Interplay between Helicobacter pylori and immune cells in immune pathogenesis of gastric inflammation and mucosal pathology

Helicobacter pylori infection is associated with an inflammatory response in the gastric mucosa, leading to chronic gastritis, peptic ulcers, gastric carcinoma and gastric mucosa-associated lymphoid tissue (MALT) lymphomas. Recent studies have shown that apoptosis of gastric epithelial cells is increased during H. pylori infection. Apoptosis induced by microbial infections are factors implicated in the pathogenesis of H. pylori infection. The enhanced gastric epithelial cell apoptosis in H. pylori infection has been suggested to play an important role in the pathogenesis of chronic gastritis and gastric pathology. In addition to directly triggering apoptosis, H. pylori induces sensitivity to tumor-necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL)-mediated apoptosis in gastric epithelial cells via modulation of TRAIL apoptosis signaling. Moreover, H. pylori infection induces infiltration of T lymphocytes and triggers inflammation to augment apoptosis. In H. pylori infection, there was significantly increased CCR6⁺CD3⁺ T-cell infiltration in the gastric mucosa, and the CCR6 ligand, CCL20 chemokine, was selectively expressed in inflamed gastric tissues. These results implicate that the interaction between CCL20 and CCR6 may play a role in recruiting T cells to the sites of inflammation in the gastric mucosa during Helicobacter infection. Through these mechanisms, chemokine-mediated T lymphocyte trafficking into inflamed epithelium is initiated and the mucosal injury in Helicobacter infection is induced. This article will review the recent novel findings on the interactions of H. pylori with diverse host epithelial signaling pathways and events involved in the initiation of gastric pathology, including gastric inflammation, mucosal damage and development of MALT lymphomas.     

Immunoglobulin G1 Antibody Response to Helicobacter pylori Heat Shock Protein 60 Is Closely Associated with Low-Grade Gastric Mucosa-Associated Lymphoid Tissue Lymphoma

Gastric mucosa-associated lymphoid tissue (MALT) lymphoma is related to Helicobacter pylori infection. Specifically, it has been pointed out that pathogenesis of MALT lymphoma involves the 60-kDa heat shock protein (hsp60). To investigate humoral immune responses to the H. pylori hsp60 in patients with gastroduodenal diseases and patients with MALT lymphoma, the hsp60 of H. pylori was expressed with a glutathione S-transferase fusion protein and was purified (recombinant hsp60). Sera were obtained from H. pylori-positive patients with gastroduodenal diseases (MALT lymphoma, n = 13; gastric ulcer, n = 20; duodenal ulcer, n = 20; gastritis, n = 20) and from H. pylori-negative healthy volunteers (n = 9). Sera from patients with MALT lymphoma were also obtained at two times: before and after eradication therapy. Antibodies to hsp60 and H. pylori were assessed by enzyme-linked immunosorbent assay. The levels of immunoglobulin G (IgG) antibodies to the hsp60 of H. pylori-positive patients with gastroduodenal diseases were significantly elevated compared to those in the controls. The levels of IgG1 antibodies to hsp60 were elevated and correlated with the levels of anti-H. pylori antibodies in patients with MALT lymphoma. Humarol immunity against hsp60 may be important and relevant to gastroduodenal diseases induced by H. pylori infection.     

When can complete regression of low‐grade gastric lymphoma of mucosa‐associated lymphoid tissue be predicted after Helicobacter pylori eradication?

AIMS: Recent studies suggest that primary low-grade gastric lymphomas of mucosa-associated lymphoid tissue (MALT) are cured in many cases between 1 and 18 months after H. pylori eradication. The aim of this study is to elucidate when complete regression (CR) of MALT lymphoma can be histologically predicted after H. pylori eradication. METHODS AND RESULTS: Twenty-one patients with low-grade gastric MALT lymphoma were treated with triple therapy (amoxicillin, clarythromycin and proton pump inhibitor) for 14 days. Subsequently, they were followed up by sequential endoscopy and biopsy (number of biopsy specimens for each endoscopy is 3-8, with an average of 4) from 91 to 657 days (average: 309 +/- 165 days). Eradication of H. pylori infection was achieved in all patients. Nine patients were free of lymphoma at 1 to 2 months after eradication and remained in CR at 163-657 days. Twelve patients showed residual lymphoma at 1 to 2 months after eradication. Five out of 12 patients revealed only one or two small foci of lymphoma-cell aggregation and showed a high incidence (80%) of CR at the latest biopsy (135-434 days, average 276 +/- 115 days after eradication), while seven patients showed diffuse remains of lymphoma cells and indicated CR in only one case (14%) at 362 days, partial regression in five cases at 130-431 days (average 227 +/- 114 days), and no change in one case at 91 days after eradication. CONCLUSIONS:: These results suggest that CR of low-grade MALT lymphoma can be predicted at 1 to 2 months after eradication therapy by checking histological changes of MALT lymphoma cells.     

