinguish the CagA type by highly sensitive real-time PCR with the objective of establishing a system to detect H. pylori and CagA subtypes from gastric biopsies. We designed primers and probe sets for Western or East Asian-cagA at Western-specific or East Asian-specific sequence regions, respectively, and H. pylori 16S rRNA. We could detect the H. pylori 16S rRNA gene, Western and East Asian-cagA gene from DNA of gastric biopsies. The sensitivity and specificity for H. pylori infection was 100% in this system. In Thai patients, 87.8% (36/41) were cagA-positive; 26.8% (11/41) were Western-cagA positive and 53.7% (22/41) were East Asian-cagA positive, while 7.3% (3/41) reacted with both types of cagA. These results suggest that this real-time PCR system provides a highly sensitive assessment of CagA type as a new diagnostic tool for the pathogenicity of H. pylori infection.

Comparison of Helicobacter pylori infection and gastric mucosal histological features of gastric ulcer patients with chronic gastritis patients.

AIM: To compare Helicobacter pylori infection and gastric mucosal histological features of gastric ulcer patients with chronic gastritis patients in different age groups and from different biopsy sites. METHODS: The biopsy specimens were taken from the antrum, corpus and upper angulus of gastric ulcer and chronic gastritis patients. Giemsa staining, improved Toluidine-blue staining and H pylori-specific antibody immune staining were performed as appropriate for the histological diagnosis of H pylori infection. Hematoxylin-eosin staining was used for the histological diagnosis of activity of H pylori infection, mucosal inflammation, glandular atrophy and intestinal metaplasia and scored into four grades according to the Updated Sydney System. RESULTS: Total rate of H pylori infection, mucosal inflammation, activity of H pylori infection, glandular atrophy and intestinal metaplasia in 3 839 gastric ulcer patients (78.5%, 97.4%, 82.1%, 61.1% and 64.2%, respectively) were significantly higher than those in 4 102 chronic gastritis patients (55.0%, 90.3%, 56.2%, 36.8%, and 37.0%, respectively, P<0.05). The rate of H pylori colonization of chronic gastritis in <30 years, 31-40 years, 41-50 years, 51-60 years, 61-70 years and >70 years age groups in antrum was 33.3%, 41.7%, 53.6%, 57.3%, 50.7%, 43.5%, respectively; in corpus, it was 32.6%, 41.9%, 53.8%, 60.2%, 58.0%, 54.8%, respectively; in angulus, it was 32.4%, 42.1%, 51.6%, 54.5%, 49.7%, 43.5%, respectively. The rate of H pylori colonization of gastric ulcer in <30 years, 31-40 years, 41-50 years, 51-60 years, 61-70 years and >70 years age groups in antrum was 60.5%, 79.9%, 80.9%, 66.8%, 59.6%, 45.6%, respectively; in corpus, it was 59.7%, 79.6%, 83.6%, 80.1%, 70.6%, 59.1%, respectively; in angulus, it was 61.3%, 77.8%, 75.3%, 68.8%, 59.7%, 45.8%, respectively. The rate of H pylori colonization at antrum was similar to corpus and angulus in patients, below 50 years, with chronic gastritis and in patients, below 40 years, with gastric ulcer. In the other age- groups, the rate of H pylori colonization was highest in corpus, lower in antrum and lowest in angulus (all P<0.05). The rates of glandular atrophy and intestinal metaplasia were higher and earlier in H pylori-positive patients than those without H pylori infection (both P<0.01). In comparison of gastric ulcer patients with chronic gastritis patients, the rate of glandular atrophy and intestinal metaplasia was higher in H pylori-positive patients with gastric ulcer than in H pylori-positive patients with chronic gastritis (both P<0.01); the rate of glandular atrophy and intestinal metaplasia were also higher in H pylori-negative patients with gastric ulcer than in H pylori-negative patients with chronic gastritis (both P<0.01). Both glandular atrophy and intestinal metaplasia were much more commonly identified in the angulus than in the antrum, lowest in corpus (all P<0.01). CONCLUSION: Rate of H pylori infection, glandular atrophy and intestinal metaplasia in gastric ulcer were higher than in chronic gastritis in all-different age -groups. Distribution of H pylori colonization is pangastric in the younger patients. It is highest in corpus, lower in antrum and lowest in angulus in the older age groups. Progression of glandular atrophy and intestinal metaplasia seem to have a key role in the distribution of H pylori colonization. H pylori appears to be the most important risk factor for the development of glandular atrophy and intestinal metaplasia, but it is not the only risk.

Helicobacter pylori infection, glandular atrophy and intestinal metaplasia in superficial gastritis, gastric erosion, erosive gastritis, gastric ulcer and early gastric cancer.

