Post‐operative care of interventional therapy for 40 liver cancer patients with obstructive jaundice

The care of 40 patients with primary liver cancer with obstructive jaundice treated with liver puncture bile drainage or biliary stent implantation was reported. Treated with the interventional therapy, patients were observed closely to identify symptoms of hepatic encephalopathy and pain; diet care was well performed. Bile drainage tube and skin acre were performed carefully. Liver function, bilirubin and other biochemical indicators were monitored; occurrence of bleeding, acute pancreatitis, biliary tract infection, leakage of ascites around drainage tube and other complication were observed with good discharge instruction. After this operation, three rounds of liver had poor function, and hepatic encephalopathy and death occurred during hospitalisation. Seven patients had bloody bile drainage fluid after operation; eight had increased blood amylase; nine had biliary infection and four had leakage of ascites around the drainage tube. After positive treatment and care, the situation was improved with varied degrees of jaundice increase.     

Detection of Helicobacter species in the liver of patients with and without primary liver carcinoma

BACKGROUND: Several studies have shown the presence of Helicobacter species in the human biliary tract and in the intestinal tract of animals. In this study, the presence of Helicobacter species in liver samples from patients with primary hepatic carcinomas was evaluated. METHODS: Sixteen liver specimens were studied (8 from patients with primary liver carcinoma and 8 from patients without primary liver carcinoma). Histology with standard stains, culture, and polymerase chain reaction (PCR) amplification using two sets of primers located in the 16S ribosomal DNA (rDNA) were used to detect the presence of bacteria. Amplified products were sequenced to determine the genus and species of the bacteria. A search for other genes that were specific for Helicobacter pylori also was carried out by PCR. RESULTS: PCR performed with the 16S rDNA primers revealed the presence of bacteria from the genus Helicobacter in all of the liver specimens from patients with primary liver carcinoma (eight of eight patients) and in one specimen from a patient without primary liver carcinoma (one of eight patients). When the nucleotide sequence of > 80% of the 16S rDNA was determined, the closest similarity was with the 16S rDNA from H. pylori in eight patients. In 1 patient sample from which only 398 nucleotides were sequenced, the closest match was Helicobacter felis. CONCLUSIONS: The results presented in this study indicate that Helicobacter species can be present in the liver of patients with primary hepatic carcinoma, but their eventual role in the carcinogenesis process, although it is plausible, remains to be proven. Based on sequence similarity, it seems that Helicobacter species that are related closely to H. pylori but are distinct from it have been found.     

Complete regression of low-grade mucosa-associated lymphoid tissue (MALT) lymphoma in the gastric stump after eradication of Helicobacter pylori

Recent studies have suggested that Helicobacter pylori (H. pylori)-associated gastritis may play an important role in the pathogenesis of primary gastric lymphoma. Recently, triple therapy using proton pump inhibitor, amoxicillin, and clarithromycin, has been established for the eradication therapy of H. pylori infection, and is also recommended for the treatment of the superficial type of low-grade gastric MALT (mucosa-associated lymphoid tissue ) lymphoma. MALT lymphoma of the gastric stump is rare, and total resection or chemotherapy for MALT lymphoma of the gastric stump has been previously reported. Therefore, there is no evidence that eradication therapy is effective for low-grade MALT lymphoma of the gastric stump. Our case illustrates the remarkable efficacy of eradication of H. pylori for low-grade MALT lymphoma of the gastric stump without other modalities such as surgery and systemic chemotherapy.     

Helicobacter pylori Infection and Dietary Factors Act Synergistically to Promote Gastric Cancer

However, the incidence of gastric cancer (GC) has been decreased in past decades; GC is the second cause of cancer related death in the world. Evidence has illustrated that several factors including Helicobacter pylori (H. pylori) infection, host genetics, and environmental factors (smoking and particularly diet) may play a crucial role in gastric carcinogenesis. It has been demonstrated that high consumption of fresh fruits, vegetables, high level of selenium and zinc in drinking water, sufficient iron, and cholesterol protect against GC, while; smoked , pickled, and preserved foods in salt, and nitrites increase the risk of GC. Epidemiological studies have also proved that H. pylori infection and a high salt diet could independently induce atrophic gastritis and intestinal metaplasia. Recently, studies have been demonstrated that dietary factors directly influence H. pylori virulence. The use of appropriate diet could reduce levels of H. pylori colonization or virulence and prevent or delay development of peptic ulcers or gastric carcinoma. This is attractive from a number of perspectives including those of cost, treatment tolerability, and cultural acceptability. This review will describe new insights into the pathogenesis of H. pylori in relation to environmental factors, especially dietary, not only to find the developed means for preventing and treating GC, but also for understanding the role of chronic inflammation in the development of other malignancies.     

