Gastric cancer prevention targeted on risk assessment: Gastritis OLGA staging

Gastric cancer (GC) ranks among the most lethal epithelial malignancies, and its striking mortality rate prompts a global prevention strategy. Helicobacter pylori (H. pylori) gastritis is the main GC promoter, and the 2014 Global Kyoto conference recognized H. pylori gastritis as a (treatable) infectious disease. It is therefore plausible that any large‐scale intervention for H. pylori eradication would result in cleansing the world of the fifth cause of cancer‐related death. Atrophic gastritis is the cancerization field in which GCs (both intestinal and diffuse histotypes) mainly develop. Discontinuing the inflammatory cascade triggered by H. pylori is tantamount to preventing GC. For patients (still infected or eradicated) who have already developed gastric atrophy, the severity/topography of the atrophic changes correlates with their cancer risk. Gastritis OLGA (Operative Link for Gastritis Assessment) staging consistently ranks the atrophy‐associated cancer risk, providing a solid clinical/biological rationale for establishing patient‐specific surveillance programs. By combining primary and secondary prevention strategies, gastric cancer is a preventable disease.     

Helicobacter pylori modulation of gastric acid

Helicobacter pylori plays major causative roles in peptic ulcer disease and gastric cancer. Elevated acid secretion in patients with duodenal ulcers (DUs) contributes to duodenal injury, and diminished acid secretion in patients with gastric cancer allows carcinogen-producing bacteria to colonize the stomach. Eradication of H. pylori normalizes acid secretion both in hyper-secreting DU patients and hypo-secreting relatives of gastric cancer patients. Therefore, we and others have asked how H. pylori causes these disparate changes in acid secretion. H. pylori gastritis more or less restricted to the gastric antrum in DU patients is associated with increased acid secretion. This is probably because gastritis increases release of the antral acid-stimulating hormone gastrin and diminished mucosal expression of the inhibitory peptide somatostatin. Bacterial products and inflammatory cytokines including TNFalpha may cause these changes in endocrine function. Gastritis involving the gastric corpus tends to diminish acid secretion, probably because bacterial products and cytokines including IL-1 inhibit parietal cells. Pharmacological inhibition of acid secretion increases corpus gastritis in H. pylori-infected subjects, so it is envisaged that gastric hypo-secretion of any cause might become self-perpetuating. H. pylori-associated mucosal atrophy will also contribute to acid hypo-secretion and is more likely in when the diet is high in salt or lacking in antioxidant vitamins. Data on gastric acid secretion in patients with esophagitis are limited but suggest that acid secretion is normal or slightly diminished. Nevertheless, H. pylori infection may be relevant to the management of esophagitis because: (i) H. pylori infection increases the pH-elevating effect of acid inhibiting drugs; (ii) proton pump inhibitors may increase the tendency of H. pylori to cause atrophic gastritis; and (iii) successful eradication of H. pylori is reported to increase the likelihood of esophagitis developing in patients who had DU disease. Points (ii) and (iii) remain controversial and more work is clearly required to elucidate the relationship between H. pylori, acid secretion, gastric mucosa atrophy and esophagitis.     

Serum OPN Expression for Identification of Gastric Cancer and Atrophic Gastritis and Its Influencing Factors

Background

Most studies have found that osteopontin (OPN) expression level is related to the poor prognosis of gastric cancer. However, few studies have examined the relationship between OPN expression and gastric precancerous diseases, and the potential role of OPN in the formation and development of GC. We investigated the relationships between serum OPN levels and the risks of gastric cancer (GC) and its precancerous disease, to explore the diagnostic efficacy of serum OPN level for GC and atrophic gastritis and its influencing factors.

Methods

A total of 1,452 patients were enrolled, including 609 with mild superficial gastritis (SG), 594 with atrophic gastritis (AG) and 249 with GC. The levels of serum OPN and serum Helicobacter pylori IgG antibody were detected by enzyme-linked immunosorbent assay.