Effect of Helicobacter pylori Eradication According to the IL-8-251 Polymorphism in Koreans

Previous studies suggested that polymorphisms of proinflammatory cytokine genes are important host genetic factors in Helicobacter pylori infection. The present study evaluated whether IL-8-251 polymorphism affected H. pylori eradication rate and to investigate the effect of H. pylori eradication on angiogenesis and the inflammatory process according to the IL-8-251 polymorphism. A total of 250 H. pylori-positive patients treated by endoscopic resection of the gastric neoplasm were classified into 3 groups (134 H. pylori-eradicated group, 19 H. pylori-eradication failure group, and 97 H. pylori-infected group). H. pylori status, histology, and angiogenic factor levels were evaluated at baseline, 6 months, and 18 months. H. pylori eradication rate was 92.9% in AA genotype, 85.7% in AT genotype and 88.4% in TT genotype (P value = 0.731). Elevated IL-8 and matrix metalloproteinase-9 concentrations in H. pylori-infected gastric mucosa were reversible by successful eradication of H. pylori, independent of the IL-8-251 polymorphism. It is suggested that elevated IL-8 and MMP-9 concentrations in H. pylori-infected gastric mucosa are altered significantly after successful eradication and these conditions continue for 18 months. However, IL-8-251 polymorphism does not affect H. pylori eradication rate and the sequential changes of related angiogenic factors after H. pylori eradication in Koreans.     

HELICOBACTER PYLORI-SPECIFIC TUMOUR-INFILTRATING T CELLS PROVIDE CONTACT DEPENDENT HELP FOR THE GROWTH OF MALIGNANT B CELLS IN LOW-GRADE GASTRIC LYMPHOMA OF MUCOSA-ASSOCIATED LYMPHOID TISSUE

Previous studies have shown that tumour cells from low-grade B-cell gastric lymphomas of mucosa-associated lymphoid tissue (MALT) type proliferate in vitro in response to heat-killed whole cell preparations of Helicobacter pylori , but only in the presence of tumour-infiltrating T cells. This response is strain-specific in that the tumours studied responded optimally to different strains of H. pylori . It was unclear from these studies, however, whether the ability to recognize the specific stimulating strains of H. pylori was a property of the tumour cells or the tumour-infiltrating T cells. This study shows that whereas the tumour cells do not respond to H. pylori , both freshly isolated tumour-infiltrating T cells and a T cell line derived from these cells proliferate in response to stimulating strains of H. pylori . T cells from the spleen of one of the patients do not share this property. These results suggest that B-cell proliferation in cases of low-grade gastric lymphoma of MALT type in vitro in response to H. pylori is due to recognition of H. pylori by tumour-infiltrating T cells, which in turn provide help for tumour cell proliferation. The observations provide an explanation for properties of gastric MALT-type lymphoma, such as regression following eradication of H. pylori and the tendency of the tumour to remain localized to the primary site.     

Chromosomal imbalances are associated with outcome of Helicobacter pylori eradication in t(11;18)(q21;q21) negative gastric mucosa-associated lymphoid tissue lymphomas

Approximately 70% of gastric mucosa-associated lymphoid tissue (MALT) lymphomas can be successfully treated with H. pylori eradication. The translocation t(11;18)(q21;q21) characteristic of MALT lymphoma is recognized as a marker for H. pylori independency, but this marker is found in only a half of the MALT lymphomas resistant to H. pylori eradication. Detailed analyses of the genomic features of eradication resistant as well as responsive groups are important for understanding their molecular basis. We performed array-based comparative genomic hybridization (array-CGH) for 29 gastric MALT lymphomas treated with H. pylori eradication. These comprised ten cases of t(11;18) positive MALT, nine cases of t(11;18) negative MALT with H. pylori dependency, and ten cases of t(11;18) negative MALT with H. pylori independency. Array-CGH analysis demonstrated that no significant genetic alterations were found in t(11;18) positive MALT lymphomas, but numerous genomic alterations were detected in t(11;18) negative MALT lymphomas. Many of these alterations were similar to those found in diffuse large B-cell lymphoma with trisomy 3 being the most recurrent alteration. Within the t(11;18) negative MALT lymphoma without large cell components group, genomic imbalances occurred more frequently in the H. pylori independent than in the H. pylori dependent group (P = 0.02). Genomic imbalances are associated with H. pylori independency in t(11;18) negative gastric MALT lymphomas. They may thus play an important role in the development of H. pylori independency.     