Helicobacter pylori infection and gastric diseases--pathogenesis and effects of eradication

H. pylori infection is associated with major gastroduodenal diseases, i.e. peptic ulcer, cancer and MALT lymphoma in the stomach. The pathogenesis of H. pylori in these diseases has been elucidated. Non-atrophic diffuse antral gastritis is correlated with duodenal ulcer and multifocal atrophic gastritis is correlated with both gastric ulcer and cancer. It is well known that Japanese tend to have multifocal atrophic gastritis. H. pylori eradication therapy dramatically reduces the recurrence rates of gastroduodenal ulcers in humans and bacterial eradication for peptic ulcer patients has been recommended in many countries. Mongolian gerbils have provided an excellent model of gastric carcinogenesis and H. pylori enhanced (promoted) chemical carcinogen-induced carcinogenesis in the stomach using this model. H. pylori eradication reduced the incidence of gastric cancer in the Mongolian gerbil model. It was a recently discovered that a transforming clone carrying the translocation t (11;18) (q21;q21) forms a MALT lymphoma, the growth of which is independent of H. pylori and will not respond to bacterial eradication. In the early stage, the tumor can be successfully treated by eradication, but at a later stage additional genetic abnormality in the lymphoma may show no response to H. pylori eradication therapy.     

Helicobacter Species are Possible Risk Factors of Cholangiocarcinoma

Several infectious agents are considered to be causes of cancer in human, mainly hepatitis B and C viruses, high-risk human pailloma viruses, Helicobacter pylori, Clonorchis sinensis, and Opisthorchis viverrini. Here we described the evident research and the association between Helicobacter spp. and biliary tract cancer particularly cholangiocarcinoma (CCA). Global epidemiological studies have suggested that Helicobacter spp. are possible risk factors for biliary tract diseases. Molecular studies support a linkage of Helicobacter spp. with CCA development. H. pylori, H. bilis, and H. hepaticus, are found in CCA, but the most common species are H. pylori and H. bilis. The type of CCA are associated with Helicobacter spp. include extrahepatic CCA, and common bile duct cancer. Up to the present, however, the results from different regions, materials and methods, sub-sites of cancer, and controls have not been consistent, thus introducing heterogeneity. Therefore, a comparison between co-Helicobacter spp.-CCA in the countries with low and high incident of CCA is required to settle the question. Furthermore, clarifying variation in the role of Helicobacter species in this CCA, including pathogenesis of CCA through enhanced biliary cell inflammation and proliferation, is necessary.     

The several problems and cautions in treatment of Helicobacter pylori infection

Helicobacter pylori (H. pylori) infection is the main cause of most gastroduodenal diseases; this discovery has been a major breakthrough in gastroenterology, hematology, dermatology and pediatrics. Triple therapy, including two antibiotics, amoxicillin and clarithromycin, and a proton pump inhibitor given for a week has been recommended as the treatment of choice in guideline for diagnosis and treatment of H. pylori infection in Japanese Journal of Helicobacter Research. However, this treatment may fail for several reasons including bacterial resistance. Our aim to review the problems and cautions in diagnosis and treatment of H. pylori infection.     

Helicobacter pylori: optimum diagnosis and test of cure

The fact that about 50% of the world's population is infected with Helicobacter (H.) pylori and the important role that this bacterium plays in public health have been important incentives in the search for accurate diagnostic methods. A large number of invasive and non-invasive methods have been used to diagnose H. pylori infection. Each method has its advantages and disadvantages and each practitioner should choose the best diagnostic method according to the facilities available. Non-invasive tests for the diagnosis of H. pylori infection are largely used in clinical practice and in management of patients with gastroduodenal disease. Serology is the most widespread test but its use is not advised in the post-treatment follow-up. The Urea Breath Test is a simple, safe and highly accurate method ideal for evaluating the short-term follow-up of H. pylori eradication after therapy.     