Results

Serum OPN levels increased from mild SG (1.99±1.91 ng/ml) to AG (2.37±2.27 ng/ml) to GC (5.94±4.52 ng/ml) (P≤0.002), along with increasing severity of gastric disease. OPN levels were significantly higher in patients with GC compared with the non-cancer population (2.17±2.10, P<0.0001). Serum OPN level was positively correlated with age and was higher in men than women, but was not correlated with H. pylori infection status. The area under the receiver operating characteristic curve was 0.805, the optimal cutoff was 2.56 ng/ml and the sensitivity and specificity were 74.3% and 71.8%, respectively, for the ability of serum OPN to discriminate GC.

Conclusions

Serum OPN expression was closely related to the risks of GC and AG, and it might be a useful marker for the discrimination of GC. OPN level was positively correlated with age and male sex, but was not affected by H. pylori infection, and it was promoted by smoking and drinking, in patients with mild SG.     

Diversity of Helicobacter pylori cagA and vacA genes in Costa Rica: its relationship with atrophic gastritis and gastric cancer

BACKGROUND: Associations between Helicobacter pylori gene diversity and gastric cancer have not been reported on in Costa Rica, despite its being one of the countries with the highest gastric cancer incidence and mortality rates in the world. The aim of this study was to determine the prevalence of H. pylori cagA and vacA genes and investigate whether it could be correlated with atrophic gastritis (AG) and gastric cancer (GC) in Costa Rica. MATERIALS AND METHODS: Genomic DNAs from isolates of 104 patients classified into two groups: non-atrophic gastritis group (n = 68) and atrophic gastritis group (n = 36), were subjected to PCR-based genotyping of cagA and vacA genes and their correlation with clinical outcome was investigated. Total DNA extractions from gastric tissues of 25 H. pylori-infected gastric cancer patients were utilized for comparative purposes. RESULTS: The presence of cagA (75.3%), vacA s1b (75.3%), and vacA m1 (74.2%) was detected, and colonization by strains with different vacA genotypes in the same stomach was found in 9.7% of the patients. Age- and sex-adjusted vacA s1b and vacA m1 were associated with GC while only vacA m1 was significantly associated with AG. A tendency for association between cagA and vacA s1b, and AG was reported. CONCLUSIONS: The prevalence status of the cagA and vacA (s1/m1) genes in Costa Rica seems to fall between that found in European/North American and East Asian countries, and both cagA and vacA seem to have clinical relevance in this country.     

Interaction of Helicobacter pylori Infection and Nonsteroidal Anti‐Inflammatory Drugs in Gastric and Duodenal Ulcers

Background: Gastric (GU) and duodenal ulcers (DU) are in most instances either induced by Helicobacter pylori infection or by nonsteroidal anti‐inflammatory drugs (NSAIDs). Whether eradication of H. pylori is beneficial in NSAID users for preventing NSAID induced GU and DU has been the focus of different studies. Materials and Methods: Mechanisms shared by both H. pylori and NSAIDs for the induction of GU and DU were reviewed and randomized controlled trials on H. pylori eradication for prevention and healing of GU and DU in patients requiring NSAID therapy were identified by a PubMed search. Results: Key factors in the induction of GU and DU for both H. pylori and NSAIDs are a decrease in pH, imbalance between apoptosis and proliferation, reduction in mucosal blood flow, and recruitment of polymorphonucleates in distinct compartments. For primary ulcer prevention, H. pylori eradication before starting an NSAID therapy reduces the risk of NSAID induced GU and virtually abolishes the risk of DU. H. pylori eradication alone is not sufficient for secondary prevention of NSAID induced GU and DU. H. pylori infection appears to further increase the protective effects of proton‐pump inhibitors (PPI) to reduce the risk of ulcer relapse. H. pylori eradication does not influence the healing of both GU and DU if NSAID intake is discontinued. Conclusions: Duodenal ulcer is more closely related to H. pylori infection than GU in NSAID users. H. pylori eradication is recommended for primary prevention of GU and DU in patients requiring NSAID therapy. PPI therapy is mandatory for secondary prevention of gastroduodenal ulcers, and appears to further reduce the risk of ulcer relapse in the presence of H. pylori.     

