Extragastric Manifestations Research Articles

Unveiling the Silent Intruder: H. pylori's Hidden Link to Ischemic Heart Disease.

Cardiovascular disease is the leading cause of death. In addition to the well-known risk factors associated with cardiovascular disease, such as age, diabetes mellitus, smoking, hypertension, and obesity, there has been a growing concern regarding cardiac complications stemming from the Gram-negative bacteria Helicobacter pylori. While H. pylori is most commonly associated with chronic gastritis, peptic ulcer disease, gastric adenocarcinoma, and gastric lymphoma, it has also been implicated in extra gastric manifestations, encompassing cardiac, neurologic, ocular, and dermatologic issues. Key virulent factors for coronary artery disease include the vacuolating cytotoxin gene A and the cytotoxin-associated gene A. The most likely pathogenic mechanism of the relationship between H. pylori and coronary artery disease is initiating a chronic inflammatory process associated with infection and the modifications of classic risk factors. These alterations lead to the creation of prothrombotic and procoagulant environments. Here, we review the cardiac manifestations of H. pylori and the underlying pathophysiological mechanisms.

Review on Helicobacteriosis Associated Diseases

Helicobacteriosis is a bacterial infection caused by Helicobacter pylori (H.pylori)(HP). which was discovered in 1982 by Australian scientists Barry Marshall and Robin Warren, who were later awarded the Nobel Prize in 2005.Epidemiological evidence has shown that H.pylori colonizes the upper gastrointestinal tract(GIT), and the infection is one of the most common human bacterial pathogens worldwide, with 4.4 billion infected individuals in 2015, but the prevalence varies according to situation and hygiene principles. Since this first isolation, it has become apparent that this organism may be one of the most common bacterial pathogens of humans, and it is one of the risk factors for adenocarcinoma. Thus, it was categorized as a group 1 carcinogen in 1994 by the World Health Organization (WHO). New infections with H.pylori are thought to occur as a consequence of direct human-to-human transmission, via either an oral-oral or fecal-oral route or both. H.pylori has been detected in stool, saliva, vomitus, and gastric refluxate, the material that has been subject to reflux, principally stomach acid that has leaked up into the esophagus. Clinically, H. pylori infection in humans is related to chronic gastritis, peptic ulceration, duodenal ulcer, and gastric cancer in addition to mucosa-associated lymphoid malignancies.According to the World Health Organization (WHO) estimates available at that time, it was supposed that about 4.4 billion infected individuals in 2015 were infected with H. pylori. These estimations can vary and are subject to change over time as recent investigations and information become obtainable. The prevalence of H. pylori is complex and affected by several factors, comprising age, clinical outcomes, geographical location, and socioeconomic status. A higher incidence was reported in unhygienic and economically poor areas; the rate of H. pylori infection in Africa, South America, and Asia was significantly higher than that in Western Europe, North America, and Australia. However, the disease spectrum of H. pylori infection shows a wide range of clinical aspects, including gastrointestinal diseases and extra gastric manifestations. In this review, we have described the general scope of these diseases.

Helicobacter pylori infection contributes to the expression of Alzheimer's disease-associated risk factors and neuroinflammation

Over time, mounting evidence has demonstrated extra-gastric manifestations of Helicobacter pylori infection. As such, a number of studies demonstrated the potential contribution of H. pylori infection to the incidence and progression of Alzheimer's disease (AD). Considering unanswered questions regarding the effect of H. pylori infection on brain activity, we sought to investigate the impact of H. pylori infection on the expression of AD-associated risk factors. We used two H. pylori clinical strains obtained from two patients with peptic ulcer and evaluated their influence on the expression level of AD-associated genes (APP, ApoE2, ApoE4, ABCA7, BIN1, Clu, CD33) and genes for inflammatory markers (TLR-4, IL-8, TNF-α) by RT-qPCR in human glioblastoma (U87MG) and astrocyte (1321N1) cell lines. The expression of inflammatory cytokines was further assessed by ELISA assay. The exposure of U97MG and 1321N1 cells to H. pylori strains resulted in a significant enhancement in the expression level of the risk allele ApoE4, while reducing the expression of the protective allele ApoE2. H. pylori infection remarkably increased the expression level of main AD-associated risk genes, and also pro-inflammatory cytokines. Furthermore, we noticed a substantial elevation in the mRNA expression level of transmembrane receptor TLR-4 following H. pylori infection. Our findings presented the potential for H. pylori to stimulate the expression of AD-associated risk genes and trigger neuroinflammation in the brain tissue. This, in principle, leads to the recommendation that AD patients should perhaps test for H. pylori infection and receive treatments upon positive detection.