AIM: To evaluate the histological features of gastric mucosa, including Helicobacter pylori infection in patients with early gastric cancer and endoscopically found superficial gastritis, gastric erosion, erosive gastritis, gastric ulcer. METHODS: The biopsy specimens were taken from the antrum, corpus and upper angulus of all the patients. Giemsa staining, improved toluidine-blue staining, and H pylori-specific antibody immune staining were performed as appropriate for the histological diagnosis of H pylori infection. Hematoxylin-eosin staining was used for the histological diagnosis of gastric mucosa inflammation, gastric glandular atrophy and intestinal metaplasia and scored into four grades according to the Updated Sydney System. RESULTS: The overall prevalence of H pylori infection in superficial gastritis was 28.7%, in erosive gastritis 57.7%, in gastric erosion 63.3%, in gastric ulcer 80.8%, in early gastric cancer 52.4%. There was significant difference (P<0.05), except for the difference between early gastric cancer and erosive gastritis. H pylori infection rate in antrum, corpus, angulus of patients with superficial gastritis was 25.9%, 26.2%, 25.2%, respectively; in patients with erosive gastritis 46.9%, 53.5%, 49.0%, respectively; in patients with gastric erosion 52.4%, 61.5%, 52.4%, respectively; in patients with gastric ulcer 52.4%, 61.5%, 52.4%, respectively; in patients with early gastric cancer 35.0%, 50.7%, 34.6%, respectively. No significant difference was found among the different site biopsies in superficial gastritis, but in the other diseases the detected rates were higher in corpus biopsy (P<0.05). The grades of mononuclear cell infiltration and polymorphonuclear cell infiltration, in early gastric cancer patients, were significantly higher than that in superficial gastritis patients, lower than that in gastric erosion and gastric ulcer patients (P<0.01); however, there was no significant difference compared with erosive gastritis. The grades of mucosa glandular atrophy and intestinal metaplasia were significantly highest in early gastric cancer, lower in gastric ulcer, the next were erosive gastritis, gastric erosion, the lowest in superficial gastritis (P<0.01). Furthermore, 53.3% and 51.4% showed glandular atrophy and intestinal metaplasia in angular biopsy specimens, respectively; but only 40.3% and 39.9% were identified in antral biopsy, and 14.1% and 13.6% in corpus biopsy; therefore, the angulus was more reliable for the diagnosis of glandular atrophy and intestinal metaplasia compared with antrum and corpus (P<0.01). The positivity rate of glandular atrophy and intestinal metaplasia of superficial gastritis with H pylori-positivity was 50.7%, 34.1%; of erosive gastritis 76.1%, 63.0%; of gastric erosion 84.8%, 87.8%; of gastric ulcer 80.6%, 90.9%; and of early gastric cancer 85.5%, 85.3%, respectively. The positivity rate of glandular atrophy and intestinal metaplasia of superficial gastritis with H pylori-negativity was 9.9%, 6.9%; of erosive gastritis 42.5%, 42.1%; of gastric erosion 51.1%, 61.9%; of gastric ulcer 29.8%, 25.5%; and of early gastric cancer 84.0%, 86.0%, respectively. The positivity rate of glandular atrophy and intestinal metaplasia of superficial gastritis, erosive gastritis, gastric erosion, and gastric ulcer patients with H pylori positivity was significantly higher than those with H pylori negativity (P<0.01); however, there was no significant difference in patients with early gastric cancer with or without H pylori infection. CONCLUSION: The progression of the gastric pre-cancerous lesions, glandular atrophy and intestinal metaplasia in superficial gastritis, gastric erosion, erosive gastritis and gastric ulcer was strongly related to H pylori infection. In depth studies are needed to evaluate whether eradication of H pylori infection will really diminish the risk of gastric cancer.

Inflammation of the gastric remnant after gastrectomy: mucosal erythema is associated with bile reflux and inflammatory cellular infiltration is associated with Helicobacter pylori infection.

BACKGROUND: Controversy exists concerning the role of bile reflux and Helicobacter pylori ( H. pylori) infection in the development of inflammation of the gastric remnant after gastrectomy. This study was designed to investigate association of bile reflux and H. pylori infection or both with inflammatory changes in the gastric remnant. METHODS: A questionnaire on GI symptoms was returned by 200 gastrectomy patients, and 24-h bilirubin monitoring in the gastric remnant was performed on 55 patients with Bilitec 2000. Upper GI endoscopy evaluated reflux gastritis in the gastric remnant, and the presence of H. pylori infection and chronic, active inflammatory cellular infiltration in the biopsy specimens were examined microscopically with the updated Sydney system. RESULTS: No difference in the incidence of GI symptoms was observed among individual gastrectomy patients. Bile reflux was lower in patients who had undergone a gastrectomy with jejunal interposition, a pylorus-preserving gastrectomy, and a gastrectomy with Roux-Y anastomosis than those who had undergone a Billroth-II (B-II) anastomosis ( P < 0.05). Endoscopy showed positive correlation between mucosal erythema and bile reflux ( P < 0.001). No correlation was observed between the mucosal erythema and chronic and active inflammatory cellular infiltration. Infection of H. pylori correlated with chronic and active inflammatory cellular infiltration ( P < 0.001). Bile reflux did not correlate with the severity of chronic and active inflammatory cellular infiltration or H. pylori infection. CONCLUSIONS: Bile reflux into the gastric remnant was observed by Bilitec 2000. Mucosal erythema and chronic, active inflammatory cell infiltration in the gastric remnant after gastrectomy may be caused by bile reflux or H. pylori infection, respectively.