Detection of monoclonality of gastric MALT lymphoma using PCR method and its clinicopathological application

Twenty cases of H. pylori-related gastric lymphoproliferative disorders including 12 cases of MALT lymphoma (Grade 5 after Wotherspoon, et al), 6 of suspicious of MALT lymphoma (Grade 4), and 2 of active chronic gastritis (Grade 3) were studied. Using the nested PCR method, paraffin-embedded gastric biopsy specimens of these 20 cases were investigated whether or not monoclonal IgH rearrangement could be demonstrated in infiltrating lymphoid cells. Monoclonal IgH rearrangement was recognized in 6 of 12 MALT lymphomas, but in other 14 cases including 6 of MALT lymphomas the monoclonality was not recognized. The result showed the sensitivity was 50% and the specificity was 100% with this method. Follow-up study after eradication of H. pylori was performed on 6 cases of MALT lymphoma which had showed the monoclonality before, using the same method. The monoclonality disappeared in 5 of 6 and histology showed a complete remission. In the remaining one case the monoclonality was yet demonstrated and lymphoma cells were histologically recognized. Thus, this method is very useful to assess not only the histological diagnosis of MALT lymphoma but also the effectiveness after treatment.     

Eradication of Helicobacter pylori Increases Ghrelin mRNA Expression in the Gastric Mucosa

It has been suggested that Helicobacter pylori eradication may influence production of some peptides in the stomach, which can affect appetite. This hypothesis is controversial. To verify the hypothesis, we conducted this randomized controlled trial using H. pylori infected subjects without any gastrointestinal symptoms. The treatment group received triple H. pylori eradication therapy for 7 days and the control group received no medication. We measured ghrelin, obestatin and the tumor necrosis factor-α (TNF-α) mRNA levels in endoscopic biopsy specimens and the changes from baseline to follow-up. The plasma active n-octanoyl ghrelin and obestatin levels were measured in both groups. The ghrelin/obestatin ratios in plasma and gastric mRNA expression were calculated at baseline and follow-up. Ghrelin mRNA expression in the fundic mucosa after H. pylori eradication increased significantly compared to the control group (4.47±2.14 vs. 1.79±0.96, P=0.009), independent of inflammatory changes. However, obestatin mRNA expression decreased in the antral mucosa (-0.57±1.06 vs. 0.41±0.72, P=0.028). The treatment group showed a marginal increase (P=0.060) in plasma ghrelin/obestatin ratio. The TNF-α mRNA expression also decreased significantly with treatment. This randomized controlled trial demonstrates that H. pylori eradication increases ghrelin mRNA expression, independent of inflammatory cell changes.     

High frequency of CagA+ Helicobacter pylori infection in high-grade gastric MALT B-cell lymphomas

A high incidence of Helicobacter pylori infection has been found in patients with gastric MALT (mucosa-associated lymphoid tissue) B-cell lymphoma. Recent studies have indicated that the aggressive strains of the bacterium containing the CagA gene may have direct effects on tumourigenesis. To investigate the involvement of CagA+ strains in MALT lymphomagenesis, a sensitive polymerase chain reaction (PCR)-based detection assay for the gene was developed. DNA extracts from paraffin sections of 123 H. pylori-related gastric biopsies from Italy were analysed, including 56 cases of chronic gastritis, 37 low-grade, and 30 high-grade MALT lymphomas: 30·3 per cent (17/56) of the gastritis cases, 37·8 per cent (14/37) of the low-grade, and 76·7 per cent (23/30) of the high-grade MALT lymphomas were found to contain the CagA gene. The frequency of CagA+ strain infection was signfiicantly higher (P<0·05) in high-grade than in low-grade MALT lymphoma or gastritis. These results suggest that high-grade gastric MALT lymphoma transformation may be more likely to occur following infection by CagA+ strains of H. pylori. © 1998 John Wiley & Sons, Ltd.     

