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World Journal of Gastroenterology Nov 2021Therapy of () requires a combination of antibiotics together with an acid suppressing agent; most treatment regimens include Amoxicillin as one of the antibiotics,... (Review)
Review
Therapy of () requires a combination of antibiotics together with an acid suppressing agent; most treatment regimens include Amoxicillin as one of the antibiotics, which is an important constituent as resistance to it is low. However, allergies to the penicillin group of antibiotics are not uncommon, and treating infection in such individuals can be challenging due to the restricted choice of regimens. The aim of this review is to summarise the evidence for therapeutic options in patients with infection and penicillin allergy. A literature search was conducted in PubMed for English language publications using the key words 'Helicobacter' and 'treatment' or 'therapy' and 'penicillin' or 'beta-lactam' and 'allergy' or 'anaphylaxis'. Eighteen studies were identified that specifically evaluated treatment success in penicillin allergic patients. The number of subjects in most of them was low and many were retrospective, uncontrolled, single cohort studies. The most effective option for first-line treatment appears to be Bismuth-based quadruple therapy for 10-14 d. The evidence supports second-line treatment with Levoflaxacin-based triple therapy for 10 d. Patients with persistent infection after 2 treatment courses should be considered for testing to confirm penicillin allergy. Further treatment should be guided by the results of culture and sensitivity testing.
Topics: Amoxicillin; Anti-Bacterial Agents; Bismuth; Drug Hypersensitivity; Drug Therapy, Combination; Helicobacter Infections; Helicobacter pylori; Humans; Metronidazole; Penicillins; Proton Pump Inhibitors; Retrospective Studies; Treatment Outcome
PubMed: 34908805
DOI: 10.3748/wjg.v27.i44.7661 -
Current Gastroenterology Reports Jul 2016Helicobacter pylori infects about 50 % of the world's population, causing at a minimum chronic gastritis. A subset of infected patients will ultimately develop gastric... (Review)
Review
Helicobacter pylori infects about 50 % of the world's population, causing at a minimum chronic gastritis. A subset of infected patients will ultimately develop gastric or duodenal ulcer disease, gastric adenocarcinoma, or MALT (mucosa-associated lymphoid tissue) lymphoma. Eradication of H. pylori requires complex regimens that include acid suppression and multiple antibiotics. The efficacy of treatment using what were once considered standard regimens have declined in recent years, mainly due to widespread development of antibiotic resistance. Addition of bismuth to standard triple therapy regimens, use of alternate antibiotics, or development of alternative regimens using known therapies in novel combinations have improved treatment efficacy in specific populations, but overall success of eradication remains less than ideal. Novel regimens under investigation either in vivo or in vitro, involving increased acid suppression ideally with fewer antibiotics or development of non-antibiotic treatment targets, show promise for future therapy.
Topics: Anti-Bacterial Agents; Bismuth; Chronic Disease; Drug Resistance, Bacterial; Drug Therapy, Combination; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Proton Pump Inhibitors
PubMed: 27177639
DOI: 10.1007/s11894-016-0509-x -
Journal of Visceral Surgery Aug 2016The spleen and pancreas are at risk for injury during abdominal trauma. The spleen is more commonly injured because of its fragile structure and its position immediately... (Review)
Review
The spleen and pancreas are at risk for injury during abdominal trauma. The spleen is more commonly injured because of its fragile structure and its position immediately beneath the ribs. Injury to the more deeply placed pancreas is classically characterized by discordance between the severity of pancreatic injury and its initial clinical expression. For the patient who presents with hemorrhagic shock and ultrasound evidence of major hemoperitoneum, urgent "damage control" laparotomy is essential; if splenic injury is the cause, prompt "hemostatic" splenectomy should be performed. Direct pancreatic injury is rarely the cause of major hemorrhage unless a major neighboring vessel is injured, but if there is destruction of the pancreatic head, a two-stage pancreatoduodenectomy (PD) may be indicated. At open laparotomy when the patient's hemodynamic status can be stabilized, it may be possible to control splenic bleeding without splenectomy; it is always essential to search for injury to the pancreatic duct and/or the adjacent duodenum. Pancreatic contusion without ductal rupture is usually treated by drain placement adjacent to the injury; ductal injuries of the pancreatic body or tail are treated by resection (distal pancreatectomy with or without splenectomy), with generally benign consequences. For injuries of the pancreatic head with pancreatic duct disruption, wide drainage is usually performed because emergency PD is a complex gesture prone to poor results. Postoperatively, the placement of a ductal stent by endoscopic retrograde catheterization may be decided, while management of an isolated pancreatic fistula is often straightforward. Non-operative management is the rule for the trauma victim who is hemodynamically stable. In addition to the clinical examination and conventional laboratory tests, investigations should include an abdominothoracic CT scan with contrast injection, allowing identification of all traumatized organs and assessment of the severity of injury. In this context, non-operative management (NOM) has gradually become the standard as long as the patient remains hemodynamically stable and there is no suspicion of injury to hollow viscera, with the patient being carefully monitored on a surgical service. The development of arteriography with splenic artery embolization has increased the rate of splenic salvage; this can be performed electively based on specific indications (blush on CT, pseudoaneurysm, arteriovenous fistula), and may also be considered for severe splenic injury, abundant hemoperitoneum, or severe polytrauma. For pancreatic injury, in addition to CT scan, magnetic resonance pancreatography (MRCP) or even endoscopic retrograde cholangiopancreatography (ERCP) may be necessary to identify a ductal rupture. If the pancreatic duct is intact, laboratory and CT imaging surveillance is performed just as for splenic injury. In case of pancreatic ductal injury, ERCP stenting can be considered. However, if this is unsuccessful, the therapeutic decision can be difficult: while NOM can still be successful, complications may arise that are difficult to treat while distal pancreatectomy, although initially more agressive may avoid these complications if performed early.