Role of noninvasive tests (C-urea breath test and stool antigen test) as additional tools in diagnosis of Helicobacter pylori infection in patients with atrophic body gastritis

BACKGROUND: Detection of Helicobacter pylori infection in atrophic body gastritis (ABG) is difficult, as during progression of body atrophy, H. pylori disappears. AIM: To increase the diagnostic yield of detection of active H. pylori infection in atrophic body gastritis patients by using noninvasive tests such as (13)C-Urea Breath Test ((13)C-UBT) and H. pylori stool antigen test (HpSA) would be useful. PATIENTS: 27 consecutive patients with newly-diagnosed atrophic body gastritis (19F/7M, age 27-73 years). METHODS: Gastroscopy with biopsies (antrum n = 3, body n = 3) and histology according to updated Sydney system, H. pylori IgG serology, (13)C-UBT, and HpSA. RESULTS: All tests used in the diagnosis of H. pylori infection were in agreement in 9/27 atrophic body gastritis patients (33.3%), being all positive in four (14.8%) and all negative in five patients (18.5%). Ten of the 27 (37%) patients were Giemsa stain-positive and serology-positive (group I). Seventeen of the 27 (63%) patients were Giemsa stain-negative: 5/17 with positive serology (group II) and 12/17 with negative serology (group III). In group I, 5/10 (50%) were (13)C-UBT positive and 4/10 (40%) HpSA positive. In group II, two patients were (13)C-UBT positive, but all were HpSA negative. Also in group III, all patients were HpSA negative, but one had a positive (13)C-UBT. CONCLUSIONS: In atrophic body gastritis patients, neither (13)C-UBT nor HpSA per se add useful information regarding active H. pylori infection, but these noninvasive tests may be important in combination with histology and serology to define the H. pylori status in some atrophic body gastritis patients.     

Apoptosis in different gastric lesions and gastric cancer: relationship with Helicobacter pylori, overexpression of p53 and aneuploidy

Apoptosis has an essential function in maintaining the integrity of the gastrointestinal mucosa. Its deregulation is associated with the occurrence of lesions such as in atrophic gastritis, peptic ulcers, intestinal metaplasia, and stomach tumorigenesis. Thus, the aim of the present study was to investigate the frequency of apoptotic cells (apoptotic index, AI) by using two different immunohistochemical techniques, TUNEL and anti-activated caspase-3 antibody (CPP32), in gastric dyspepsia [chronic gastritis (CG, N = 34), chronic atrophic gastritis (CAG, N = 11), gastric ulcer (GU, N = 17), and intestinal metaplasia (IM, N = 15)], normal gastric mucosae (NM, N = 8), and gastric adenocarcinoma (GC, N = 12). The relationship was investigated between the AI and Helicobacter pylori infection, diagnosed by PCR, overexpression of p53 protein determined by immunohistochemistry, and aneuploidy by fluorescence in situ hybridization, as performed by our laboratory in previous studies. No significant differences were observed in AI between the different groups, whether by the TUNEL technique (F = 1.60; p = 0.1670) or by CPP32 antibody (F = 1.70; p = 0.1420). Nonetheless, CAG and CG groups had AI statistically higher than those of normal mucosae. These two groups (CAG and CG) also showed a higher frequency of apoptosis-positive cases (TUNEL+ or CPP32+). Generally, there was no correlation between the AI detected by the TUNEL and CPP32 techniques in the groups studied, except in the GC group (r = 0.70). Moreover, there was no significant association between apoptosis and H. pylori infection, overexpression of p53 protein and aneuploidy, but the H. pylori-positive cases only of GU (p = 0.0233) and IM (p = 0.0253) groups displayed a statistically higher AI compared to H. pylori-negative NM, when the CPP32 antibody technique was used. Thus, CG and CAG have increased apoptosis, which may occur independent of an association with H. pylori infection, aneuploidy and overexpression of p53 protein.     