Helicobacter pylori induces DNA damage in vitro

A close association between Helicobacter pylori infection and the development of gastric adenocarcinoma in humans has been demonstrated. Therefore, the direct induction of DNA damage by H. pylori was investigated here using the in vitro micronucleus assay. After 5 days of incubation with bacterial lysate a dose-dependent formation of micronuclei was found, which was not limited to cytotoxic protein concentrations and was not observed after treatment with Escherichia coli lysate (control). This induction of DNA damage may be a link between chronic H. pylori infection and development of adenocarcinoma of the stomach.     

The Carcinogenic Liver Fluke Opisthorchis viverrini is a Reservoir for Species of Helicobacter

There has been a strong, positive correlation between opisthorchiasis-associated cholangiocarcinoma andinfection with Helicobacter. Here a rodent model of human infection with Opisthorchis viverrini was utilized tofurther investigate relationships of apparent co-infections with O. viverrini and H. pylori. A total of 150 hamsterswere assigned to five groups: i) Control hamsters not infected with O. viverrini; ii) O. viverrini-infected hamsters;iii) non-O. viverrini infected hamsters treated with antibiotics (ABx); iv) O. viverrini-infected hamsters treatedwith ABx; and v) O. viverrini-infected hamsters treated both with ABx and praziquantel (PZQ). Stomach,gallbladder, liver, colonic tissue, colorectal feces and O. viverrini worms were collected and the presence ofspecies of Helicobacter determined by PCR-based approaches. In addition, O. viverrini worms were cultured invitro with and without ABx for four weeks, after which the presence of Helicobacter spp. was determined. In situlocalization of H. pylori and Helicobacter-like species was performed using a combination of histochemistry andimmunohistochemistry. The prevalence of H. pylori infection in O. viverrini-infected hamsters was significantlyhigher than that of O. viverrini-uninfected hamsters (p≤0.001). Interestingly, O. viverrini-infected hamsters treatedwith ABx and PZQ (to remove the flukes) had a significantly lower frequency of H. pylori than either O. viverriniinfectedhamsters treated only with ABx or O. viverrini-infected hamsters, respectively (p≤0.001). QuantitativeRT-PCR strongly confirmed the correlation between intensity H. pylori infection and the presence of liver flukeinfection. In vitro, H. pylori could be detected in the O. viverrini worms cultured with ABx over four weeks. Insitu localization revealed H. pylori and other Helicobacter-like bacteria in worm gut. The findings indicate thatthe liver fluke O. viverrini in the biliary tree of the hamsters harbors H. pylori and Helicobacter-like bacteria.Accordingly, the association between O. viverrini and H. pylori may be an obligatory mutualism.     

Helicobacter pylori eradication therapy does not prevent gastric cancer development in all patients

We previously reported that eradication of Helicobacter pylori reduced the risk of gastric cancer developing in patients with peptic ulcer diseases. In the present study, we followed up with our patient group to investigate the occurrences and clinical features of gastric cancers that developed after cure of the infection. Prospective post-eradication evaluations were conducted on 1, 674 consecutive patients who had received successful H. pylori eradication therapy. The patients underwent endoscopic examination before eradication therapy to test for peptic ulcers, background gastric mucosal atrophy, and H. pylori infection. After confirmation of the cure of infection, the annual follow-up endoscopy was performed. The patients were followed up to more than 10 years. During the follow-up, their risk of developing gastric cancer after the cure of infection was almost the same as we reported previously. There was still a risk of developing gastric cancer of both the intestinal and diffuse types. The grade of gastric mucosal atrophy present before receiving eradication therapy was closely related to the development of gastric cancer after eradication of H. pylori. The stage of most gastric cancer was at the early TNM stage, but advanced cancer was observed in patients who skipped regular endoscopic surveillance. H. pylori eradication therapy does not prevent gastric cancer development in all infected patients. Thus, it is important to inform patients about the risk of gastric cancer after eradication therapy and to offer them surveillance endoscopy.     

The role of Helicobacter pylori infection in hematological diseases - a review

Helicobacter pylori (H. pylori) infection has been known to be the most closely associated with extra-gastrointestinal diseases. Above all, the association between H. pylori and hematological diseases, including immune thrombocytopenic purpura ( ITP), gastric MALT lymphoma and iron deficiency anemia (IDA) has been focused. Although the molecular mechanisms have not yet been fully understood, H. pylori eradication resulted in high response rates without major adverse effects. We focus here on a comprehensive review of the current literature of ITP, gastric MALT lymphoma and IDA.     