Topics: Abdominal Injuries; Angiography; Embolization, Therapeutic; Hemoperitoneum; Humans; Infections; Laparotomy; Pancreas; Pancreaticoduodenectomy; Postoperative Complications; Spleen; Splenectomy
PubMed: 27402320
DOI: 10.1016/j.jviscsurg.2016.04.005 -
Cancer Jul 2021Coronavirus disease 2019 (COVID-19) restrictions on visitation policies have created barriers for cancer caregivers and patients. Awareness of the critical role that...
Coronavirus disease 2019 (COVID-19) restrictions on visitation policies have created barriers for cancer caregivers and patients. Awareness of the critical role that cancer caregivers play should lead to better integration of the caregiver into clinical care and research after the pandemic ends.
Topics: Aged; Ampulla of Vater; COVID-19; Common Bile Duct Neoplasms; Decision Making; Humans; Male; Narration; Pandemics; Physician-Patient Relations; Visitors to Patients
PubMed: 33761133
DOI: 10.1002/cncr.33291 -
World Journal of Gastroenterology Jul 2015Aspirin, even at low doses, has been known to cause upper gastro-intestinal complications, such as gastroduodenal ulcers, despite the definite benefits from its... (Review)
Review
Aspirin, even at low doses, has been known to cause upper gastro-intestinal complications, such as gastroduodenal ulcers, despite the definite benefits from its antithrombotic effects. Helicobacter pylori (H. pylori) is major pathogen responsible for gastroduodenal ulcer formation. There have been conflicting results about the potential interaction between these two ulcerogenic factors and the geographic areas involved. In Western countries, the prevalence of gastroduodenal ulcers is consistently higher in H. pylori-positive low-dose aspirin (LDA) users than in H. pylori-negative ones, suggesting that H. pylori infection exacerbates LDA-induced gastroduodenal mucosal injury in these geographic areas. Meanwhile, previous studies from Japan have generally reported a similar prevalence of LDA-induced gastroduodenal mucosal injury regardless of the presence of H. pylori infection, indicating that the infection is not an overall exacerbating factor for drug-induced injury. H. pylori infection could have a synergistic or antagonistic interaction with LDA use in adverse gastroduodenal events depending on gastric acid secretion. It is well-recognized that the net effect of H. pylori infection on gastric acid secretion shows considerable geographic variation at the population level. While gastric acid secretion levels were not decreased and were well-preserved in most patients with H. pylori infection from Western countries, the majority of Japanese patients with H. pylori infection exhibited decreased gastric acid secretion. Such large geographic differences in the net effect of H. pylori infection on gastric acid secretion could be at least partly responsible for the geographically distinct interaction between LDA use and H. pylori infection on adverse gastroduodenal lesions.