Assessment of the mixed origin of the gastric epithelial extracellular vesicles in acellular transfer of Helicobacter pylori toxins and a systematic review

BackgroundH. pylori are generally considered as extracellular organisms, with exclusive colonization of the gastric milieu. Yet, several extra gastric manifestations are associated with this infection. The aim of the present study was to investigate the feasibility of toxin transfer by extracellular vesicles, from bacterial and epithelial origins. MethodsTox-positive H. pylori and its two cagA and vacA mutant strains were used to produce bacterial vesicles (BVs) and to infect AGS cells. The produced BVs and the infected cell vesicles (ICVs) were collected by ultracentrifugation and evaluated by western blotting, DLS and electron microscopy. These two sets of vesicles were applied to a second set of recipient AGS cells, in which the acellular transfer of toxins, IL-8 production and downstream morphologic changes were assessed, by western blotting, ELISA and light microscopy, respectively. ResultsThe BVs were positive for H. pylori membrane markers (BabA and UreB), VacA and CagA toxins, except for from the corresponding mutant strains. The ICVs were larger in size and positive for bacterial markers, as well as epithelial markers of CD9, LGR5, but negative for nuclear (Ki76) or cytoplasmic (β-actin) markers. Bacteria-independent transfer of CagA and VacA into the recipient cells occurred upon treatment of cells with BVs and ICVs, followed by cellular vacuolation and elongation. IL-8 production was induced in recipient AGS cells, treated with BVs (1279.4 ± 19.79 pg/106 cells), early (8 h, 1171.4 ± 11.31 pg/106 cells) and late (48 h, 965.4 ± 36.77 pg/106 cells) ICVs (P < 0.0001). ConclusionOur data indicates that ICVs, with mixed bacterial and epithelial constituents, similar to BVs, are capable of transferring bacterial toxins into the recipient cells, inducing IL-8 production and subsequent morphologic changes, in an acellular manner.

Učestalost Helicobacter pylori infekcije i antibiotska rezistencija kod bolesnika sa akutnim dekompenzacijama jetre

Introduction: Helicobacter pylori (H. pylori) infection is a global healthcare challenge. In its course of infection, Helicobacter pylori infection leads to a systemic increase of post-inflammatory cytokines and can have extra gastric manifestations, affecting the worsening of metabolic and cardiovascular diseases and endangering normal liver function, especially when liver cirrhosis is present. Aim: The aim of this study was to examine the frequency of H. pylori infection in patients with cirrhosis of the liver in stage AD or ACLF. The frequency of antibiotic resistance to clarithromycin and fluoroquinolones was also investigated. Material and methods: A prospective study with 45 patients was conducted which included both sexes. Samples of gastric mucosa were taken from all patients included in the study during the upper endoscopy and were sent to the Institute of Microbiology of the Faculty of Medicine University of Belgrade. A molecular method, Polymerase chain reaction (PCR) was used to detect H. pylori and mutations responsible for resistance to clarithromycin and fluoroquinolones. Results: The presence of H. pylori infection was registered in 15 decompensated patients (33.33%), while 30 (66.67%) were negative. In H. pylori positive patients, PCR detection of genotypes responsible for antibiotic resistance revealed clarithromycin resistance in 11 patients (73.33%), while fluoroquinolone resistance was detected in 7 patients (46.66%). In 6 patients (40.0%), an associated resistance to clarithromycin and fluoroquinolones was found. Conclusion: The H. pylori infection in cirrhotic patients with acute decompensation or ACLF has no significant effect on the severity of the clinical condition, elevated laboratory parameters and survival. Resistance rates to fluoroquinolones and clarithromycin or both antibiotics are high in decompensated patients with cirrhosis. There is a need to increase awareness of the rational use of antibiotics based on further investigations.