Plasma obestatin levels in men with chronic atrophic gastritis

Obestatin is a recently discovered active peptide isolated from the stomach. The purpose of the present study was to investigate the modification of plasma obestatin levels in men with chronic atrophic gastritis. Men older than 65 years undergoing upper gastrointestinal endoscopy were included. All patients with chronic atrophic gastritis underwent multiple biopsies. Fasting plasma obestatin and ghrelin levels were examined in 50 men with chronic atrophic gastritis and 50 healthy men. Plasma obestatin levels were significantly lower in patients with chronic atrophic gastritis than in healthy subjects. Plasma ghrelin levels and ghrelin to obestatin ratio was decreased in men with chronic atrophic gastritis. There was a significant relationship between atrophy and decreased obestatin. A negative correlation was found between circulating obestatin levels and body mass index (BMI) in healthy subjects, but not in patients with chronic atrophic gastritis. The data indicated that chronic atrophic gastritis influenced plasma obestatin levels as well as ghrelin to obestatin ratio in elderly men.     

Serum and Gastric Luminal Epidermal Growth Factor in Helicobacter Pylori—Associated Gastritis and Peptic Ulcer Disease

Background Helicobacter pylori is the cause of chronic (type B) gastritis, duodenal ulceration (DU), and gastric ulceration (GU). Smoking is associated with delayed ulcer healing. Epidermal growth factor (EGF) is produced in the salivary and Brunner's glands of the upper gastrointestinal tract, inhibits gastri acid secretion, and is a powerful mitogen. Materials and Methods. We sought to determine gastric luminal EGF (GL-EGF) in smokers and patients with Hp-associated DU and the effect of Hp eradication. Our aim was to determine GL-EGF in patients with GU and the effect of ulcer healing and to measure serum EGF in patients with Hp gastritis with or without DU disease. Results. GL-EGF was reduced in smokers compared to control (p= .008). Subjects with HP gastritis had reduced GL-EGF compared to controls (p= .0002). There was no difference in GL-EGF between Hp-positive subjects who had DU and those with chronic gastritis alone. Eradication of Hp from those patients with DU had no effect on the low levels of GL-EGF. There was no difference between GL-EGF in Hp gastritis alone and in Hp-associated active GU. GL-EGF fell after ulcer healing (p= .04), a difference confirmed by analysis of paired samples from patients before and after ulcer healing (p= .03). There was no difference in serum EGF between controls and subjects with Hp infection. There was no difference in serum EGF in subjects with DU-associated and non-ulcer-associated gastritis. Conclusions. Subjects with Hp gastritis, or those who smoke, had low concentrations of GL-EGF regardless of whether DU was present. Eradication of Hp did not return the concentrations of GL-EGF to normal in DU subjects. Individuals with Hp gastritis and inactive GU had low levels of GL-EGF compared to non-ulcer Hp infection. The relative increase in GL-EGF that occurred with ulceration of the gastric mucosa may have resulted from the development of an ulcer-associated cell lineage. Serum EGF did not play a role in the pathogenesis of Hp gastritis or of associated DU ulcer disease.     

Functional variability of cagA gene in Japanese isolates of Helicobacter pylori

CagA protein of Helicobacter pylori is injected into the epithelium, where CagA undergoes tyrosine phosphorylation and activates proliferation signals. However, the importance of these CagA activities for pathogenesis has yet to be resolved. The aim of this study is to analyze the genetic and functional variability of cagA gene of clinical strains in relation to gastric diseases. Thirty-six H. pylori strains were isolated from Japanese patients with various gastric diseases and examined. All 36 strains were found to contain cagA and cagE gene and to induce CagA phosphorylation upon infection. The intensity of CagA phosphorylation expressed in HeLa cells by transfection was highly correlated to the number of R1 region. The phosphorylation intensity was slightly higher in strains from chronic atrophic gastritis (CG); however, the differences were not statistically significant. These CagA proteins also activated the serum response element (SRE) reporter by 5- to 14-fold, above the level of the control. CagA proteins which lack R2 or R3 region exhibited smaller ability for SRE activation. The average of SRE activation was slightly higher in strains from cases of gastric cancer (GC; 11.4+/-1.6), MALT lymphoma (ML; 10.7+/-1.0), and chronic atrophic gastritis (CG; 11.2+/-1.6) than in those of duodenal ulcer (DU; 8.3+/-1.9) or gastric ulcer (GU; 9.0+/-1.1). In summary, most Japanese H. pylori strains contained CagA transport system and induced CagA phosphorylation, and the levels of the intensity of phosphorylation and the ability to induce SRE varied among strains. Although the association between CagA activities and disease outcome shown in this study is not very strong, variety of CagA structure, which induces variable activities, may be one of the reasons why H. pylori induces distinct diseases on host.     

