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World Journal of Emergency Surgery :... 2019Duodeno-pancreatic and extrahepatic biliary tree injuries are rare in both adult and pediatric trauma patients, and due to their anatomical location, associated injuries... (Review)
Review
Duodeno-pancreatic and extrahepatic biliary tree injuries are rare in both adult and pediatric trauma patients, and due to their anatomical location, associated injuries are very common. Mortality is primarily related to associated injuries, but morbidity remains high even in isolated injuries. Optimal management of duodeno-bilio-pancreatic injuries is dictated primarily by hemodynamic stability, clinical presentation, and grade of injury. Endoscopic and percutaneous interventions have increased the ability to non-operatively manage these injuries. Late diagnosis and treatment are both associated to increased morbidity and mortality. Sequelae of late presentations of pancreatic injury and complications of severe pancreatic trauma are also increasingly addressed endoscopically and with interventional radiology procedures. However, for moderate and severe extrahepatic biliary and severe duodeno-pancreatic injuries, immediate operative intervention is preferred as associated injuries are frequent and commonly present with hemodynamic instability or peritonitis. The aim of this paper is to present the World Society of Emergency Surgery (WSES) and American Association for the Surgery of Trauma (AAST) duodenal, pancreatic, and extrahepatic biliary tree trauma management guidelines.
Topics: Abdominal Injuries; Bile Ducts, Extrahepatic; Duodenum; Focused Assessment with Sonography for Trauma; General Surgery; Guidelines as Topic; Humans; Pancreas; Tomography, X-Ray Computed; Trauma Centers; Triage; Ultrasonography
PubMed: 31867050
DOI: 10.1186/s13017-019-0278-6 -
Pathologica Sep 2020Celiac disease is a multi-factorial chronic inflammatory intestinal disease, characterized by malabsorption resulting from mucosal injury after ingestion of wheat gluten... (Review)
Review
Celiac disease is a multi-factorial chronic inflammatory intestinal disease, characterized by malabsorption resulting from mucosal injury after ingestion of wheat gluten or related rye and barley proteins. Inappropriate T-cell-mediated immune response against ingested gluten in genetically predisposed people, leads to characteristic histological lesions, as villous atrophy and intraepithelial lymphocytosis. Nevertheless, celiac disease is a comprehensive diagnosis with clinical, serological and genetic characteristics integrated with histological features. Biopsy of duodenal mucosa remains the gold standard in the diagnosis of celiac disease with the recognition of the spectrum of histological changes and classification of mucosa damage based on updated Corazza-Villanacci system. Appropriate differential diagnosis evaluation and clinical context also for the diagnosis of complications is, moreover, needed for correct histological features interpretation and clinical management.
Topics: Biopsy; Celiac Disease; Diagnosis, Differential; Duodenitis; Duodenum; Genetic Predisposition to Disease; Glutens; Humans; Intestinal Mucosa; Intestine, Small
PubMed: 33179621
DOI: 10.32074/1591-951X-157 -
Neurogastroenterology and Motility Nov 2022Functional dyspepsia (FD) is a common and debilitating gastrointestinal disorder attributed to altered gut-brain interactions. While the etiology of FD remains unknown,... (Review)
Review
BACKGROUND
Functional dyspepsia (FD) is a common and debilitating gastrointestinal disorder attributed to altered gut-brain interactions. While the etiology of FD remains unknown, emerging research suggests the mechanisms are likely multifactorial and heterogenous among patient subgroups. Small bowel motor disturbances, visceral hypersensitivity, chronic microinflammation, and increased intestinal tract permeability have all been linked to the pathogenesis of FD. Recently, alterations to the gut microbiome have also been implicated to play an important role in the disease. Changes to the duodenal microbiota may either trigger or be a consequence of immune and neuronal disturbances observed in the disease, but the mechanisms of influence of small intestinal flora on gastrointestinal function and symptomatology are unknown.