Helicobacter pylori infection: is there circulating vacuolating cytotoxin A or cytotoxin-associated gene A protein?

BackgroundHelicobacter pylori infection is a well-recognized cause of gastric diseases, including chronic gastritis, peptic ulcer, and gastric cancer. Vacuolating cytotoxin-A (VacA) and cytotoxin-associated gene A protein (CagA) play a role in the pathogenesis of H. pylori-related gastric diseases. Also, extragastric disorders are frequent morbid complications in patients with H. pylori infection. However, the direct pathologic implication of these virulence factors in extragastric manifestations remains unclear. Our hypothesis in the present study is that VacA and CagA released by H. pylori in the gastric mucosa leak into the systemic circulation, and therefore they can be measured in serum.ResultsSixty-two subjects were enrolled. They were allocated into the H. pylori-positive and H. pylori-negative groups. VacA and CagA were measured by immunoassays. The serum levels of VacA and CagA above an upper limit cut-off (mean plus two standard deviations of the mean in patients without H. pylori infection) were considered positive for antigen circulating level. Five out of 25 H. pylori-positive patients were positive for both serum VacA and serum CagA. The serum levels of VacA and CagA were significantly correlated with the serum levels of anti- H. pylori antibody and interleukin-12p70 among all H. pylori-positive and H. pylori-negative patients.ConclusionsThis study suggests that spill-over of VacA and CagA antigens in the systemic circulation may occur in some patients with H. pylori infection.

A 2022 focus on extragastric manifestations of Helicobacter pylori

A 2022 focus on extragastric manifestations of Helicobacter pylori

Helicobacter pylori Infection and Chronic Immune Thrombocytopenia.

Approximately half of the world’s population is infected with Helicobacter pylori, which causes gastric disease. Recent systematic reviews and meta-analyses have reported that H. pylori may also have extragastric manifestations such as hematologic diseases, including chronic immune thrombocytopenia (cITP). However, the molecular mechanisms by which H. pylori induces cITP remain unclear, and may involve the host immune response, bacterial strain diversity, and delivery of bacterial molecules to the host blood vessels. This review discusses the important pathophysiological mechanisms by which H. pylori potentially contributes to the development of cITP in infected patients.

On the Association between Gastrointestinal Symptoms and Extragastric Manifestations.

The aim of this study was to investigate the relationship between gastrointestinal (GI) symptoms and extragastric manifestations such as headache, fatigue, and dizziness. A prospective cohort study was conducted in a tertiary hospital in Athens, where patients with GI problems and extragastric symptoms were treated only for their GI problems, and improvement in extragastric manifestations was recorded. Inclusion criteria were an age older than 18 years, the presence of at least one of the three extragastric symptoms investigated in this study (headache, dizziness, and fatigue), and the concomitant presence of at least one gastrointestinal symptom (e.g., nausea, belching, abdominal tenderness, epigastric pain, halitosis, flatulence, diarrhea, bad odor of flatulence, flatulence, and constipation). A standardized questionnaire was used to collect demographic data (such as age, weight, and height), patients' symptoms, laboratory findings (gastric biopsy, gastroscopy, and colonoscopy), and intensity/frequency of GI and extragastric symptoms. Statistically significant associations were found between GI symptoms (nausea, constipation, halitosis, and belching) and dizziness, fatigue, and headache (frequency, intensity, and duration). Treatment of GI problems resulted in a significant improvement in extragastric symptoms within one month of treatment initiation. It should be emphasized that the actual reason for the improvement in extragastric symptoms was solely the resolution of the GI problems, as patients did not receive specific treatments for headache, dizziness or fatigue, or other changes in daily life. This study demonstrates the association between extragastric manifestations and GI disorders.

Diagnostic approach to Helicobacter pylori-related gastric oncogenesis.