Host-environment interactions: their impact on progression from gastric inflammation to carcinogenesis and on development of new approaches to prevent and treat gastric cancer.

Revelation of the connection between Helicobacter pylori infection and gastric adenocarcinoma has prompted new investigations pertaining to its basic and clinical aspects. H. pylori-induced persistent and uncontrolled gastric inflammation nearly always precedes the development of cancer and is instrumental in initiating a multistep process leading to carcinogenesis. Despite initial optimism about the potential of combination anti-H. pylori therapy to ultimately eradicate gastric adenocarcinoma, recent investigations suggest its use should be targeted and tailored to a selected patient group considering the multifaceted role of H. pylori in disease and the disease heterogeneity of gastric adenocarcinoma. The clinical spectrum of H. pylori infection ranges from asymptomatic gastritis and peptic ulcer to gastric malignancies. The occurrence of one versus another is the result of differences in the magnitude of gastritis, and the current disease paradigm suggests gastric inflammation is common to all H. pylori-associated gastroduodenal diseases. Therefore, the host inflammatory responses to environmental triggers, rather than to bacteria or environmental factors per se, would dictate the variable outcomes of H. pylori infection. Putative factors that are expected to play an important role in stimulating inflammatory pathways and modulating the cross-talk between host and environment are age at the time of infection, environmental cofactors, H. pylori virulence, and host genetics. Elucidation of the intimate relationship between host-environment interaction and gastric inflammation, although currently a formidable task, is essential in the development of new prevention and treatment strategies. Such knowledge might provide clues that allow more accurate prediction of variable outcomes of gastric inflammation and appropriate adjustment of treatment strategies, and might open up novel areas for studying gastric carcinogenesis. The evolving new technologies, such as microarray, proteomic, and functional genomic analyses, promise to shed new light on the immense complexity of the presumed host-environment interactions and will reveal more useful markers for the diagnosis and prognosis of gastric adenocarcinoma.     

Helicobacter pylori and gastric epithelial cells: from gastritis to cancer

Helicobacter pylori is a spiral, gram-negative rod-shaped pathogen that attaches to gastric epithelial cells in the human stomach and is a causative agent of chronic active gastritis, peptic ulcer and neoplasia. H. pylori is one of the most common pathogens afflicting humans and is the major environmental factor in the development of gastric cancer increasing from 4 to 6 folds the risk of its development. Several specific virulence factors are implicated in the mechanism of H. pylori infection like the bacterial motility; the secretion of large amounts of urease; specific adhesins for the interaction between H. pylori and the gastric surface epithelium; the traslocation into gastric ephitelial cells of the cytotoxin-associated gene A (CagA), the vacuolating cytotoxin A (VacA) and the heat shock protein HspB. Adherence of H. pylori to the gastric epithelium and secretion of interleukins are believed to be an important step in the induction of active inflammation of the mucosal layer. Several studies have demonstrated that H. pylori infection induces gastric epithelial cell proliferation activating ERK and MAPK pathways and increase of mitosis and mutations. Therefore, H. pylori infection seems to increase apoptosis, implying increased gastric epithelial cell turnover. Recently, it has been shown that H. pylori-induced apoptosis in gastric epithelial cells is mediated via the CD95-receptor/ ligand system but that TRAIL also plays an important role in this regulation.     

Gut and liver involvement in pediatric hematolymphoid malignancies

Hematolymphoid malignancies are common neoplasms in childhood. The involvement of the gastrointestinal (GI) tract, liver, biliary system, pancreas, and peritoneum are closely interlinked and commonly encountered. In leukemias, lymphomas, and Langerhans cell histiocytosis (LCH), the manifestations result from infiltration, compression, overwhelmed immune system, and chemotherapy-induced drug toxicities. In acute leukemias, major manifestations are infiltrative hepatitis, drug induced gastritis, neutropenic typhlitis and chemotherapy related pancreatitis. Chronic leukemias are rare. Additional presentation in lymphomas is cholestasis due to infiltration or biliary obstruction by lymph nodal masses. Presence of ascites needs a thorough workup for the underlying pathophysiology that may modify the therapy and affect the outcome. Uncommon hematolymphoid malignancies are primary hepatic, hepatosplenic, and GI lymphomas which have strict definitions. In advanced diseases with extensive spread, it may be impossible to distinguish these diseases from the primary site of origin. LCH produces biliary strictures that mimic as sclerosing cholangitis. Liver infiltration is associated with poor liver recovery even after chemotherapy. The heterogeneity of gut and liver manifestations in hematolymphoid malignancies has a clinical impact on their management. Though chemotherapy is the mainstay of therapy in all hematolymphoid malignancies, debulking surgery and radiotherapy have an adjuvant role in specific clinical scenarios. Rare situations presenting as liver failure or end-stage liver disease require liver transplantation. At their initial presentation to a primary care physician, given the ambiguity in clinical manifestations and the prognostic difference with time-bound management, it is vital to recognize them early for optimal outcomes. Pooled data from robust registries across the world is required for better understanding of these complications.     

