Helicobacter Infections ; complications ; Helicobacter pylori ; Hematologic Diseases ; complications ; Humans

No abstract available
Cardiovascular Diseases/*microbiology/physiopathology ; Helicobacter Infections/*complications ; *Helicobacter pylori ; Humans

Helicobacter pylori (HP) is an infectious pathogen which can easily infringe gastric mucosa. If the body is infected by HP, it can release cytokines, such as TNF-alpha, IL-1 and IL-6. These cytokines can regulate the absorption and transformation of bone, promote the formation of osteoclast, and then cause localized or systemic osteoporosis. HP infection may decrease the level of estrogen and vitamin B12, which is considered as a risk factor for osteoporosis. Helicobacter pylori infection is related with the occurrence of gastritis, peptic ulcer and gastric malignancies, and these diseases and treatments are associated with osteoporosis. Meanwhile the application of proton pump inhibitor (PPI) can influence absorption of calcium, decrease the level of serum calcium and increase the risk of fracture. Gastrostomy may cause bone metabolism disorders.
Helicobacter Infections ; complications ; drug therapy ; Helicobacter pylori ; Humans ; Osteoporosis ; etiology

Helicobacter pylori (H. pylori) is the causative agent of chronic gastritis and peptic ulcer diseases and is an important risk factor for the development functional dyspepsia, peptic ulceration, gastric adenocarcinoma and mucosa-associated lymphoid tissue lymphoma. H. pylori has very high rates of infection in human populations, and it is estimated that over 50% of the world population is infected. Recently, certain extra-gastric manifestations, linked to H. pylori infection, have been widely investigated. Noteworthy, a growing body of evidences supports an association between H. pylori infection with lung cancer. The present review intend to highlight not only the most recent evidences supporting this association, but also some missed points, which must be considered to validate this emerging association.
Helicobacter Infections ; complications ; Helicobacter pylori ; physiology ; Humans ; Lung Neoplasms ; complications ; microbiology

The relationship between Helicobacter pylori (H. pylori) infection and gastro-esophageal reflux disease (GERD) is complex. Since some studies have suggested that H. pylori eradication may result in an increased incidence of GERD in duodenal ulcer patients, there have been debates about the protective function of H. pylori infection on GERD. H. pylori-associated antral gastritis can induce increased gastric acid output via increasing gastrin secretion. Changes in gastric acid secretion depend on the distribution (e.g. antral, corpus or pangastritis) or severity of gastritis, not on H. pylori infection itself. Patients with H. pylori infection are at risk of developing gastric mucosal atrophy, and a cohort study suggested that long-term proton pump inhibitor therapy for GERD may accelerate this process. Therefore, it has been recommended that H. pylori should be treated in GERD patients in whom a long-term antisecretory therapy is planned. The previous hypothesis that 'H. pylori infection protects from the development of GERD' is thought to be an erroneous concept recently.
Gastritis/microbiology ; Gastroesophageal Reflux/drug therapy/*microbiology ; Helicobacter Infections/*complications/drug therapy ; *Helicobacter pylori ; Humans