Helicobacter pylori (H. pylori) is a causative agent of peptic ulcer disease and plays an important role in the development of various other upper and lower gastrointestinal tract and systemic diseases; in addition to carcinogenesis and the development of mucosa-associated lymphoid tissue lymphoma, extragastric manifestations of H. pylori are increasingly being unraveled. Therefore, prompt and accurate diagnosis is essential. Within this narrative review we present an overview of the current trend in the diagnosis of H. pylori infection and its potential oncogenic sequelae, including gastric mucosa atrophy, intestinal metaplasia, dysplasia and gastric cancer. Signs of H. pylori-related gastric cancer risk can be assessed by endoscopy using the Kyoto classification score. New technology, such as optical or digital chromoendoscopy, improves diagnostic accuracy and provides information regarding H. pylori-related gastric preneoplastic and malignant lesions. In addition, a rapid urease test or histological examination should be performed, as these offer a high diagnostic sensitivity; both are also useful for the diagnosis of sequelae including gastric and colon neoplasms. Culture is necessary for resistance testing and detecting H. pylori-related gastric dysbiosis involved in gastric oncogenesis. Likewise, molecular methods can be utilized for resistance testing and detecting H. pylori-related gastric cancer development and progression. Noninvasive tests, such as the urea breath and stool antigen tests, can also be implemented; these are also suitable for monitoring eradication success and possibly for detecting H. pylori-related gastric malignancy. Serological tests may help to exclude infection in specific populations and detect gastric and colon cancers. Finally, there are emerging potential diagnostic biomarkers for H. pylori-related gastric cancer.

Extragastric Manifestations of Helicobacter Pylori Infection: A Commentary

Helicobacter pylori (Hp) is characterized as a gram-negative bacterium with microaerophilic metabolism, flagellated and helix-shaped that affects approximately 50% of the world population and, in some regions, this rate can exceed 80% [1,2]. Hp infection is well known to infect the epithelial tissue of the stomach, being involved with development of many stomach diseases, including gastric carcinoma

Helicobacter pylori infection and other bacteria in pancreatic cancer and autoimmune pancreatitis.

Helicobacter pylori (H. pylori) is an infectious agent influencing as much as 50% of the world’s population. It is the causative agent for several diseases, most especially gastric and duodenal peptic ulcer, gastric adenocarcinoma and mucosa-associated lymphoid tissue lymphoma of the stomach. A number of other, extragastric manifestations also are associated with H. pylori infection. These include neurological disorders, such as Alzheimer’s disease, demyelinating multiple sclerosis and Parkinson’s disease. There is also evidence for a relationship between H. pylori infection and such dermatological diseases as psoriasis and rosacea as well as a connection with infection and open-angle glaucoma. Generally little is known about the relationship between H. pylori infection and diseases of the pancreas. Most evidence about H. pylori and its potential role in the development of pancreatic diseases concerns pancreatic adenocarcinoma and autoimmune forms of chronic pancreatitis. There is data (albeit not fully consistent) indicating modestly increased pancreatic cancer risk in H. pylori-positive patients. The pathogenetic mechanism of this increase is not yet fully elucidated, but several theories have been proposed. Reduction of antral D-cells in H. pylori-positive patients causes a suppression of somatostatin secretion that, in turn, stimulates increased secretin secretion. That stimulates pancreatic growth and thus increases the risk of carcinogenesis. Alternatively, H. pylori, as a part of microbiome dysbiosis and the so-called oncobiome, is proven to be associated with pancreatic adenocarcinoma development via the promotion of cellular proliferation. The role of H. pylori in the inflammation characteristic of autoimmune pancreatitis seems to be explained by a mechanism of molecular mimicry among several proteins (mostly enzymes) of H. pylori and pancreatic tissue. Patients with autoimmune pancreatitis often show positivity for antibodies against H. pylori proteins. H. pylori, as a part of microbiome dysbiosis, also is viewed as a potential trigger of autoimmune inflammation of the pancreas. It is precisely these relationships (and associated equivocal conclusions) that constitute a center of attention among pancreatologists, immunologists and pathologists. In order to obtain clear and valid results, more studies on sufficiently large cohorts of patients are needed. The topic is itself sufficiently significant to draw the interest of clinicians and inspire further systematic research. Next-generation sequencing could play an important role in investigating the microbiome as a potential diagnostic and prognostic biomarker for pancreatic cancer.