TFF2在胃癌中的表达及与幽门螺杆菌感染关系的研究

目的探讨三叶因子Ⅱ(Trefoil factors2,TFF2)在胃癌和癌前病变中的表达及与幽门螺杆菌感染(Helicobacter pylori,H.pylori)的关系。方法选取经病理证实的慢性浅表性胃炎、胃溃疡、慢性萎缩性胃炎和胃癌4种不同胃黏膜病变的标本140例,用免疫组化法检测标本中TFF2的表达及H.pylori的感染情况,并分析TFF2的表达与H.pylori的感染的关系。结果在慢性浅表性胃炎、胃溃疡、慢性萎缩性胃炎和胃癌中,TFF2和H.pylori的表达率依序呈逐渐增加的趋势,但TFF2在胃癌组织中表达降低。H.pylori阳性组TFF2的表达率低于阴性组,TFF2的阳性率与H.pylori感染率之间呈负相关(r=-0.335,P<0.05)。结论 TFF2的表达和H.pylori的感染与肿瘤的发生密切相关,检测该指标可为胃癌诊断、判断预后和指导治疗提供理论依据。     

CagA and VacA: Virulence Factors of Helicobacter pylori in Thai patients with Gastroduodenal Diseases

Background. The aim of this study was to assess the seroprevalence of cytotoxin-associated gene A ( cag A) and vacuolating cytotoxin gene A ( vac A) of Helicobacter pylori in selected Thai populations with specific gastroduodenal diseases.
Materials and Methods. The immunoblot assay was used to detect serum antibodies against CagA and VacA obtained from the following patients: 87 cases of nonulcer dyspepsia (NUD), 61 cases of duodenal ulcer (DU), 49 cases of gastric ulcer (GU), and 10 cases of gastric cancer (GC).
Results. Serum antibodies to CagA were detected in 75.4% of all patients (70.1% of NUD, 78.7% of DU, 77.6% of GU, and 90% of GC). Although the prevalence of CagA seropositivity in GC patients was higher than in the other three groups, the difference was not statistically significant ( p > .05).
Conclusions. The high seroprevalence of the CagA-positive H. pylori strain in patients with peptic ulcer, GC, and NUD indicates that this strain is common in Thai patients with gastroduodenal diseases. Furthermore, phenotypic classification of H. pylori into type 1 (CagA-positive, VacA-positive) and type 2 (CagA-negative, VacA-negative) is not a useful marker for screening patients with severe forms of gastroduodenal diseases.     

Gastritis of the Herniated Stomach in Patients with Esophageal Hiatus Hernia

Seven illustrative cases of gastritis of the herniated stomach in patients with sliding esophageal hiatus hernia are reported. Five had superficial gastritis (three mild, one moderate and one severe); two had atrophic gastritis. Gastritis was present in two patients whose mucosa appeared normal at esophagoscopy. Interstitial hemorrhage into the lamina propria was present in four of the seven biopsy specimens. The possibility that interstitial hemorrhage may be related to the development of gastric erosions is considered. The pathogenesis of this form of gastritis is discussed.     

Helicobacter pylori associated gastric pathology.