胃肠道黏膜相关边缘区B细胞淋巴瘤和弥漫性大B细胞淋巴瘤中API2-MALT1融合基因表达的差异

目的 比较t(11;18)(q21;q21)/API2-MALX1融合基因在胃肠道黏膜相关边缘区B细胞淋巴瘤(MALN淋巴瘤)和弥漫性大B细胞淋巴瘤(DLBCL)中的发生情况,探讨t(11;18)(q21;q21)与胃肠道MALT淋巴瘤和DLBCL间演进的关系.方法 收集57例胃肠道MALT淋巴瘤(包括38例胃和19例肠),32例胃肠道DLBCL(包括28例胃和4例肠)和7例胃DLBCL同时合并MALT淋巴瘤成分,用荧光原位杂交(FISH)检测API2-MALT1融合基因.使用的探针包括API2-MALT1双色融合易位探针和MALT1双色分离重排探针.结果 在MALT淋巴瘤中有21.1%(12/57,包括10例胃和2例肠)发现API2-MALT1融合基因,而在32例DLBCL和7例DLBCL与MALT淋巴瘤混合的病例中均未检测出API2-MALT1融合基因.两组经统计学比较差异有统计学意义(X~2=9.383,P=0.001).结论 API2-MALT1融合基因是MALT淋巴瘤中特异的遗传学异常,而不见于DLBCL或DLBCL与MAIX淋巴瘤共存的病例中,提示至少在胃肠道API2-MALT1阳性的MALT淋巴瘤一般不会发生大细胞转化,而胃肠道DLBCL可能为原发或由t(11;18)阴性的部分MALT淋巴瘤转化而来.     

Simultaneous gastric adenocarcinoma and MALT-type lymphoma in Helicobacter pylori infection

A 79-year-old women with upper abdominal pain, vomiting and weight loss was found at endoscopy to have a large tumour mass in the gastric body. Histology of forceps biopsies revealed an adenocarcinoma of intestinal type. Gastrectomy was performed, but extensive lymph node metastasis precluded a curative surgical approach. Histopathological study of the specimen, however, revealed two distict malignancies, which arose in the setting of Helicobacter pylori-associated chronic gastritis with partial mucosal atrophy. One tumour was a gastric carcinoma, while the other was a primary B-cell lymphoma of the stomach (CD20-positive). The lymphoma comprised both a low-grade component (mucosa-associated lymphoid tissue- or MALT-type lymphoma), and a high-grade component (large cell lymphoma with CD30-positive giant cells). Infection with H. pylori was confirmed by the serological presence of IgG antibodies to H. pylori-antigens, including antibodies against the 128 kDa protein of the cytotoxin-associated gene (cagA gene) of H. pylori.     

Helicobacter pylori Eradication for Prevention of Metachronous Recurrence after Endoscopic Resection of Early Gastric Cancer

Controversies persist regarding the effect of Helicobacter pylori eradication on the development of metachronous gastric cancer after endoscopic resection of early gastric cancer (EGC). The aim of this study was to assess the efficacy of Helicobacter pylori eradication after endoscopic resection of EGC for the prevention of metachronous gastric cancer. A systematic literature review and meta-analysis were conducted using the core databases PubMed, EMBASE, and the Cochrane Library. The rates of development of metachronous gastric cancer between the Helicobacter pylori eradication group vs. the non-eradication group were extracted and analyzed using risk ratios (RRs). A random effect model was applied. The methodological quality of the enrolled studies was assessed by the Risk of Bias table and by the Newcastle-Ottawa Scale. Publication bias was evaluated through the funnel plot with trim and fill method, Egger''s test, and by the rank correlation test. Ten studies (2 randomized and 8 non-randomized/5,914 patients with EGC or dysplasia) were identified and analyzed. Overall, the Helicobacter pylori eradication group showed a RR of 0.467 (95% CI: 0.362-0.602, P < 0.001) for the development of metachronous gastric cancer after endoscopic resection of EGC. Subgroup analyses showed consistent results. Publication bias was not detected. Helicobacter pylori eradication after endoscopic resection of EGC reduces the occurrence of metachronous gastric cancer.     

Deregulation of a distinct set of microRNAs is associated with transformation of gastritis into MALT lymphoma

The mechanisms underlying the transformation from chronic Helicobacter pylori gastritis to gastric extranodal marginal zone lymphoma (MALT lymphoma) are poorly understood. This study aims to identify microRNAs that might be involved in the process of neoplastic transformation. We generated microRNA signatures by RT-PCR in 68 gastric biopsy samples representing normal mucosa, gastritis, suspicious lymphoid infiltrates, and overt MALT lymphoma according to Wotherspoon criteria. Analyses revealed a total of 41 microRNAs that were significantly upregulated (n = 33) or downregulated (n = 8) in succession from normal mucosa to gastritis and to MALT lymphoma. While some of these merely reflect the presence of lymphocytes (e.g. miR-566 and miR-212) or H. pylori infection (e.g. miR-155 and let7f), a distinct set of five microRNAs (miR-150, miR-550, miR-124a, miR-518b and miR-539) was shown to be differentially expressed in gastritis as opposed to MALT lymphoma. This differential expression might therefore indicate a central role of these microRNAs in the process of malignant transformation.     