Possible relation between H. pylori and bilateral nasal polypi

Background: H.pylori is a Gram-negative bacterium known to be associated with peptic ulcer disease, gastric cancer, gastric lymphoma. Recently it was detected in mucosa of patients with CRS, but relation with bilateral nasal polyposis has not been demonstrated yet. Objectives: H. pyloriis a pathogen that lives in the gastrointestinal tract (GIT) and has extragastric manifestations. Nasal polypi may be one of these manifestations. This study aims to detect the relation between H.pylori and bilateral nasal polypi. Patients and methods: This study includes 80 cases of nasal polypi, 40 of them were de novo bilateral nasal polypi and 40 were recurrent nasal polypi, biopsies of nasal polypi were taken under sterile conditions and stained with Giemsa stain and Hematoxylin and eosin(H&E) stain. Stool analysis was done to detect presence of H.pylori using rapid urease test. Results: Both groups are age and sex matched. Nasal polyp biopsies showed positive results in 10 % of denovo group and 15 % of recurrent group with p value 0.449 which is not statistically significant. Stool antigen test showed positive results in 52.5 % of denovo group and 60 % of recurrent group with p value 0.449 which is not statistically significant. Conclusion: There is no statistically significant relation between H.pylori and the pathogenesis of bilateral nasal polypi, further studies with large number of patients is recommended.

Helicobacter pylori Infection and Association with Anaemia in Cameroon Patients, Using GastroPanel® Serological Biomarkers (Pepsinogen I; Pepsinogen II; Gastrin-17; Helicobacter pylori IgG)

Introduction: Helicobacter pylori (H. pylori) together with chronic atrophic gastritis have also been associated to extragastric manifestations including neurological, dermatological, ocular, cardiovascular, metabolic, allergic diseases and hematologic disorders. Several studies have associatedH. pylori with anaemia, iron deficiency and iron deficiency anemia. Little or no data on the association of H. pylori infection andanaemia exist in Cameroon. We therefore evaluated the prevalence H. pylori infection among patients with anaemia.&#x0D; Methodology: Blood samples were aseptically collected for the measurements Helicobacter pylori IgG antibodies, pepsinogene I et II levels, gastrine-17 in a total of 150 patients during the period February to July 2020. The blood samples required for the study were collected prospectively. Ethical clairance was obtained from the Centre Regional Ethics Committee for Human Sciences. An authorization of research was obtained from the authorities of General Hospital of Yaounde. All participants signed an informed consent form.&#x0D; Results: The GastroPanel® results showed that the prevalence of H. pyloriinfection was 90(60.00%).We observeda strong association of H. pylori with anaemia (OR 2.19, 95% CI 1.08–4.46; p=0,02).&#x0D; Conclusion: The prevalence of H. pylori infection is high in patients with anaemia and thus requires continuous monitoring of these patients.

Autoimmune gastritis, with or without pernicious anemia: epidemiology, risk factors, and clinical management.

Autoimmune gastritis (AIG) is a chronic immune-mediated, inflammatory condition that involves the destruction of the gastric oxyntic mucosa through the autoimmune-mediated loss of parietal cells, with replacement by atrophic and metaplastic tissue. Diagnosing AIG is important, given the need for ongoing clinical management and vigilance with respect to downstream complications, the most serious of which is gastric adenocarcinoma. Other clinical consequences include gastric neuroendocrine tumors, consequences related to decreased gastric acid and decreased intrinsic factor due to parietal cell destruction and antibodies against intrinsic factor (e.g. micronutrient deficiencies), as well as concomitant autoimmune disorders. Considering the prevalence of AIG and the potential for severe clinical outcomes, it is important to engage in efforts to reduce practice pattern variability related to diagnosis and management. Accordingly, herein, we review of the epidemiology, pathogenesis, clinical presentation of AIG, including both gastric and extragastric manifestations, and provide an overview of clinical management.