Objective: To investigate the characteristics of duodenal bulbar microbiota in children with duodenal ulcer and Helicobacter pylori (Hp) infection. Methods: This prospective cohort study enrolled 23 children with duodenal ulcers diagnosed by gastroscopy who were admitted to the Children's Hospital of Zhejiang University School of Medicine due to abdominal pain, abdominal distension, and vomiting from January 2018 to August 2018. They were divided into Hp-positive and Hp-negative groups according to the presence or absence of Hp infection. Duodenal bulbar mucosa was sampled to detect the bacterial DNA by high-throughput sequencing. The statistical difference in α diversity and β diversity, and the relative abundance in taxonomic level between the two groups were compared. Microbial functions were predicted using the software PICRUSt. T-test, Rank sum test or χ² test were used for comparison between the two groups. Results: A total of 23 children diagnosed with duodenal ulcer were enrolled in this study, including 15 cases with Hp infection ((11.2±3.3) years of age, 11 males and 4 females) and 8 cases without Hp infection ((10.1±4.4) years of age, 6 males and 2 females). Compared with Hp-negative group, the Hp-positive group had higher Helicobacter abundance (0.551% (0.258%, 5.368%) vs. 0.143% (0.039%, 0.762%), Z=2.00, P=0.045) and lower abundance of Fusobacterium, Streptococcus and unclassified- Comamonadaceae (0.010% (0.001%, 0.031%) vs. 0.049% (0.011%, 0.310%), Z=-2.24, P=0.025; 0.031% (0.015%, 0.092%) vs. 0.118% (0.046%, 0.410%), Z=-2.10, P=0.036; 0.046% (0.036%, 0.062%) vs. 0.110% (0.045%, 0.176%), Z=-2.01, P=0.045). Linear discriminant analysis (LDA) effect sized showed that at the genus level, only Helicobacter was significantly enriched in Hp-positive group (LDA=4.89, P=0.045), while Streptococcus and Fusobacterium significantly enriched in Hp-negative group (LDA=3.28, 3.11;P=0.036,0.025, respectively). PICRUSt microbial function prediction showed that the expression of oxidative phosphorylation and disease-related pathways (pathways in cancer, renal cell carcinoma, amoebiasis, type 1 diabetes mellitus) in Hp-positive group were significantly higher than that in Hp-negative group (all P<0.05), while the expression of pathways such as energy metabolism and phosphotransferase system pathways were significantly lower than that in Hp-negative group (all P<0.05). Conclusion: In children with Hp-infected duodenal ulcers, the mucosal microbiota of the duodenal bulb is altered, characterized by an increased abundance of Helicobacter and a decreased abundance of Clostridium and Streptococcus, and possibly alters the biological function of the commensal microbiota through specific metabolic pathways.
Male ; Female ; Humans ; Child ; Duodenal Ulcer/diagnosis* ; Helicobacter Infections/complications* ; Helicobacter pylori/genetics* ; Prospective Studies ; Microbiota

DNA Methylation ; Helicobacter Infections ; complications ; Helicobacter pylori ; Humans ; Stomach Neoplasms ; etiology ; genetics ; Telomerase ; physiology

Adult ; Female ; Helicobacter Infections ; complications ; Helicobacter pylori ; Humans ; Hyperemesis Gravidarum ; etiology ; Pregnancy

Helicobacter pylori (Hp) is a high prevalence of chronic infectious pathogens, though not necessarily lead to symptoms, but it can affect the immune system. More than of the world's population harbors the bacterium, and most adult Hp infection was obtained in childhood. Hp infection is a major cause of peptic ulcer, although children rarely suffer from peptic ulcer disease. Hp infection is closely related to chronic gastritis, dyspepsia, chronic diarrhea and recurrent abdominal pain in children. In recent years, Hp infection may also participate in some of non-digestive diseases, such as children's nutritional iron deficiency anemia, growth retardation, malnutrition, autoimmune idiopathic thrombocytopenic purpura, chronic urticaria, as well as the development of adult atherosclerosis-related cardiovascular diseases and some nervous system diseases. Hp infection can be a lifetime issues of children. Hp infection of children will bring many socio-economic problems. In this paper, the correlation of Hp infection in stomach and oral cavity, and diagnostic technology, prevention as well as treatment strategies for Hp infection will be discussed.
Helicobacter Infections ; complications ; diagnosis ; epidemiology ; genetics ; Helicobacter pylori ; Humans ; Mouth ; microbiology ; Stomach ; microbiology

OBJECTIVETo probe into the correlativity of Helicobacter pylori (HP) with cerebral infarction and the possible mechanism.

METHODSComprehensively discuss the data of studies on the clinical correlativity of HP with cerebral infarction and the possible pathogenic mechanisms.

CONCLUSIONMost scholars hold that HP infection is one of risk factors of cerebral infarction. At present, the theory about positive correlation tendency between HP infection and occurrence of cerebral infarction has not been defined. For the mechanism about HP infection possibly inducing cerebral infarction, studies indicate that HP is involved in attack of cerebral infarction possibly alone or via influencing other risk factors, and the pathogenic mechanism mainly include inflammation, immunology and metabolism and so on. However, whether HP infection is a risk factor for attack of cerebral infarction, and the accurate pathogenic mechanisms need further be studied scientifically.