Factors associated with gastro-duodenal disease in patients undergoing upper GI endoscopy at the Korle-Bu Teaching Hospital,Accra, Ghana

BackgroundThere is a high prevalence of gastro-duodenal disease in sub-Saharan Africa. Peptic ulcer disease in dyspeptic patients, 24.5%, was comparable to prevalence of gastro-duodenal disease among symptomatic individuals in developed countries (12 — 25%). Limited data exists regarding its associated risk factors despite accumulating evidence indicating that gastroduodenal disease is common in Ghana.ObjectivesThis study investigates risk factors associated with gastro-duodenal disease at the Korle-Bu Teaching Hospital, Accra, Ghana.MethodsThis study utilized a cross-sectional design to consecutively recruit patients referred with upper gastro-intestinal symptoms for endoscopy. The study questionnaire was administered to study participants. Helicobacter pylori infection was confirmed by rapid-urease examination at endoscopy.ResultsOf 242 patients sampled; 64 had duodenal ulcer, 66 gastric ulcer, 27gastric cancer and 64 non-ulcer dyspepsia. Nineteen (19) had duodenal and gastric ulcer while 2 had gastric ulcer and cancer. A third (32.6%) of patients had history of NSAID-use. H. pyloriwas associated with gastric ulcer (p=0.033) and duodenal ulcer (p=0.001). There was an increased prevalence of duodenal ulcer in H. pylori-infected patients taking NSAIDs, P=0.003.ConclusionH. pylori was a major risk factor for peptic ulcer disease. However, NSAID-related gastro-duodenal injury has been shown to be common in H. pylori infected patients. It highlights the need for awareness of the adverse gastro-intestinal effects in a H. pylori endemic area.     

Differing degree and distribution of gastritis in Helicobacter pylori-associated diseases

Infection with Helicobacter pylori (H. pylori) causes gastritis, and may be associated with gastric and duodenal ulcers and also with such malignant diseases as MALT lymphoma and gastric carcinoma. In order to determine whether there are differences in the degree and distribution of gastritis, each patient with H. pylori gastritis only (n = 50) was matched for sex and age with four patients, one each with H. pylori-associated duodenal ulcer, gastric ulcer, gastric carcinoma or MALT lymphoma. From each patient, two biopsies were taken from the antrum and two from the corpus for histopathological examination of H. pylori gastritis. The median summed gastritis score decreases in the following order: antrum: gastric ulcer > duodenal ulcer > gastritis alone > carcinoma > MALT lymphoma, and corpus: gastric ulcer > carcinoma > MALT lymphoma > gastritis alone and duodenal ulcer. We conclude that the degree and distribution of H. pylori gastritis differs significantly among H. pylori-associated diseases. These differences may explain some of the underlying pathomechanisms associated with H. pylori infection.     

A case of multiple mucosa-associated lymphoid tissue (MALT) lymphoma of the colon identified as simple mucosal discoloration

Most colonic multiple mucosa-associated lymphoid tissue (MALT) lymphomas are confirmed with a histologic and immunohistochemical staining of the mucosal biopsy specimen obtained during colonoscopic examinations. Endoscopically, colonic MALT lymphomas frequently appear as protruding and/or ulcerative lesions, and there are not so many reports of colonic MALT lymphoma as compared to the frequent reports of MALT lymphoma of stomach. We report a unique case of colonic MALT lymphoma presenting as a simple reddish discoloration of mucosa; this presentation has never been describe before. Our patient was a 47-yr-old male who suffered from tenesmus and mucoid stool. A colonoscopy was accomplished, followed by a histologic examination and we diagnosed a colonic MALT lymphoma. Staging of the disease was done because this was necessary for choosing the modality of treatments. The patient was then treated with polychemotherapy in conjunction with radiation therapy.     