EFFECT OF HELICOBACTER PYLORY ON THE COURSE OF EARLY EMESIS GRAVIDARUM IN PREGNANT WOMEN WITH CHRONIC GASTRITIS

Introduction. The questions of the role of the infectious factor in the course of pregnancy, delivery and the newborn state are important due to the need of the determination of the appropriate management to prevent adverse maternal and fetal outcomes.&#x0D; Currently, the issues of extragastric manifestations associated with Helicobacter pylori (Hp) are being investigated, suggesting possible involvement of Hp in pregnancy complications.&#x0D; Study objective is to evaluate the course of early gestosis (emesis gravidarum), depending on the presence of Helicobacter infection in women with chronic gastritis.&#x0D; Material and methods. We examined 120 pregnant women in the gestation period of 8-12 weeks who had early gestational complications: emesis gravidarum, threatened miscarriage, spontaneous miscarriage and stillbirth, which were divided into 2 groups according to the presence of chronic gastritis: group 1 of 58 pregnant women with gastritis and Group 2 of 62 pregnant women without gastritis.&#x0D; Pregnant women with this form of pregnancy complication were additionally examined to perform the study objective of determining the features and frequency of early gestosis (emesis gravidarum).&#x0D; In addition to clinical and laboratory studies performed in accordance with the protocols of the Ministry of Health of Ukraine for the monitoring of pregnant women, the examined patients were diagnosed with a non-invasive Helicobacter pylory method by rapid chromatographic immunoassay for the detection of serum IgG antibodies to Hp.&#x0D; To determine the type of gastritis, the determination of the level of basal secretion of gastrin 17 (G-17) in the serum was performed with the stimulating test with which the presence and severity of atrophy of the mucous membrane of the antral gastric department can be determined.&#x0D; Pregnant women of both groups who had early gestosis (emesis gravidarum) were evaluated for the severity of pregnancy vomiting using a questionnaire method that included an evaluation of clinical and laboratory parameters.&#x0D; The obtained results were processed by methods of mathematical and statistical analysis with the determination of mean values (M ± m), Student’s test and reliability indicator (difference р&lt;0.05 was considered statistically significant).&#x0D; Results. Among the early gestational complications in pregnant women of groups 1 and 2, early gestosis (emesis gravidarum) had the same frequency and was 29.3% among pregnant women with chronic gastritis and 29.0% among women without gastritis.&#x0D; The positive result of detection of IgG antibodies to Helicobacter pylory in group 1 was 88,2%, in group 2 – 27,8%. When comparing the frequency of detection of antibodies in pregnant groups examined at different severity of emesis gravidarum, it was found that positive results were more common in group 1 with moderate (66,7%) and severe (26,7%) course. In group 2, a positive result was observed in mild emesis gravidarum (60,0%).&#x0D; When investigating the frequency of Hp detection in women with different types of gastritis and emesis gravidarum, it was found that Hp antibodies were more common in women of group 1 with hyperacid type of gastritis (53.3%), and in group 2 with hypoacid type of gastritis (80.0).&#x0D; The evaluation of the clinical course and laboratory data showed the difference, which was more often associated with the type of gastritis, which was responsible for the clinical course of pregnancy in women with chronic gastritis and early gestosis and the degree of emesis gravidarum.&#x0D; Conclusion. The presence of Helicobacter pylory infection is more common in pregnant women with chronic gastritis and vomiting of pregnant women. The clinical course of early gestosis in these conditions depends on the level of gastric acidity, which determines the severity of emesis gravidarum.

Helicobacter pylori and Metabolic Diseases

&lt;i&gt;Helicobacter pylori&lt;/i&gt; (&lt;i&gt;H. pylori&lt;/i&gt;) is one of the most common pathogens that can cause certain gastrointestinal disorders, such as gastritis, peptic ulcers, and gastric cancer. Recently, interest in the systemic effects of &lt;i&gt;H. pylori&lt;/i&gt; on extragastric manifestations is increasing. Representative diseases include hematologic, cardiovascular, neurodegenerative, autoimmune, dermatologic, allergic, hepatobiliary, and metabolic diseases. Among them, since the prevalence of metabolic diseases is on the rise worldwide, the relationship between &lt;i&gt;H. pylori&lt;/i&gt; infection and metabolic diseases has become an interesting research issue. Many studies have been conducted to clarify any association. However, the results of those studies still remain controversial. This review focuses on recently published studies to investigate the relationship between &lt;i&gt;H. pylori&lt;/i&gt; infection and metabolic diseases, including diabetes mellitus, metabolic syndrome, obesity, and non-alcoholic fatty liver disease, and their associated pathophysiology.