PURPOSE
This review summarizes and synthesizes the literature on the link between the microbiota, low-grade inflammatory changes in the duodenum and FD. This review is not intended to provide a complete overview of FD or the small intestinal microbiota, but instead outline some of the key conceptual advances in understanding the interactions between altered gastrointestinal bacterial communities; dietary factors; host immune activation; and stimulation of the gut-brain axes in patients with FD versus controls. Current and emerging treatment approaches such as dietary interventions and antibiotic or probiotic use that have demonstrated symptom benefits for patients are reviewed, and their role in modulating the host-microbiota is discussed. Finally, suggested opportunities for diagnostic and therapeutic improvements for patients with this condition are presented.
Topics: Anti-Bacterial Agents; Duodenum; Dyspepsia; Gastrointestinal Diseases; Gastrointestinal Microbiome; Humans
PubMed: 35403776
DOI: 10.1111/nmo.14372 -
Cell Reports Mar 2021The upper gastrointestinal tract, consisting of the esophagus, stomach, and duodenum, controls food transport, digestion, nutrient uptake, and hormone production. By...
The upper gastrointestinal tract, consisting of the esophagus, stomach, and duodenum, controls food transport, digestion, nutrient uptake, and hormone production. By single-cell analysis of healthy epithelia of these human organs, we molecularly define their distinct cell types. We identify a quiescent COL17A1 KRT15 stem/progenitor cell population in the most basal cell layer of the esophagus and detect substantial gene expression differences between identical cell types of the human and mouse stomach. Selective expression of BEST4, CFTR, guanylin, and uroguanylin identifies a rare duodenal cell type, referred to as BCHE cell, which likely mediates high-volume fluid secretion because of continual activation of the CFTR channel by guanylin/uroguanylin-mediated autocrine signaling. Serotonin-producing enterochromaffin cells in the antral stomach significantly differ in gene expression from duodenal enterochromaffin cells. We, furthermore, discover that the histamine-producing enterochromaffin-like cells in the oxyntic stomach express the luteinizing hormone, yet another member of the enteroendocrine hormone family.
Topics: Animals; Autoantigens; Bestrophins; Cystic Fibrosis Transmembrane Conductance Regulator; Duodenum; Esophagus; Gene Expression; Humans; Intestinal Mucosa; Keratin-15; Luteinizing Hormone; Mice; Mice, Inbred C57BL; Non-Fibrillar Collagens; Single-Cell Analysis; Stem Cells; Stomach; Upper Gastrointestinal Tract; Collagen Type XVII
PubMed: 33691112
DOI: 10.1016/j.celrep.2021.108819 -
Nature Nov 2021Tissue maintenance and repair depend on the integrated activity of multiple cell types. Whereas the contributions of epithelial, immune and stromal cells in intestinal...
Tissue maintenance and repair depend on the integrated activity of multiple cell types. Whereas the contributions of epithelial, immune and stromal cells in intestinal tissue integrity are well understood, the role of intrinsic neuroglia networks remains largely unknown. Here we uncover important roles of enteric glial cells (EGCs) in intestinal homeostasis, immunity and tissue repair. We demonstrate that infection of mice with Heligmosomoides polygyrus leads to enteric gliosis and the upregulation of an interferon gamma (IFNγ) gene signature. IFNγ-dependent gene modules were also induced in EGCs from patients with inflammatory bowel disease. Single-cell transcriptomics analysis of the tunica muscularis showed that glia-specific abrogation of IFNγ signalling leads to tissue-wide activation of pro-inflammatory transcriptional programs. Furthermore, disruption of the IFNγ-EGC signalling axis enhanced the inflammatory and granulomatous response of the tunica muscularis to helminths. Mechanistically, we show that the upregulation of Cxcl10 is an early immediate response of EGCs to IFNγ signalling and provide evidence that this chemokine and the downstream amplification of IFNγ signalling in the tunica muscularis are required for a measured inflammatory response to helminths and resolution of the granulomatous pathology. Our study demonstrates that IFNγ signalling in enteric glia is central to intestinal homeostasis and reveals critical roles of the IFNγ-EGC-CXCL10 axis in immune response and tissue repair after infectious challenge.