Topics: Anti-Inflammatory Agents, Non-Steroidal; Asia; Aspirin; Australia; Duodenal Ulcer; Duodenum; Europe; Gastric Acid; Gastric Mucosa; Helicobacter Infections; Helicobacter pylori; Humans; Intestinal Mucosa; North America; Prevalence; Risk Assessment; Risk Factors; Stomach Ulcer
PubMed: 26167071
DOI: 10.3748/wjg.v21.i25.7709 -
Briefings in Bioinformatics Jul 2019Helicobacter pylori (H. pylori) infection remains a cause of significant morbidity and mortality worldwide. Comprehensive understanding of the pathogenic mechanism of H.... (Review)
Review
Helicobacter pylori (H. pylori) infection remains a cause of significant morbidity and mortality worldwide. Comprehensive understanding of the pathogenic mechanism of H. pylori and its interaction with host will contribute to developing novel prophylactical and therapeutical strategies. Here, we first determined microRNA (miRNA) levels in H. pylori-infected patients with gastritis, duodenal ulcer, gastric cancer or mucosa-associated lymphoid tissue lymphoma using miRNA data sets. Thirty-four differentially expressed miRNAs were identified and functional enrichment analysis of those miRNA target genes revealed that H. pylori infection were strongly associated with pathway in cancer and regulation of mRNA synthesis. Using disease connectivity analysis of 28 hub genes, we found that H. pylori may increase the risk of many extragastric diseases (e.g. cardiovascular disease, hemic and lymphatic diseases and nervous system disease). Altogether, our integrated analysis provided a new method to predict pathogen-human disease connectivity based on miRNA-mRNA interaction network and indicated anti-H. pylori therapy as an effective means of human diseases prevention.
Topics: Computational Biology; Gene Expression Regulation; Gene Ontology; Gene Regulatory Networks; Helicobacter Infections; Helicobacter pylori; Host Microbial Interactions; Humans; MicroRNAs; Protein Interaction Maps; RNA, Messenger
PubMed: 29579224
DOI: 10.1093/bib/bby018 -
Journal of Investigative Medicine High... 2021(also referred to as and ) is the most common intestinal parasite in the world, affecting approximately 200 million people annually. Symptoms of include foul-smelling... (Review)
Review
(also referred to as and ) is the most common intestinal parasite in the world, affecting approximately 200 million people annually. Symptoms of include foul-smelling diarrhea, abdominal cramping, bloating, gas, and nausea. Although usually self-limiting, can progress to dehydration, malnutrition, and failure to thrive, especially in immunocompromised individuals. Early diagnosis and treatment is imperative to prevent and control infection of . Infectious Disease Society of America diagnostic guidelines recommend obtaining stool studies to diagnose ; when stool studies are negative but suspicion remains high, duodenal aspirate microscopy is the only alternative diagnostic strategy suggested. We report a patient diagnosed incidentally with from a duodenal biopsy specimen obtained during a workup for a gastrointestinal bleed. There are limited cases of diagnosed by duodenal biopsy reported in the literature. We review studies that suggest duodenal biopsy can be a very sensitive strategy for the diagnosis of .
Topics: Biopsy; Duodenum; Feces; Giardia lamblia; Giardiasis; Humans
PubMed: 33733914
DOI: 10.1177/23247096211001649 -
Gastroenterology Mar 2022The protozoa Giardia duodenalis is a major cause of gastrointestinal illness worldwide, but underlying pathophysiological mechanisms remain obscure, partly due to the...
BACKGROUND & AIMS
The protozoa Giardia duodenalis is a major cause of gastrointestinal illness worldwide, but underlying pathophysiological mechanisms remain obscure, partly due to the absence of adequate cellular models. We aimed at overcoming these limitations and recapitulating the authentic series of pathogenic events in the primary human duodenal tissue by using the human organoid system.
METHODS
We established a compartmentalized cellular transwell system with electrophysiological and barrier properties akin to duodenal mucosa and dissected the events leading to G. duodenalis-induced barrier breakdown by functional analysis of transcriptional, electrophysiological, and tight junction components.
RESULTS
Organoid-derived cell layers of different donors showed a time- and parasite load-dependent leak flux indicated by collapse of the epithelial barrier upon G. duodenalis infection. Gene set enrichment analysis suggested major expression changes, including gene sets contributing to ion transport and tight junction structure. Solute carrier family 12 member 2 and cystic fibrosis transmembrane conductance regulator-dependent chloride secretion was reduced early after infection, while changes in the tight junction composition, localization, and structural organization occurred later as revealed by immunofluorescence analysis and freeze fracture electron microscopy. Functionally, barrier loss was linked to the adenosine 3',5'-cyclic monophosphate (cAMP)/protein kinase A-cAMP response element-binding protein signaling pathway.
