胃粘膜局部抗幽门螺杆菌抗体IgA的研究

采用胃粘膜体外培养技术和免疫印迹技术研究了５１例慢性胃炎和消化性溃疡患者胃粘膜局部抗幽门螺杆菌（Ｈｐ）抗体ＩｇＡ，同时对其中１０例Ｈｐ阳性患者的血清ＩｇＡ作了分析。结果表明：４０例Ｈｐ阳性患者除１例外，其粘膜抗ＨｐＩｇＡ抗体均为阳性；１１例Ｈｐ阴性患者中，２例胃粘膜局部ＩｇＡ阳性，９例为阴性。该方法与常规方法检测Ｈｐ的符合率为９２．２％。粘膜局部ＩｇＡ识别５条左右条带，且识别条带具多样性。１０例Ｈｐ阳性且局部ＩｇＡ阳性患者的血清ＩｇＡ亦为阳性，但血清ＩｇＡ的识别条带较局部ＩｇＡ少，且染色浅，说明抗ＨｇＩｇＡ抗体以局部为主，该局部ＩｇＡ的作用值得进一步研究。     

Diagnosis of Helicobacter pylori infection by specific gastric mucosal IgA and IgG pylori antibodies.

AIMS--To investigate the diagnostic value of mucosal IgA and IgG Helicobacter pylori antibodies. METHODS--The study population comprised 209 consecutive patients with severe dyspeptic complaints referred for upper gastrointestinal endoscopy. A positive culture or histological identification of H pylori in gastric biopsy specimens, or both, were used to confirm infection. Specific IgA and IgG H pylori antibodies were determined using a modified ELISA technique. RESULTS--Of the 209 patients, 137 were infected with H pylori. The diagnostic value of systemic IgA and IgG H pylori antibodies was confirmed. Systemic IgA antibodies had a sensitivity of 76.6% (95% confidence interval 69.5-83.7) and a specificity of 94.4% (89.1-99.7). The sensitivity and specificity for systemic IgG antibodies were, respectively, 97.1% (94.3-99.9) and 98.6% (95.9-100). A moderate but clinically important correlation was found between local and systemic IgA and IgG. Mucosal IgA H pylori antibodies had a sensitivity of 98.5% (96.5-100) and a specificity of 91.7% (85.3-98.1), while for IgG these figures were, respectively, 88.3% (82.9-93.7) and 98.6% (95.9-100). As a diagnostic test mucosal IgA H pylori antibodies were comparable with culture and histology. CONCLUSION--Determination of local IgA and IgG H pylori antibody levels is a highly sensitive and specific test for the diagnosis of H pylori infection.     

PPARγ2 Pro12Ala基因多态性与我国胃癌关系的研究

目的：研究PPARγ2 Pro12Ala基因多态性在我国普通人群和胃癌患者中的分布，探讨我国汉人PPARγ2 Pro12Ala基因多态性、幽门螺杆菌 (Hp)感染与胃癌的关系。方法:胃癌患者、健康志愿者各104例，两组人群在性别以及年龄均匹配。采用限制性片段长度多态性（PCR-RFLP）分析PPARγ2 Pro12Ala基因多态性，采用酶联免疫吸附法（ELISA）检测血清抗Hp-IgG抗体。结果:胃癌人群Hp感染率明显高于对照人群 (81.7% vs 59.6%，2=12.27，P<0.01；OR=3.0，95%CI=1.6-5.7)。我国汉人普通人群PPARγ2 CC、CG和GG基因型频率分别为91.3%、8.7%、0，G等位基因频率为4.3%。胃癌患者中携带有PPARγ2 G等位基因者比率明显高于对照人群 (19.2% vs 8.7%, P<0.05；OR＝2.5，95%CI=1.1-5.8)，并使Hp感染后胃癌发生的危险性增加 (P<0.01, OR=8.9, 95% CI=2.2-35.7)。结论:PPARγ2 G等位基因与我国汉族人群胃癌的发生有关，增加Hp感染后胃癌发生的危险性。     

Prevalence of antibodies against heat-stable antigens from Helicobacter pylori in patients with dyspeptic symptoms and normal persons.