Topography of chronic active gastritis in Helicobacter pylori-positive Asian populations: age-, gender-, and endoscopic diagnosis-matched study.

BACKGROUND: The incidence and mortality of gastric cancer is high among Japanese and Chinese populations but extremely low in Thailand and low in Vietnam. The aim of this study was to compare the degree of corpus-predominant gastritis, which is considered to be one of risk factors of gastric cancer, in Helicobacter pylori-positive Asian adult populations. METHODS: H. pylori-positive Chinese (Beijing and Fuzhou), Thai, and Vietnamese patients were paired with Japanese patients by age, gender, and endoscopic diagnosis to compare the ratio of corpus gastritis to antrum gastritis (C/A ratio) (105, 85, 195, and 154 pairs, respectively). RESULTS: The Japanese C/A ratio was significantly higher than that in other groups. Corpus-predominant gastritis (C/A ratio > 1.00) was characteristic in aged Japanese and Chinese (Fuzhou), but Chinese (Beijing), Thai, and Vietnamese were antrum predominant (C/A ratio < 1.00) in every age group except for the Vietnamese over-70 group. There was a similarity between degree of H. pylori colonization and neutrophil activity score. CONCLUSIONS: Corpus-predominant gastritis was found in aged Japanese and Chinese (Fuzhou) and antrum-predominant gastritis was found in Chinese (Beijing), Thai, and Vietnamese patients. These results correlate with the low incidence of gastric cancer in Thai and Vietnamese populations. The incidence and mortality of gastric cancer is high among Japanese and Chinese populations but extremely low in Thailand and low in Vietnam. The aim of this study was to compare the degree of corpus-predominant gastritis, which is considered to be one of risk factors of gastric cancer, in Helicobacter pylori-positive Asian adult populations.

Surgical outcome of 483 patients with early gastric cancer: prognosis, postoperative morbidity and mortality, and gastric remnant cancer.

BACKGROUND/AIMS: The aim of this retrospective study was to evaluate the characteristics, treatment, postoperative morbidity, mortality, and prognosis of early gastric cancer patients as well as the incidence of gastric remnant cancer after curative surgery based on an analysis of the surgical results of Nippon Medical School Hospital over the past 10 years (1991-2000). METHODOLOGY: Out of 1057 patients with gastric cancer (all stages), 483 patients (301 males and 182 females; mean age 60.9 years) underwent surgery for early gastric cancer. Early gastric cancer, defined as that invading the m or sm layer regardless of lymph node metastasis, was classified according to the Japanese Classification of Gastric Carcinoma. The survival rate was calculated using the Kaplan-Meier method. RESULTS: The stages of the 483 patients were as follows: stage Ia patients, 443 cases; stage Ib, 29 cases; stage II, 7 cases; and stage IV, 4 cases. The overall 5- and 10-year survival rates were 95.9% and 95.9% for stage Ia, 82.9% and 80.2% for stage Ib, 73.2% and 68.6% for stage II and 0% for stage IV, respectively. No difference was observed in the 5- and 10-year survival rates between patients with D1 and D2 dissections in cases without lymph node metastasis. In patients with n1 positive sm cancer, however, the 5-year survival rate of the patients who underwent D2 dissection was 91.0% while that of those who underwent D1 dissection was 80.0% (P<0.05). The incidences of postoperative morbidity from various cancers included 4.2% from surgical site infections, 1.6% from anastomotic dehiscence, 1.6% from intestinal obstructions, and 3.9% from respiratory and/or heart dysfunction. Three patients (0.6%) died of multiple organ failure. Five patients who had undergone gastrectomy for early gastric cancer were diagnosed as having early cancer in the gastric remnant during a periodic follow-up endoscopy and underwent regastrectomy. CONCLUSIONS: The prognosis of early gastric cancer is usually excellent, and the morbidity and mortality rates are satisfactory. D2 lymph node dissection is necessary in patients with n1 positive sm cancer. Periodic follow-up endoscopies in gastrectomized patients may be useful for the early detection of gastric remnant cancer.