The Relation of Cytotoxin-Associated Gene-A Seropositivity with Vitamin B12 Deficiency in Helicobacter pylori-Positive Patients.

Background and Aim As a worldwide infectious bacterium, H. pylori leads to stomach pathologies such as gastritis, peptic ulcer, gastric cancer, MALToma, and various extragastric manifestations. In our study, we aimed to investigate the association between serum vitamin B12 level and cytotoxin-associated gene-A (CagA) seropositivity, which is one of the virulence factors of Helicobacter pylori (H. pylori). Method This study has been conducted on 289 patients who have met the inclusion criteria. Within these patients, 213 of them were H. pylori positive and 76 were negative. Vitamin B12 and CagA-IgG levels were assessed in consecutive dyspeptic patients undergoing upper endoscopy. Results Out of 289 patients, 51.9% were women (n = 150) and H. pylori was detected in 213 (73.7%) patients. Histopathological evaluation with modified Sydney classification revealed lymphocyte infiltration in 66.8% (n = 193), activation in 46% (n = 133), metaplasia in 11.4% (n = 33), atrophy in 11.4% (n = 33), and lymphoid follicles in 21.1% (n = 61) of the patients. Within H. pylori-positive patients, the ratio of CagA positivity was 57.3% (n = 122). Low B12 vitamin level was significantly correlated with existence of H. pylori (p=0.02), CagA (p=0.002), lymphocyte (p=0.006), metaplasia (p=0.001), atrophy (p=0.001), and lymphoid follicles (p=0.006). Positivity of CagA has been detected to be statistically corelated with lymphocyte (p=0.001) and activation (p=0.005); however, the same relation was not present with atrophy (p=0.236). Conclusion In conclusion, B12 deficiency was positively correlated with CagA positivity and gastric inflammatory activity.

Association of Chronic Urticaria with Helicobacter pylori Infection in Duhok City, Kurdistan Region of Iraq

Background: Helicobacter pylori (H. pylori) infection is associated with gastric and extra-gastric manifestations such as idiopathic urticaria. Objectives: The aim of this report was to investigate the relationship between H. pylori positivity and chronic urticaria. Methods: This case control study was carried out between June 2018 and March 2019. The study was conducted at the Dermatology Consultation Unit, Azadi Teaching Hospital, Duhok, Iraq. A total of 49 patients with chronic urticaria were recruited in the study. During the study period, 95 subjects were recruited as a control. Results: The overall H. pylori positivity was 106/144 (73.6%). A significant association was found between family members number and H. pylori positivity (P = 0.04; OR = 1.15; CI = 1 - 1.3). The positivity was 38/49 (77.6%) positive for the patients’ group versus 70/95 (73.7%) for the control group (P = 0.7; OR = 1.16; CI = 0.53 - 2.57). Conclusions: The prevalence of H. pylori infections was high in the region. No association was found between H. pylori positivity and chronic urticaria. Further study is needed to explore the effect of H. pylori eradication on urticaria treatment outcome.

Bone of Contention: Helicobacter pylori and Osteoporosis-Is There an Association?

Helicobacter pylori (H. pylori) infection is a common disease that can cause chronic gastritis, peptic ulcers, and gastric cancer. Nevertheless, due to its ability to elicit a systemic inflammatory response, it has also been related to several extra-gastric manifestations including endocrine disorders, such as autoimmune thyroid diseases, diabetes mellitus, dyslipidemia, and obesity. H. pylori infection has also been linked to osteoporosis, although currently available data are equivocal. This brief review will focus on the possible association between H. pylori infection and osteoporosis, a silent disease characterized by decreased bone mass that can increase the occurrence of fractures, disability, and mortality.