Topics: Adventitia; Animals; Chemokine CXCL10; Duodenum; Female; Gliosis; Homeostasis; Humans; Inflammation; Interferon-gamma; Intestines; Male; Mice; Nematospiroides dubius; Neuroglia; Regeneration; Signal Transduction; Strongylida Infections
PubMed: 34671159
DOI: 10.1038/s41586-021-04006-z -
Gut Jan 2021Type 1 diabetes (T1D) is characterised by islet autoimmunity and beta cell destruction. A gut microbiota-immunological interplay is involved in the pathophysiology of... (Randomized Controlled Trial)
Randomized Controlled Trial
OBJECTIVE
Type 1 diabetes (T1D) is characterised by islet autoimmunity and beta cell destruction. A gut microbiota-immunological interplay is involved in the pathophysiology of T1D. We studied microbiota-mediated effects on disease progression in patients with type 1 diabetes using faecal microbiota transplantation (FMT).
DESIGN
Patients with recent-onset (<6 weeks) T1D (18-30 years of age) were randomised into two groups to receive three autologous or allogenic (healthy donor) FMTs over a period of 4 months. Our primary endpoint was preservation of stimulated C peptide release assessed by mixed-meal tests during 12 months. Secondary outcome parameters were changes in glycaemic control, fasting plasma metabolites, T cell autoimmunity, small intestinal gene expression profile and intestinal microbiota composition.
RESULTS
Stimulated C peptide levels were significantly preserved in the autologous FMT group (n=10 subjects) compared with healthy donor FMT group (n=10 subjects) at 12 months. Small intestinal was inversely related to residual beta cell function (r=-0.55, p=0.02), whereas plasma metabolites 1-arachidonoyl-GPC and 1-myristoyl-2-arachidonoyl-GPC levels linearly correlated with residual beta cell preservation (rho=0.56, p=0.01 and rho=0.46, p=0.042, respectively). Finally, baseline CD4 +CXCR3+T cell counts, levels of small intestinal and CCL22 and CCL5 gene expression in duodenal biopsies predicted preserved beta cell function following FMT irrespective of donor characteristics.
CONCLUSION
FMT halts decline in endogenous insulin production in recently diagnosed patients with T1D in 12 months after disease onset. Several microbiota-derived plasma metabolites and bacterial strains were linked to preserved residual beta cell function. This study provides insight into the role of the intestinal gut microbiome in T1D.
TRIAL REGISTRATION NUMBER
NTR3697.
Topics: Adolescent; Adult; C-Peptide; Diabetes Mellitus, Type 1; Duodenum; Fecal Microbiota Transplantation; Female; Gastrointestinal Microbiome; Humans; Insulin-Secreting Cells; Male; Transplantation, Autologous; Young Adult
PubMed: 33106354
DOI: 10.1136/gutjnl-2020-322630 -
Internal Medicine (Tokyo, Japan) 2021
Topics: Colitis, Ulcerative; Crohn Disease; Duodenitis; Humans
PubMed: 34776467
DOI: 10.2169/internalmedicine.7592-21 -
The New England Journal of Medicine Oct 2020Eosinophilic gastritis and duodenitis are characterized by gastrointestinal mucosal eosinophilia, chronic symptoms, impaired quality of life, and a lack of adequate... (Randomized Controlled Trial)
Randomized Controlled Trial
BACKGROUND
Eosinophilic gastritis and duodenitis are characterized by gastrointestinal mucosal eosinophilia, chronic symptoms, impaired quality of life, and a lack of adequate treatments. Mast-cell activity may contribute to the pathogenesis of the conditions. AK002 (lirentelimab) is an anti-Siglec-8 antibody that depletes eosinophils and inhibits mast cells and that has shown potential in animal models as a treatment for eosinophilic gastritis and duodenitis.