Helicobacter pylori (HP), undoubtedly, the most common world-wide infection plays an important role in pathogenesis of peptic ulcer. Proof for a causal role for HP in peptic ulcer rests in two major points; 1) the majority of ulcer patients are HP infected and the prevalence of this infection for both gastric ulcer (GU) and duodenal ulcer (DU) is much higher than for gender- and age-adjusted controls and 2) the cure of HP infection dramatically reduces ulcer recurrence. Conclusions regarding the mechanisms by which HP induces peptic ulcer are restricted mainly to studies observing the consequences of its eradication by antibiotics combined with gastric inhibitors or bismuth agents. Several specific virulence factors such as cytotoxin-associated gene A (CagA) and vacuolating cytotoxin A (VacA) as well as other noxious substances including ammonia, lipopolysaccharide (endotoxin), platelet activating factor (PAF), nitric oxide (NO) and others have been implicated in gastritis and were found to be significantly more frequent in gastric cancer than in gender- and age-matched controls, especially in younger generation. Chronic inflammation, atrophic gastritis, intestinal metaplasia, impaired defense mechanisms combined with hypergastrinemia, deficiency of vitamin C in the stomach , excessive oxygen metabolites and epithelial cell proliferation have been associated with gastric cancer. This multi-step pathway originally proposed by Correa and his colleagues, long before the HP was discovered in the stomach, leads to cancer but may be reversed by eradication of HP. This is, however, a controversial issue because gastric atrophy and intestinal metaplasia may be also caused by other factors such as bile reflux, dietary irritants, and autoimmunity. The implication of HP in MALT-lymphoma is based on the observations that eradication of HP in early stage of low-grade of this tumor leads to complete remission. The significance of HP in non-ulcer dyspepsia remains questionable and requires further studies.     

Risk factors associated with gastric cancer in patients with a duodenal ulcer

Background: Although gastric cancer (GC) and duodenal ulcer (DU) are both strongly associated with Helicobacter pylori infection, a DU is negatively associated with the risk of GC. The aim of the study is to evaluate histologic risk factors for GC among patients with a DU. Materials and Methods: A total of 541 consecutive patients with GC were prospectively evaluated for the presence of a DU. Control patients with only a DU (n = 89) were recruited from health screening population. Histologic grading was assessed using the updated Sydney system for six gastric biopsies from three regions. GC risk among patients with a DU was evaluated using logistic regression analysis. Results: Among patients with GC, 7.6% (41/541) had a concomitant DU or an ulcer scar. Corpus‐predominant/pangastritis were more frequently found in concomitant GC patients with a DU (90%) than in patients with a DU alone (62%) (p = .001). In patients with a DU, moderate–severe chronic inflammation at the lesser and greater curvatures of corpus was associated with GC risk (OR, 3.70; 95% CI, 1.46–9.36, and OR, 7.72; 95% CI, 3.18–18.7, respectively). Additionally, moderate–severe intestinal metaplasia (IM) at the antrum and corpus lesser curvature was associated with GC risk (OR, 7.52; 95% CI, 3.06–18.5, and OR, 9.25, 95% CI, 2.39–35.8, respectively). Conclusions: A DU is not rare in patients with GC in a high‐risk region of GC. Patients with a DU with chronic corpus gastritis and IM have an increased risk of GC, thus those patients should be followed up for GC development.     

幽门螺杆菌相关胃癌发生不同阶段miRNAs表达与临床研究

目的 观察幽门螺杆菌（Helicobacter pylori, H. pylori）感染的慢性非萎缩性胃炎（no-atrophic gastritis,NAG）→萎缩性胃炎（chronic atrophic gastritis,CAG）→肠上皮化生（intestinal metaplasia,IM）→非典型增生（dysplasia,DYS）→胃癌（gastric cancer,GC）五个不同阶段miR-1、miR-20a、miR-34a、miR-423-5p表达变化规律及其与临床的关系。方法 收集胃镜及病理证实的上述胃癌发生五个不同阶段且H. pylori感染的患者（依次为44、47、43、50、45例）,胃癌无H. pylori感染者46例,胃黏膜正常（normal gastric mucose,NGM）63例的血清标本,采用Real-time PCR法检测无H. pylori感染者miR-1、miR-20a、miR-34a、miR-423-5p表达。结果 H. pylori感染NAG→GC不同阶段,miR-1、miR-20a、miR-34a、miR-423-5p表达逐渐升高（P<0.05）,GC阶段最高,miR-1、miR-20a CAG→GC阶段均高于NGM（P<0.05）,与NGM比较差异有统计学意义（P<0.05）;其表达程度与GC发生阶段呈正相关（P<0.001）;GC组H. pylori感染者较无H. pylori感染者miR-1、miR-20a、miR-34a、miR-423-5p表达升高（P<0.05）。结论 H. pylori感染CAG→GC阶段miR-1、miR-20a、miR-34a、miR-423-5p表达升高,向胃癌演进中呈逐渐升高趋势,miR-1、miR-20a、miR-34a、miR-423-5p高表达可能是H. pylori感染后导致胃癌发生发展的重要机制,miR-1、miR-20a、miR-34a可作为诊断早期胃癌的标记物。     