High Fluoroquinolone Resistant Strains of Helicobacter Pylori in the Golden Triangle

Background and aims: Helicobacter pylori (H. pylori) infections, associated with fatal GI diseases such as gastric cancer and MALT lymphoma, remain a major health problem in ASEAN countries. The Golden triangle has long been known as one of Asia’s main opium-producing areas. There have been no prior studies of H. pylori infection in this area. The major objectives of this project were therefore to establish prevalence, antibiotic resistance patterns and associated predictive in the Golden triangle. Methods: We recruited dyspeptic patients in Chiang khong and Chiang saen districts, Chiangrai province of Thailand. All subjects underwent gastroscopy, and 3 antral gastric biopsies were collected for rapid urease tests and H. pylori culture. E-tests were used to evaluate the MICs for metronidazole (MNZ), levofloxacin (LVX), ciprofloxacin (CIP), amoxicillin(AMX), tetracycline (TET) and clarithromycin (CLR). Results: Total of 148 patients was included. H. pylori infection was present in 36.3%(37/102) of Chiang khong and 34.8 % (16/46) of Chiang saen subjects and the overall H. pylori infection rate was 35.8% (53/148). Antibiotic resistance was demonstrated in 44%, including 2% for CLR and 26% for MNZ, whereas fluoroquinolone resistance was demonstrated to be as high as 25% in Chiang khong. Multi-drug resistant H. pylori was detected in 4%. There was no AMX and TET resistance in this study. The prevalence of CLR resistance on a background of gastritis was significantly higher than peptic ulcer disease in the golden triangle area (100%vs 0%: P= 0.04). Conclusions: H. pylori remains a common infection in the Golden triangle. MNZ resistance appears to be high, whereas fluoroquinolone resistance is prevalent and is becoming a significant problem in this area. Diagnosis of gastritis might be a predictor of CLR resistance in the Golden triangle. H. pylori eradication with an appropriate regimen by using the local antibiotic resistant pattern is a key important tool to reduce H. pylori associated GI diseases in this particular part of the world.     

Management of Helicobacter pylori infection: gastroenterological and surgical perspectives

Diagnosis and treatment of Helicobacter pylori is a crucial point in the management of the different gastroduodenal disorders. Management involves the general practitioner and different specialists such as internists, gastroenterologists and surgeons. Among the most frequent H. pylori-related gastroduodenal disorders of medical interest are some diseases such as dyspepsia and gastroesophageal reflux, where the role of the bacterium is not well defined and therefore the importance H. pylori eradication is still controversial. On the contrary, the relationship of H. pylori and gastric and duodenal peptic ulcer is widely and definitively proven, and there are no doubts regarding the importance of curing the bacterium in these disorders. However, the surgical aspect of peptic ulcer, in particular the relevance and management of its complications, has not been widely investigated so far. In fact, the prevalence of H. pylori in perforated, bleeding and stenotic peptic ulcers seem to be lower that in non-complicated peptic ulcer, and whenever H. pylori eradication virtually prevents the re-bleeding of peptic ulcer in all cases, the effect of curing the bacterium in perforated and stenotic ulcers is still largely unknown. The management of H. pylori infection after gastric surgery is also still controversial. Most studies suggest that H. pylori can persist after gastric surgery whenever its incidence is much lower than that before operation. However it seems most unlikely that the infection plays a major role in the development of ulcer recurrence after gastric surgery or in the induction of gastric carcinoma. In any case, there are no convincing data that its cure may prevent the occurrence of gastric carcinoma following gastrectomy procedures.     