Heat-stable antigens from Helicobacter pylori were investigated for the detection of serum IgG, IgA and IgM antibodies against H. pylori by an ELISA technique. Antibody titers against H. pylori were measured in 167 dyspeptic patients, of whom 96 were H. pylori positive confirmed by culture or microscopy, and in 482 controls (0-98 years). Increased IgG antibody titers were found significantly more often in dyspeptic patients with active chronic gastritis than in patients with normal morphology, as well as in H. pylori-positive patients as compared to H. pylori-negative patients, independent of the endoscopic findings. The heat-stable antigens were compared with acid glycine-extracted antigens and a high degree of concordance was found in the results obtained with the two antigen preparations. The differences in the IgA antibody titers against H. pylori between H. pylori-positive and H. pylori-negative dyspeptic patients were significant and may be useful to confirm a borderline IgG result. No differences were found in IgM antibody titer between H. pylori-positive and -negative patients. The greatest age-dependent increase in IgG and IgA antibody titers was found in children, and if a lower cut-off level is used for children than for adults, as has been proposed, the proportion of people with increased antibody titers against H. pylori would be almost constant from the age of between five and 10 years until the time between 61 and 80 years. Comparison of H. pylori IgG antibodies with IgG antibodies against Campylobacter jejuni and total antibodies against cytomegalovirus (CMV) showed a greater similarity between H. pylori and C. jejuni (R = 0.51) than between H. pylori and CMV (R = 0.22). This may possibly be caused by cross-reactions between H. pylori and C. jejuni. The H. pylori heat-stabile antigen seems not to be very different from other crude H. pylori antigens like acid glycine-extracted antigens, but purification and characterization of the antigens are needed to improve antibody assays.     

Impact of Helicobacter pylori infection on the humoral immune response to MUC1 peptide in patients with chronic gastric diseases and gastric cancer

Many investigators have demonstrated alteration of gastric mucins in H. pylori infected individuals. The inflammatory environment induced by H. pylori leading to aberrant glycosylation of MUC1 and demasking of core peptide MUC1 epitope could enhance immune responses to MUC1. IgG and IgM immune response to MUC1 in patients with gastric cancer (n = 214) chronic gastroduodenal diseases (n = 160) and healthy blood donors (n = 91) was studied with ELISA using bovine serum albumin-MUC1 60-mer peptide as antigen. H. pylori serologic status was evaluated with ELISA and CagA status by immunoblotting. Gastric mucosa histology was scored according to the Sydney system. Compared to H. pylori seronegative individuals, higher levels of IgG antibody to MUC1 were found in H. pylori seropositive patients with benign gastric diseases (p < 0.01) and blood donors (p < 0.03). Higher MUC1 IgG antibody levels were associated with a higher degree of gastric corpus mucosa inflammation in patients with chronic gastroduodenal diseases (p < 0.0025). There was a positive correlation between the levels of anti-H. pylori IgG and MUC1 IgG antibody levels in blood donors (p = 0.03), and in patients with benign diseases (p < 0.0001). In patients with gastric cancer (n = 214) a significantly higher level of anti-MUC1 IgG than in blood donors was observed (p < 0.001) irrespective of H. pylori status or stage of cancer. MUC1 IgM antibody levels were not related to the H. pylori serology. IgG immune response to tumor-associated MUC1 is up regulated in H. pylori infected individuals. This increase is associated with a higher IgG immune response to H. pylori and with a higher degree of gastric mucosa inflammation. High levels of MUC1 IgG antibody irrespective of H. pylori serologic status characterized patients with gastric cancer. The findings suggest that, in some individuals, the H. pylori infection may stimulate immune response to tumor-associated MUC1 peptide antigen thus modulating tumor immunity.     

Diagnostic value of detection of IgM antibodies to Helicobacter pylori.