[Clinical significance of a standardized clinical pathway in gastrectomy patients].

UNLABELLED: In traditional practice patterns, physicians take care of all clinical decisions, such as diagnosis, treatment, and recovery. In the Nippon Medical School Hospital a clinical pathway for distal gastrectomy patients, recorded as a post-operative care map, was introduced in August 2000. In January 2001 the post-operative management was analyzed and standardization of practice was carried out with printed order sets, such as drugs and infusion solutions. The aim of this study was to evaluate the clinical significance of the clinical pathway for gastrectomy patients by employing standardized postoperative management and printed order sets. PATIENTS AND METHODS: From January 2001 to December 2001, 87 patients underwent distal (43), total (28), proximal (7) and partial gastrectomy (9) for gastric cancer (stage IA: 47, IB: 9, II: 7, IIIA: 8, IIIB 2, IV: 10) and gastrointestinal stromal tumor (4). These patients were randomly assigned to either the main building or the east building of our hospital. In the main building 38 patients were looked after using traditional practice (control group). In the east building 47 patients were looked after according to the clinical pathway (path group) and 2 patients were excluded from the path group because of neo-adjuvant chemotherapy and severe heart failure. Aspects of the patients' outcomes, including length of stay, the first day of the diet, morbidity, and medical costs, were compared between the path group and the control group. All data were expressed as means+/-standard deviation. Statistical analyses were made using Student t-test, Mann-Whitney U-test, and chi(2) test, and the 5%level was chosen for statistical significance. RESULTS: The length of the hospital stay was 27.1+/-10.0 and 40.8+/-26.1 days (p<0.005) and the length of post-operative stay was 18.1+/-9.5 and 28.2+/-22.3 days (p<0.01) in the path group and the control group, respectively. The post-operative day when the diet was started for the path and control groups was 6.8+/-8.9 and 8.2+/-7.2, respectively; however, the length of the intravenous infusion for the two groups was 11.8+/-1.1 and 16.5+/-1.2 days (p<0.01), respectively. There was no statistically significant difference in the morbidity rate between the path group (3/47) and the control group (5/38). The total cost was 1,502,587 yen +/-41,650 in the path group and 1,932,197 yen +/-131,030 in the control (p<0.001). CONCLUSION: A clinical pathway for gastrectomy patients proved useful to optimize their postoperative care, including medication management and diet education. It is suggested that the implementation of a standardized clinical pathway for gastrectomy patients reduced the length of the hospital stay and the medical costs.

Helicobacter pylori eradication therapy for the remnant stomach after gastrectomy.

BACKGROUND: The remnant stomach after surgery for gastric cancer is at high risk for the metachronous development of multiple gastric cancers. Here, we report on eradication therapy of Helicobacter pylori in the remnant stomach, comparing the eradication rate with that in unoperated stomachs. We examined gross and histological changes after treatment. METHODS: Forty H. pylori-positive patients after distal gastrectomy were treated with proton pump inhibitor (PPI)-based dual and triple therapies. After eradication, histological changes were classified on the basis of the updated Sydney system. RESULTS: The eradication rate in the remnant stomach was 70% (14 of 20) after dual therapy and 90% (18 of 20) after triple therapy, using per-protocol analysis, and these rates were comparable to the rates of 70% (186 of 264) and 88% (58 of 66), respectively, in nonsurgery patients. After eradication, three sites in the remnant stomach showed similar histological changes: significant decreases in inflammation and activity scores (P < 0.001) and no significant changes in glandular atrophy and intestinal metaplasia scores. CONCLUSION: PPI-based therapy was as effective for H. pylori eradication in the remnant stomach as in the unoperated stomach, and eradication therapy resulted in a significant decrease in inflammatory cell infiltration of the mucosal layer.

[An economic evaluation on the clinical pathway for gastrectomy].

OBJECTIVE: To analyze the costs of gastrectomy patients treated with the clinical pathway. PATIENTS AND METHODS: Seventy-six patients (path group 44, control 32) had undergone gastrectomy in our hospital in 2001. The clinical pathway included the same care map. Treatment costs were estimated from medical cost receipt data. The economical analysis was performed from the point of the direct cost payer's view. RESULTS: The length of hospital stay in the path group was 27.1 +/- 5.9 days and decreased 8.3 days in comparison with the control(p < 0.001). The cost of the path group was 145.290 +/- 23.773 points and 19.278 points less than the control(p < 0.005). In the path group the operation case per bed was increased 30% and the cost per bed was also increased 15% more than the control. CONCLUSIONS: The implementation of the clinical pathway decreased the length and the cost of hospital stay. The clinical pathway is effective to use the hospital resources, such as bed.