METHODS
In this phase 2 trial, we randomly assigned adults who had symptomatic eosinophilic gastritis, eosinophilic duodenitis, or both conditions in a 1:1:1 ratio to receive four monthly infusions of low-dose AK002, high-dose AK002, or placebo. The primary end point was the change in gastrointestinal eosinophil count from baseline to 2 weeks after the final dose; to maximize statistical power, we evaluated this end point in the placebo group as compared with the combined AK002 group. Secondary end points were treatment response (>30% reduction in total symptom score and >75% reduction in gastrointestinal eosinophil count) and the change in total symptom score.
RESULTS
Of the 65 patients who underwent randomization, 43 were assigned to receive AK002 and 22 were assigned to receive placebo. The mean percentage change in gastrointestinal eosinophil count was -86% in the combined AK002 group, as compared with 9% in the placebo group (least-squares mean difference, -98 percentage points; 95% confidence interval [CI], -121 to -76; P<0.001). Treatment response occurred in 63% of the patients who received AK002 and in 5% of the patients who received placebo (difference, 58 percentage points; 95% CI, 36 to 74; P<0.001). The mean change in total symptom score was -48% with AK002 and -22% with placebo (least-squares mean difference, -26 percentage points; 95% CI, -44 to -9; P = 0.004). Adverse events associated with AK002 were similar to those with placebo, with the exception of higher percentages of patients having mild-to-moderate infusion-related reactions with AK002 (60% in the combined AK002 group and 23% in the placebo group).
CONCLUSIONS
In patients with eosinophilic gastritis or duodenitis, AK002 reduced gastrointestinal eosinophils and symptoms. Infusion-related reactions were more common with AK002 than with placebo. (Funded by Allakos; ENIGMA ClinicalTrials.gov number, NCT03496571.).
Topics: Adolescent; Adult; Aged; Antibodies, Monoclonal, Humanized; Antigens, CD; Antigens, Differentiation, B-Lymphocyte; Dose-Response Relationship, Drug; Double-Blind Method; Duodenitis; Enteritis; Eosinophilia; Eosinophils; Female; Gastritis; Gastrointestinal Tract; Humans; Infusions, Intravenous; Lectins; Leukocyte Count; Male; Middle Aged; Young Adult
PubMed: 33085861
DOI: 10.1056/NEJMoa2012047 -
Revista Espanola de Enfermedades... Apr 2023Gastrointestinal tuberculosis (TB) is a rare disease and only involves the duodenum in 2-2,5% of all cases. A 60-year-old female with no reported medical history,...
Gastrointestinal tuberculosis (TB) is a rare disease and only involves the duodenum in 2-2,5% of all cases. A 60-year-old female with no reported medical history, presented with constitutional syndrome with a 10 kg weight loss in three months, epigastric pain, bloating and vomiting. She denied fever or respiratory symptoms. Laboratory examination revealed elevated C-reactive protein levels and low prealbumin. Abdominal computed tomography (CT) showed duodenal wall thickening, mainly in its third part, with infiltration of the root of the mesentery and numerous subcentimeter adenopathies at that level.
Topics: Female; Humans; Middle Aged; Duodenum; Abdomen; Abdominal Pain; Mesentery; Tuberculosis, Gastrointestinal
PubMed: 36695766
DOI: 10.17235/reed.2023.9373/2022 -
Revista Espanola de Enfermedades... Feb 2023We herein report a case of jejunal lymphangioma. A CT scan showed non-enhancing cystic masses in the jejunum. Enteroscopy revealed multiple cystic swelling with whitish...
We herein report a case of jejunal lymphangioma. A CT scan showed non-enhancing cystic masses in the jejunum. Enteroscopy revealed multiple cystic swelling with whitish carpet-like villi. Histopathology disclosed dilated lymphatic channels, lined by a single layer of endothelial cells, which were positive for the lymphatic endothelial marker by the immunohistochemical staining. Clinical manifestations of intestinal lymphangioma are briefly discussed.
Topics: Humans; Jejunum; Endothelial Cells; Lymphangioma; Duodenum; Tomography, X-Ray Computed
PubMed: 36043534
DOI: 10.17235/reed.2022.9088/2022