CONCLUSIONS
Data suggest a previously unknown sequence of events culminating in intestinal barrier dysfunction upon G. duodenalis infection during which alterations of cellular ion transport were followed by breakdown of the tight junctional complex and loss of epithelial integrity, events involving a cAMP/protein kinase A-cAMP response element-binding protein mechanism. These findings and the newly established organoid-derived model to study G. duodenalis infection may help to explore new options for intervening with disease and infection, in particular relevant for chronic cases of giardiasis.
Topics: Apoptosis; Caco-2 Cells; Chlorides; Cyclic AMP; Cyclic AMP-Dependent Protein Kinases; Cystic Fibrosis Transmembrane Conductance Regulator; Duodenum; Electric Impedance; Giardia lamblia; Giardiasis; Humans; Interleukin-1; Intestinal Mucosa; Ion Transport; NF-kappa B; Organoids; Parasite Load; Signal Transduction; Solute Carrier Family 12, Member 2; Tight Junctions; Transcriptome; Tumor Necrosis Factor-alpha
PubMed: 34822802
DOI: 10.1053/j.gastro.2021.11.022 -
World Journal of Gastroenterology Jul 2014The bacterial pathogen Helicobacter pylori (H. pylori) colonizes in over half of the world's population. H. pylori that establishes life-long infection in the stomach is... (Review)
Review
The bacterial pathogen Helicobacter pylori (H. pylori) colonizes in over half of the world's population. H. pylori that establishes life-long infection in the stomach is definitely associated with gastro-duodenal diseases and a wide variety of non-gastrointestinal tract conditions such as immune thrombocytopenia. Triple therapy which consists of a proton pump inhibitor and combinations of two antibiotics (amoxicillin, clarithromycin or amoxicillin, metronidazol) is commonly used for H. pylori eradication. Recently, the occurrence of drug-resistant H. pylori and the adverse effect of antibiotics have severely weakened eradication therapy. Generally antibiotics induce the disturbance of human gastrointestinal microflora. Furthermore, there are inappropriate cases of triple therapy such as allergy to antibiotics, severe complications (liver and/or kidney dysfunction), the aged and people who reject the triple therapy. These prompt us to seek alterative agents instead of antibiotics and to develop more effective and safe therapy with these agents. The combination of these agents actually may result in lower a dose of antibiotics. There are many reports world-wide that non-antibiotic substances from natural products potentially have an anti-H. pylori agent. We briefly review the constituents derived from nature that fight against H. pylori in the literature with our studies.
Topics: Animals; Anti-Bacterial Agents; Complementary Therapies; Dietary Supplements; Drug Resistance, Bacterial; Drug Therapy, Combination; Gastrointestinal Agents; Helicobacter Infections; Helicobacter pylori; Humans; Phytotherapy; Plant Extracts; Plants, Medicinal; Proton Pump Inhibitors; Treatment Outcome
PubMed: 25083070
DOI: 10.3748/wjg.v20.i27.8971 -
The Korean Journal of Internal Medicine May 2016One in 10 people suffer from functional dyspepsia (FD), a clinical syndrome comprising chronic bothersome early satiety, or postprandial fullness, or epigastric pain or... (Review)
Review
One in 10 people suffer from functional dyspepsia (FD), a clinical syndrome comprising chronic bothersome early satiety, or postprandial fullness, or epigastric pain or burning. Postprandial distress syndrome (PDS, comprising early satiety and/or postprandial fullness) and epigastric pain syndrome (EPS) are increasingly accepted as valid clinical entities, based on new insights into the pathophysiology and the results of clinical trials. Diagnosis is based on the clinical history, and exclusion of peptic ulcer and cancer by endoscopy. Evidence is accumulating FD and gastroesophageal ref lux disease are part of the same disease spectrum in a major subset. The causes of FD remain to be established, but accumulating data suggest infections and possibly food may play an important role in subsets. FD does not equate with no pathology; duodenal eosinophilia is now an accepted association, and Helicobacter pylori infection is considered to be causally linked to dyspepsia although only a minority will respond to eradication. In those with EPS, acid suppression therapy is a first line therapy; consider a H2 blocker even if proton pump inhibitor fails. In PDS, a prokinetic is preferred. Second line therapy includes administration of a tricyclic antidepressant in low doses, or mirtazapine, but not a selective serotonin reuptake inhibitor.
Topics: Anti-Bacterial Agents; Antidepressive Agents, Tricyclic; Dyspepsia; Gastrointestinal Agents; Genetic Predisposition to Disease; Helicobacter Infections; Helicobacter pylori; Histamine H2 Antagonists; Humans; Predictive Value of Tests; Proton Pump Inhibitors; Risk Factors; Treatment Outcome
PubMed: 27048251
DOI: 10.3904/kjim.2016.091