This report describes the diagnostic value of anti-Helicobacter pylori IgM detection. Serum samples from 9043 symptomatic and asymptomatic individuals were evaluated with ELISA for the presence of anti-H. pylori IgG, IgM, and IgA. The specificity of detected IgM was confirmed by inhibition and cross-reactivity assays. Treatment of IgM-positive specimens with 1% 2-mercaptoethanol resulted in approximately 90% inhibition. Our data suggest a low level of cross-reactivity (5%) between H. pylori and four different enteropathogenic bacteria tested. The specificity of anti-H. pylori IgM was also demonstrated by Western blot and linearity studies. Data show that the detected IgM is highly specific. Western blot analysis revealed a variable IgM response to H. pylori antigens among patients, with the most reactive antigenic fractions being in the range of 55- to 100-kDa. Overall, the data confirm the diagnostic value of anti-H. pylori IgM detection. The prevalence of IgM antibodies to H. pylori in tested sera was significantly higher in symptomatic patients (10.4%) than in asymptomatic individuals (1.1%). Likewise, the percentage of sera positive for IgM alone was higher in symptomatic than in asymptomatic groups (3.8 vs 0.22%). About 5% of sera were positive only for IgA. We concluded that ELISA can be used for the detection of specific IgM to H. pylori and that the presence or absence of IgM antibodies to H. pylori may reflect whether or not an acute infection exists.     

以壳聚糖为佐剂的Hp疫苗诱导的体液免疫应答及其免疫保护效应

目的：探讨以壳聚糖为佐剂的Hp疫苗的免疫保护作用及其机制。方法:BALB/c小鼠随机分为9组：①空白对照组：PBS溶液；②壳聚糖酸溶液组；③壳聚糖颗粒组；④Hp抗原组；⑤Hp抗原+壳聚糖酸溶液组；⑥Hp抗原+壳聚糖颗粒组；⑦Hp抗原+CT组；⑧Hp抗原+壳聚糖酸溶液+CT组；⑨Hp抗原+壳聚糖颗粒+CT组，各组于第0、7、14、21 d 灌胃各免疫1次，免疫后4周给予1×1012CFU/L的SS1 Hp菌液每只 0.5 mL进行攻击，隔日1次，共2次。4周后，采用定量Hp培养和病理改良Giemsa染色法检测胃黏膜内Hp感染。用ELISA法检测血清抗Hp IgG、IgG1、IgG2a及唾液和胃黏膜内抗Hp IgA，用SP免疫组织化学法检测胃黏膜内分泌型IgA（sIgA）。结果:①以壳聚糖为佐剂的Hp疫苗的免疫保护率达60%，与以CT为佐剂的Hp疫苗的免疫保护率（58.33%）相似，显著高于单纯Hp抗原组及其它不含Hp抗原组（P<0.01或P<0.05），同时以CT＋壳聚糖为佐剂的Hp疫苗的保护率为84.62%、85.71%，其Hp的定植评分显著低于无佐剂组及以CT为佐剂组（P<0.01，P<0.05）。②含佐剂的Hp疫苗所诱导产生的Hp IgG水平显著高于对照组及无佐剂组（P<0.01，P<0.05），而以CT＋壳聚糖为佐剂组所产生的抗Hp IgG水平显著高于仅以 CT或壳聚糖为佐剂组（P<0.05）。③胃黏膜内sIgA及特异性抗Hp IgA水平在壳聚糖为佐剂组与以CT为佐剂组无差别（P>0.05），显著高于无佐剂组，而壳聚糖与CT联合应用组显著高于单以CT为佐剂组（P<0.01，P<0.05）。结论:以壳聚糖为佐剂的Hp疫苗对Hp感染具有免疫保护作用，并可成功诱导黏膜局部的特异性体液免疫应答，从而发挥免疫防御作用。     

High prevalence of IgG and IgA antibodies to 19-kDa Helicobacter pylori-associated lipoprotein in chronic urticaria