Stomach lymphomas: minimum diagnostic requirements for gastrointestinal histopathological diagnosis

Gastric lymphomas have been the subject of intensive studies in the last years and important progress has been made regarding their etiopathogenesis and therapy. Diagnosis of gastric lymphoma is usually made on bioptic material taken at endoscopy. Histopathologic diagnosis is frequently difficult. This paper summarizes the main diagnostic criteria of this setting. It analyses the morphological, immunohistochemical and molecular features to be considered for the differential diagnosis between: reactive process vs low grade B-cell gastric MALT lymphoma, B-cell MALT lymphoma vs other low grade lymphomas involving the stomach and low grade vs high grade gastric lymphoma. The histopathological aspects of gastric biopsies after antibiotic treatment for Helicobacter pylori eradication and the role of molecular analysis in the follow-up of these patients are also considered.     

The prevalence of helicobacter pylori among dyspeptic patients in an earthquake-stricken area

OBJECTIVES:

Helicobacter pylori is a gram-negative, spiral-shaped, urease-producing bacterium with multiple unipolar flagella. Humans are a major reservoir for H. pylori; however, there are no data on the prevalence of H. pylori among dyspeptic patients who have experienced natural disasters. Therefore, the aim of this study was to examine the prevalence of H. pylori in dyspeptic patients who survived a recent natural disaster and to compare the data between the pre-disaster and post-disaster periods.

METHODS:

Between December 2011 and February 2012 (∼ one month following an earthquake), 209 dyspeptic patients who underwent gastroscopy were included in the study. For microorganism identification, gastric biopsy materials from the 209 disaster survivors with dyspeptic complaints were tested for urease activity in a medium containing urea and a pH indicator. The obtained results were compared with pre-disaster data from dyspeptic patients in the same city during the corresponding period of the previous year. Furthermore, the current H. pylori prevalence was evaluated among 139 dyspeptic patients between January 2014 and May 2014.

RESULTS:

We found a significantly higher prevalence of H. pylori in disaster survivors with dyspepsia compared with dyspeptic patients in the pre-disaster period (p<0.005). Interestingly, the current H. pylori prevalence was found to be significantly higher than the prevalence in both the disaster and pre-disaster periods (p<0.005).

CONCLUSION:

These results suggest that a recent earthquake could contribute to the development of H. pylori infection in subjects who live in the disaster-stricken area. These data also highlight the exceptionally high H. pylori prevalence in dyspeptic patients. Regional variations require further analyses.     

Is Helicobacter pylori good or bad?

Helicobacter pylori remains a controversial organism with regards to humans, with its epidemiology still being unclear nearly two decades after its discovery. The association between H. pylori infection and subsequent development of chronic active gastritis, peptic ulcer disease, gastric cell carcinoma, and B cell mucosa-associated lymphoid tissue (MALT) lymphoma has been well established. Current studies, however, suggest that fewer than 20 % of all infected patients will develop any consequences from their infection. Hence, should the infection be considered a disease not at all or, on the contrary, is the microorganism harmful in only some circumstances? This article attempts to weigh the currently available evidence supporting that H. pylori may be good and not always bad.     

Evaluation of Helicobacter pylori infection in patients with common migraine headache

Introduction

Migraine can cause headache in different communities so that 12-15% are suffering worldwide. Recently the relationship between infectious diseases such as Helicobacter pylori infection and migraine headache has been the focus of many studies. The current study was designed to evaluate IgG and IgM antibodies to H. pylori in patients suffering from migraine headaches.

Material and methods

Patients who had diagnostic criteria for migraine were chosen as cases compared to some healthy individuals as the control group amongst which immunoglobulin G (IgG), immunoglobulin M (IgM), age, job, gastro-intestinal (GI) disorders, history of migraine, special meals, medications, sleeping disorders, stress, environmental factors etc were analysed.

Results

The prevalence of disease was 38.6%. Household women had the highest prevalence (40%). Among them menstruation was related to high prevalence of migraine. 75.6% of patients had gastrointestinal disorders of which the gastric reflux was the most important sign (47.1%). The mean optical density (OD) value of IgG and IgM antibody to H. pylori was 60.08 ±7.7 and 32.1 ±8.7 for the case group, 21.82 ±6.2 and 17.6 ±9.4 for the control group, respectively.

Conclusions

There was a significant difference in mean OD value of both antibodies to H. pylori amongst the case and control groups. As a result, active H. pylori infection is strongly related to the outbreak and severity of migraine headaches, and H. pylori treatment reduces migraine headaches significantly. Hopefully, the definite treatment and eradication of this infection can cure or reduce the severity and course of migraine headaches significantly if not totally.