胆管支架和(或)引流术治疗恶性胆管梗阻30天内死亡原因分析

目的 分析胆管支架和（或）引流术治疗恶性胆管梗阻３０ｄ内死亡原因及手术有关的近期并发症,探讨更有效的临床治疗方法及手术适应证。方法 １０７例恶性胆管梗阻者实行经皮经肝穿刺担管支架和（或）引流术,术后３０ｄ内共死亡１２例,其中原发性肝癌４例,肝门淋巴结转移瘤３例,胆管癌５例,死亡率为１１．２％。结果 １２例恶性胆管梗阻者,９例放置胆管支架,其中５例同时置引流管;３例仅置胆管引流管。手术后１０例胆管梗     

Lymphoma of the gastrointestinal tract.

Non-Hodgkin's lymphoma (NHL) of the gastrointestinal (GI) tract accounts for 4% to 20% of all NHLs and is the most common extranodal site of presentation. The stomach is the major organ involved by GI lymphoma. Helicobacter pylori infection, immunosuppression after solid-organ transplantation, celiac disease, inflammatory bowel disease, and human immunodeficiency virus (HIV) infection may be risk factors for GI lymphoma. A significant proportion of gastric lymphomas are of low-grade histology and arise from mucosal-associated lymphoid tissue (MALT). Such MALT lymphomas may be associated with H. pylori infection and may undergo complete regression following eradication of H. pylori. Lymphoma of the small bowel, colon, and rectum may also occur, but are less common than gastric lymphoma. Distinct clinicopathologic entities, such as primary intestinal T-cell lymphoma, immunoproliferative small intestinal disease, and multiple lymphomatous polyposis have been described. Surgery, radiation therapy, and chemotherapy have been used in the treatment of GI lymphomas. However, the optimal management of these lymphomas has never been determined by prospective randomized clinical trials. Such trials by cooperative groups are needed to answer many of the vital unanswered questions concerning extranodal lymphomas of the GI tract.     

Helicobacter pylori and Arteriosclerosis

Helicobacter pylori (H. pylori) infection-related diseases are known to include gastritis, gastric and duodenal ulcer, gastric cancer, gastric MALT lymphoma, idiopathic thrombocytopenic purpura, iron-deficient anemia, urticaria, reflux esophagitis, and some lifestyle-related diseases. It is indicated that homocysteine involved with arteriosclerosis induces lifestyle-related diseases. Homocysteine is decomposed to methionine and cysteine (useful substances) in the liver, through the involvement of vitamin B?? (VB??) and folic acid. However, deficiency of VB?? and folic acid induces an increase in unmetabolized homocysteine stimulating active oxygen and promoting arteriosclerosis. VB?? and folic acid are activated by the intrinsic factors of gastric parietal cells and gastric acid. The question of whether homocysteine, as a trigger of arteriosclerosis, was influenced by H. pylori infection was investigated. H. pylori infection induces atrophy of the gastric mucosa, and the function of parietal cells decreases with the atrophy to inactivate its intrinsic factor. The inactivation of the intrinsic factor causes a deficiency of VB?? and folic acid to increase homocysteine's chances of triggering arteriosclerosis. The significance and usefulness of H. pylori eradication therapy was evaluated for its ability to prevent arteriosclerosis that induces lifestyle-related diseases. Persons with positive and negative results of H. pylori infection were divided into a group of those aged 65 years or more (early and late elderly) and a group of those under 65 years of age, and assessed for gastric juice. For twenty-five persons from each group who underwent gastrointestinal endoscopy, the degree of atrophy of the gastric mucosa was observed. Blood homocysteine was measured as a novel index of arteriosclerosis, as well as VB?? and folic acid that affect the metabolism of homocysteine, and then activated by gastric acid and intrinsic factors. Their arterioscleroses, measured by pulse wave velocity (PWV), were investigated and compared. The levels of homocysteine were significantly high in the elderly persons and those with H. pylori infection. On the contrary, the levels of VB?? and folic acid were low in these persons. The results of PWV showed a positive correlation with the levels of gastrin and homocysteine and an inverse correlation with the levels of VB?? and folic acid. Persons with a negative result of H. pylori infection showed a lower degree of arteriosclerosis than those with a positive result who were of the same age group. Persons with a positive result of H. pylori infection tended to show an improvement from arteriosclerosis after eradication therapy without a significant difference. 1 ) It is suggested that severity of atrophy of the gastric mucosa are correlated with the severity of arteriosclerosis. 2 ) It is hypothesized that H. pylori infection may induce arteriosclerosis.