BACKGROUND: Chronic urticaria has been described in patients with Helicobacter pylori infection. We studied the titer of IgG and IgA type antibodies against H. pylori in patients with and without urticaria of unknown etiology. We also investigated the prevalence of antibodies against H. pylori-associated lipoprotein 20 (lpp20) in patients with and without chronic urticaria. METHODS: The concentration of anti-H. pylori antibodies (IgG and IgA) was determined by the RIDA test. The level of anti-lpp20 antibodies was determined by Western blot using various H. pylori antigens (from 19 to 120 kDa). RESULTS: Patients with chronic urticaria and H. pylori infection (subgroup 1, n = 33) had high IgG and IgA titers whereas all patients with chronic urticaria and without H. pylori infection (subgroup 2, n = 23) were seronegative (P = 0.0128 for IgG and P = 0.003 for IgA). Titers in subgroup 1 did not differ significantly from a control group (n = 33) with severe H. pylori-associated gastritis without urticaria. The prevalence of the anti-lpp20 antibodies was significantly higher in subgroup 1 compared to the control group (93.9 vs 21.2%, P < 0.0001 for IgG, and 46.1 vs 6.3%, P < 0.0029 for IgA). CONCLUSIONS: We suggest that IgG and IgA antibodies to H. pylori-associated lpp20 may play role in the pathogenesis of chronic urticaria.     

Local immune response in Helicobacter pylori-infected cats and identification of H. pylori in saliva, gastric fluid and faeces.

Helicobacter pylori-infected cats were screened by culture and polymerase chain reaction (PCR) for the presence of H. pylori in salivary secretions, gastric juice, gastric tissue and faeces. H. pylori was cultured from salivary secretions in six of 12 (50%) cats and from gastric fluid samples in 11 of 12 (91%) cats. A 298 base pair polymerase chain reactions (PCR) product specific for an H. pylori 26000 MW surface protein was amplified from dental plaque samples from five of 12 (42%) cats and from the faeces of four of five (80%) cats studied. Analyses of serum and mucosal secretions by enzyme-linked immunosorbent assay (ELISA) revealed an H. pylori-specific immunoglobulin G (IgG) response, and elevated IgA anti-H. pylori antibody levels in salivary and local gastric secretions. Immunohistochemical analyses of gastric tissue revealed the presence of IgM+ B cells assembled into multiple lymphoid follicles surrounded by clusters of CD4+ and CD8+ T cells. The lamina propria also contained single cells or aggregates of IgA+ and IgM+ B cells. These observations show that H. pylori can be identified in feline mucosal secretions, and that a localized IgA immune response develops in gastric tissue of H. pylori-infected cats. The findings suggest a zoonotic risk from exposure to personnel handling H. pylori-infected cats in vivaria.     

CagA antibodies in Japanese children with nodular gastritis or peptic ulcer disease

cagA(+) Helicobacter pylori strains have been linked to more severe gastric inflammation, peptic ulcer disease, and gastric cancer in adults, but there have been few studies of cagA in children. We examined the relationship between H. pylori cagA status and clinical status in Japanese children. Forty H. pylori-positive children were studied: 15 with nodular gastritis, 5 with gastric ulcers, and 20 with duodenal ulcers. H. pylori status was confirmed by biopsy-based tests and serum anti-H. pylori immunoglobulin G (IgG) antibody. As controls, 77 asymptomatic children with sera positive for anti-H. pylori IgG were enrolled. Levels of IgG antibodies to CagA in serum were measured by an antigen-specific enzyme-linked immunosorbent assay. In 16 patients with successful H. pylori eradication, posttreatment levels of CagA and H. pylori IgG antibodies also were studied. The CagA antibody seropositivities of asymptomatic controls (81.8%) and patients with nodular gastritis, gastric ulcers, and duodenal ulcers (80.0 to 95.0%) were not significantly different. Compared with pretreatment levels of CagA antibodies, posttreatment levels decreased progressively and significantly. We conclude that, as in Japanese adults, a high prevalence of cagA(+) H. pylori strains was found in Japanese children, and that there was no association with nodular gastritis or peptic ulcer disease. In the assessment of eradicative therapies, monitoring of serum anti-CagA antibodies does not appear to offer any direct benefit over monitoring of anti-H. pylori antibodies.     