Gastritis cystica and carcinoma arising in old gastrojejunostomy stoma.

Gastritis cystica and carcinoma developed 35 years after partial gastectomy and gastrojejunostomy for benign peptic ulcer. Although chronic atrophic gastritis and carcinoma are well recognized complications of gastrojejunostomy, gastritis cystica appears to be rare. The resemblance of the lesion to that of colitis cystica profunda is striking.     

Flow cytometric analysis of the cell cycle in chronic gastritis.

Flow cytometric cell cycle analysis was recorded in gastric biopsy specimens from patients with normal gastric mucosa (GM), superficial gastritis (SG) and chronic atrophic gastritis (CAG). Cell-cycle analysis showed significantly higher percentages of cells in S- and S+G2/M-phase in CAG than in SG and normal GM (P < 0.0001). Moreover, CAG with severe or moderate atrophy showed significantly higher percentages of cells in S-phase (P < 0.05) and S+G2/M-phase (P < 0.02) than CAG with mild atrophy in antrum. In fundus, even if this increase was observed, it did not reach statistical significance. Consideration of concomitant pathologic findings such as oesophagite, gastric or duodenal ulcer, duodenite or benign polyp allowed a better differentiation of CAG both in antrum and in fundus. Significantly higher S-phase was observed in CAG with severe or moderate atrophy than in CAG with mild atrophy (P < 0.05). No statistically significant results were observed in patients with normal gastric mucosa or chronic gastritis and a concomitant pathologic finding.     

帕罗西汀对慢性萎缩性胃炎患者血清胃泌素和胃动素水平的影响

目的:探讨帕罗西汀对慢性萎缩性胃炎患者血清胃泌素和胃动素水平的影响及临床意义。方法:选取我院收治的80例慢性萎缩性胃炎患者,根据治疗方案不同分为常规组及试验组。常规组采用奥美拉唑治疗,试验组采用帕罗西汀治疗,观察并比较两组患者治疗前后血清胃酸度、总酸排出量、复发率、胃动素及胃泌素水平的变化情况。结果:与治疗前比较,两组患者治疗后胃酸及总酸排出量均升高,胃动素及胃泌素水平均降低,且试验组患者胃酸及总酸排出量明显高于常规组,胃动素及胃泌素水平明显低于常规组,差异均具有统计学意义(P0.05)。治疗后,试验组复发率为7.5%(3/40),常规组复发率为30.0%(12/40),试验组复发率明显低于常规组,差异具有统计学意义(P0.05)。结论:帕罗西汀可促进慢性萎缩性胃炎患者血清胃泌素及胃动素水平的改善,可作为临床治疗慢性萎缩性胃炎的有效方案。     

人慢性胃炎与神经内分泌G、D细胞关系的研究

探讨神经内分泌G、D细胞与慢性胃炎的关系,用免疫细胞化学方法对52例慢性胃炎及9例对照者进行胃窦粘膜内G、D细胞密度计数。结果显示慢性胃炎病人的G、D细胞数均低于对照组,特别是萎缩性胃炎G、D细胞显著减少,同时还发现不同组别、不同程度的萎缩性胃炎,其G细胞的数量均大于D细胞,G／D细胞的比值在中、重度性胃炎与其它组相比有显著性差异（P＜0.01）。资料还显示G、D细胞的计数不仅可以判断胃窦粘膜的萎缩程度,而且可作为观察临床疗效的一项重要指标。