Presence of Helicobacter pylori Antibodies in Haemodialysis Patients

Aim:  Renal dysfunction may influence the colonization of gastric mucosa by urea-splitting bacteria such as Helicobacter pylori , by increasing urea concentrations in the gastric juice. Our aim was to investigate the prevalence of H. pylori in patients with end-stage renal disease (ESRD), receiving long-term haemodialysis treatment.
Methods:  This study included 40 sera from patients with ESRD (29 male and 11 female) undergoing periodic haemodialysis; mean time of treatment was 42.6 months. Using ELISA technique, we investigated the presence of IgG and IgA antibodies against H. pylori as well as IgG CagA (antibodies specific for CagA(+) strains of H. pylori ). Sera from 40 healthy blood donors were used as a control group.
Results:  H. pylori IgG antibodies were detected in 32 out of 40 (80%) patients in the dialysis group, while 31/40 (77.5%) tested positive for IgA. IgG CagA antibodies were present in 13 out of 40 (32.5%). Prevalence of H. pylori IgG, IgA and CagA IgG antibodies in the control group was 33, 7 and 15%, respectively.
Conclusions:  Although international data suggest that prevalence of H. pylori infection is the same in ESRD patients as in healthy individuals, in our study that seems not to be the case. The higher blood and gastric juice urea levels may be a risk factor (among many others), but more studies are required in order to understand the relation of H. pylori infection in this group of patients.     

State of local and total humoral immunity in duodenal ulcer with Campylobacter pylori infection

A total of 83 patients with duodenal ulcer and a varying degree of gastric mucosa contamination with C. pylori were examined. Secretory IgA was less frequently detectable in the gastric juice of patients with higher level of gastric mucosa contamination with C. pylori and in lower concentrations than in the patients with a lesser C. pylori contamination. Healing of duodenal ulcer defects was associated with a decrease of gastric mucosa contamination and elevation of secretory IgA content in the gastric juice. The role of serum immunoglobulins in the gastric juice is less significant: IgG and IgA are rarely detected. Salivary content of secretory IgA depended on the gastric mucosa contamination and ulcer stage. Secretory IgA level increased by the ulcer remission, and C. pylori contamination decreased. Normal blood serum IgA, IgG, and IgM ratios were shifted in the patients with C. pylori contamination, particularly so in those with a higher level of contamination. These findings suggest a contribution of local and total immune reactions related to C. pylori to the pathogenesis of duodenal ulcer.     

Disparity between mucosal and serum IgA and IgG in <Emphasis Type="Italic">Helicobacter pylori</Emphasis> infection

Mucosal IgA and IgG are involved in the immune defense against Helicobacter pylori in infected patients. In contrast to IgG, IgA is transported into the gastric lumen and is responsible for the first-line defense. Therefore antigens recognized by mucosal IgA are possible candidates for vaccination. This study compared the IgA and IgG immune response to H. pylori in the gastric mucosa and that in the serum of 21 patients with H. pylori gastritis by the immunoblotting technique. In particular, mucosal IgA immune response against the urease antigen of H. pylori was studied in detail, as vaccination with this antigen was not curative in men. The results show that mucosal IgA was not represented by serum IgA and IgG, and that the H. pylori specific mucosal IgA and IgG immune responses differ in antigen-recognition pattern. This disparity may reflect the different transport ways and functions of these two immunoglobulin isotypes. Furthermore, mucosal IgA specific for urease was found inconsistently in patients with H. pylori gastritis. As vaccination antigens should induce an appropriate mucosal IgA immune response against H. pylori, our findings may have important implications for the selection of antigens for vaccination against H. pylori.     

Helicobacter pylori infection and chronic gastritis in gastric cancer.

AIMS: To investigate the prevalence of Helicobacter pylori associated chronic gastritis in patients with gastric cancer. METHODS: Serum IgG antibodies for H pylori were determined in 54 consecutive patients with gastric carcinoma. The prevalence of H pylori in gastric mucosa was also examined histologically (modified Giemsa) in 32 patients from whom adequate biopsy specimens of the antrum and corpus were available. Thirty five patients with gastrointestinal tumours outside the stomach and 48 with non-gastrointestinal malignancies served as controls. RESULTS: Of the 54 patients, 38 (70%) had H pylori antibodies (IgG) in their serum (three additional patients had H pylori antibodies IgA, class specific but not IgG specific). This prevalence was significantly higher (p less than 0.05) than that (49%) in the 35 controls. No differences in prevalence of H pylori antibodies were found between gastric cancer cases of intestinal (IGCA) or diffuse (DGCA) type, both these types showing H pylori antibodies (IgG) in 71% of the patients. In the subgroup of 32 subjects, five patients had normal gastric mucosa and four showed corpus limited atrophy ("pernicious anaemia type" atrophy of type A). All of these nine patients had no evidence of current or previous H pylori infection in serum (no IgG antibodies) or in tissue sections (negative Giemsa staining). The remaining 23 patients had antral or pangastritis, and all had evidence of current or previous H pylori infection. CONCLUSIONS: H pylori associated chronic gastritis was the associated disease in 75% of the patients with gastric cancer occurring equally often in both IGCA and DGCA groups. About 25% of cases seem to have a normal stomach or severe corpus limited atrophy, neither of which showed evidence of concomitant H pylori infection.     

Type or extension of intestinal metaplasia and immature/atypical "indefinite-for-dysplasia" lesions as predictors of gastric neoplasia

At present, no information exists on the neoplastic potential of the immature hyperproliferative and atypical lesions of the gastric mucosa, which have been recently labeled "indefinite for dysplasia." In addition, uncertainties still exist concerning the risk contribution of intestinal metaplasia (IM) type and extension, as well as Helicobacter pylori infection. In this study, 471 dyspeptic patients showing IM 10% or higher (median, 40; 25th-75th percentile, 20-60) in antral, angulus, or corpus endoscopic biopsies were submitted to repeated examinations (median, 3; 2-5) over 52 (26-85) months of follow-up, during which 44 neoplastic cases were recorded. IM extension, incomplete, sulfomucin-positive, or CAR5 antigen-positive IM; H pylori infection; and indefinite-for-dysplasia lesions (IDLs), as found at first examination, all showed significant neoplastic potential. However, only IDL, ongoing H pylori infection, and patient's age retained independent predictive power in a multivariate model. On the other hand, IM extension 20% or higher proved to be more sensitive as first screening parameter for identification of subjects with increased neoplastic risk. We suggest that patients with IM, when infected, should undergo H pylori eradication to reduce their cancer risk; only those bearing IDL or very extensive IM (which strongly correlates with IDL) should be followed up with endoscopies and biopsies.     

Diagnosis of Helicobacter pylori infection by using pyloriset EIA-G and EIA-A for detection of serum immunoglobulin G (IgG) and IgA antibodies.

We evaluated the performance of new enzyme immunoassay (EIA) kits (Pyloriset; Orion Corporation, Orion Diagnostica, Espoo, Finland) for the detection of immunoglobulin G (IgG) and IgA antibodies to Helicobacter pylori in serum. Serum samples from 195 patients with upper abdominal complaints were collected. Biopsy specimens of the gastric mucosae were taken for histological analysis and bacterial culture. The sensitivity, specificity, and positive and negative predictive values, and efficacy of the Pyloriset EIA-G in detecting IgG antibodies to H. pylori were 92, 84, 88, 90, and 89%, respectively, when compared with those of the reference methods used. The corresponding data for detection of IgA antibodies were 80, 89, 89, 79, and 84%, respectively. The overall prevalence of defined H. pylori positivity was 54%. Moreover, the antibody tests showed a very good correlation with the biopsy findings. IgG antibodies were found in 93% of sera from patients with documented gastritis and H. pylori positivity, whereas only 4% of the sera from patients with documented gastritis and H. pylori-negative patients was positive. The results obtained for IgA antibodies were 81 and 6%, respectively. We conclude that the Pyloriset EIA-G, the test for IgG antibodies, is a good and reliable test for the detection of antibodies to H. pylori and as an indication of H. pylori infection. The determination of IgA antibodies may be used as a test that complements the IgG antibody assay.     

Neonatal Fc receptor for IgG (FcRn) expressed in the gastric epithelium regulates bacterial infection in mice

Neonatal Fc receptors for immunoglobulin (Ig)G (FcRn) assume a central role in regulating host IgG levels and IgG transport across polarized epithelial barriers. We have attempted to elucidate the contribution of FcRn in controlling Helicobacter infection in the stomach. C57BL/6J wild-type or FcRn(-/-) mice were infected with Helicobacter heilmannii, and gastric lesions, bacterial load and the levels of antigen-specific IgG in serum and gastric juice were analyzed. The elevated levels of anti-H. heimannii IgG in gastric juice were observed exclusively in wild-type mice but not in FcRn(-/-) mice. In contrast, an increase in lymphoid follicles and bacterial loads along with deeper gastric epithelium invasion were noted in FcRn(-/-) mice. C57BL/6J wild-type or FcRn(-/-) mice were also infected with Helicobacter pylori SS1, and the results of the bacterial load in stomachs of these mice and the anti-H. pylori IgG levels in serum and gastric juice were similar to those from H. heilmannii infection. Our data suggest that FcRn can be functionally expressed in the stomach, which is involved in transcytosis of IgG, and prevent colonization by H. heilmannii and the associated pathological consequences of infection.     

Salivary immunoglobulin G assay to diagnose Helicobacter pylori infection in children.

An in-house enzyme-linked immunosorbent assay (ELISA) for measurement of Helicobacter pylori-specific immunoglobulin G (IgG) and IgA in saliva was evaluated by comparison with histopathologic (Giemsa staining) and biochemical (urease quick test) examination of gastric biopsy specimens obtained from 112 children referred for diagnostic gastroscopy. Serum H. pylori IgG was also measured in a subgroup of 50 children by the same ELISA. Salivary H. pylori IgG levels were significantly higher in H. pylori-positive (n = 57) than in H. pylori-negative (n = 55) children (P < 0.001). The sensitivity and specificity of the salivary IgG test were 93 and 82%, respectively; the positive and negative predictive values were 84 and 92%, respectively; and the accuracy was 87.5%. Salivary H. pylori IgA did not distinguish H. pylori-positive from H. pylori-negative children. The performance of serum H. pylori IgG was slightly (3 to 6%) better than that of salivary H. pylori IgG. The salivary IgG test can be considered a useful tool for the screening of H. pylori infection in children.     

Inverse relation of serum Helicobacter pylori antibody titres and extent of intestinal metaplasia.

AIMS: To clarify the relation between the serum titre of anti-Helicobacter pylori (H pylori) antibody and the extent of intestinal metaplasia of the gastric mucosa. METHODS: The serum anti-H pylori IgG titres of 95 asymptomatic individuals (mean age 65 years) undergoing an annual health examination were measured and compared with the extent of intestinal metaplasia (absent, moderate, or extensive), determined by examination of multiple endoscopic mucosal biopsy specimens. Serum pepsinogen I (PGI) levels, as a marker for gastric atrophy, were also measured. RESULTS: The prevalence of seropositivity for H pylori antibody was high (> 80%), regardless of the extent of metaplasia. However, there was a negative association between the extent of metaplasia and the anti-H pylori titre: 75% of the subjects in the group without metaplasia had high (3+) antibody levels, as did 43% with moderate, and 37% with extensive metaplasia (absent v extensive). The inverse relation between the titre and the extent of metaplasia was evident when examined in those with normal PGI (> 30 ng/ml), whereas no such relation was apparent in subjects with low PGI (< or = 30 ng/ml). CONCLUSIONS: The anti-H pylori titre correlates inversely with the extent of intestinal metaplasia, particularly in subjects with less marked gastric atrophy.     

Antral histopathological changes in acid peptic disease associated with Helicobacter pylori

The histopathology of the antral mucosa of patients with acid peptic disease was studied in relation to Helicobacter pylori infection. Three hundred and fifty-five patients underwent gastroscopy and biopsy on 443 occasions. During each gastroscopy, two antral samples were taken for Rapid Urease Test (RUT) for H. pylori and two antral samples for histopathology. Haematoxylin and Eosin and modified Giemsa stained sections were studied. Histopathological changes in the antrum and the density of H. pylori were graded according to the Sydney System criteria. There was a significant association between the RUT and histology results for detection of H. pylori. The overall prevalence of H. pylori was 61.4% with a maximum incidence in the third and fourth decades of life, and an equal sex distribution. H. pylori colonisation was seen in 90.7% of patients with duodenal ulcer, 66.7% with gastric ulcer and 44.3% with non-ulcer dyspepsia. H. pylori colonisation was associated with more severe antral chronic active gastritis, lymphoid follicles, intestinal metaplasia and dysplasia. Elimination of H. pylori by treatment with anti-H. pylori regimens resulted in regression of the changes.