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Endocrinology Aug 2019Glucagon-like peptide-2 (GLP-2), secreted from enteroendocrine cells, attenuates gut motility, enhances barrier function, and augments nutrient absorption, actions...
Glucagon-like peptide-2 (GLP-2), secreted from enteroendocrine cells, attenuates gut motility, enhances barrier function, and augments nutrient absorption, actions mediated by a single GLP-2 receptor (GLP-2R). Despite extensive analyses, the precise distribution and cellular localization of GLP-2R expression remains controversial, confounded by the lack of suitable GLP-2R antisera. Here, we reassessed murine Glp2r expression using regular and real-time quantitative PCR (qPCR), in situ hybridization (ISH), and a Glp2rLacZ reporter mouse. Glp2r mRNA expression was detected from the stomach to the rectum and most abundant in the jejunum. Glp2r transcripts were also detected in cerebral cortex, mesenteric lymph nodes, gallbladder, urinary bladder, and mesenteric fat. Surprisingly, Glp2r mRNA was found in testis by qPCR at levels similar to jejunum. However, the testis Glp2r transcripts, detected by different primer pairs and qPCR, lacked 5' mRNA coding sequences, and only a minute proportion of them corresponded to full-length Glp2r mRNA. Within the gut, Glp2r-driven LacZ expression was localized to enteric neurons and lamina propria stromal cells, findings confirmed by ISH analysis of the endogenous Glp2r mRNA. Unexpectedly, vascular Glp2rLacZ expression was localized to mesenteric veins and not arteries. Moreover, mesenteric fat Glp2rLacZ expression was detected within blood vessels and not adipocytes. Reporter LacZ expression was not detected in all tissues expressing an endogenous Glp2r transcript, such as gallbladder, urinary bladder, and mesenteric lymph nodes. Collectively, these findings extend our understanding of the cellular domains of Glp2r expression and highlight limitations inherent in application of commonly used technologies to infer analysis of gene expression.
Topics: Animals; Gastrointestinal Tract; Glucagon-Like Peptide-2 Receptor; Mice; Mice, Inbred C57BL; RNA, Messenger; Real-Time Polymerase Chain Reaction; beta-Galactosidase
PubMed: 31237617
DOI: 10.1210/en.2019-00398 -
Cureus Aug 2022Diverticulitis is a common gastrointestinal complaint that refers to inflammation of colonic diverticula. Its incidence has increased partly due to the increase in...
Diverticulitis is a common gastrointestinal complaint that refers to inflammation of colonic diverticula. Its incidence has increased partly due to the increase in prevalence of diverticulosis, which results from poor dietary habits and chronic constipation. An acute diverticulitis episode can vary in severity, ranging from outpatient management of mild abdominal discomfort to inpatient admission requiring emergent surgery. Some common complications associated with diverticulitis include bowel wall perforation, microperforation, abscess formation, bowel obstruction, and colonic fistulas. A lesser-known complication of diverticulitis is pylephlebitis. Pylephlebitis refers to thrombosis of the portal vein resulting from sepsis secondary to an intra-abdominal or pelvic infection. Initially thought to be most associated with appendicitis, literature has emerged that implicates diverticulitis as the most likely culprit. Less frequently, pylephlebitis can also include thrombosis of the abdominal vasculature that drains into the portal vein such as the mesenteric veins and splenic vein. Despite antibiotic therapy, mortality in patients with pylephlebitis is high as it can lead to bowel ischemia, liver failure, or liver abscesses. While antibiotic therapy is the mainstay of treatment, anticoagulation can also be used in conjunction, especially when thrombosis extends beyond the portal vein. Herein, we present a case of a patient who was diagnosed with pylephlebitis with thrombosis extension into the splenic and mesenteric veins, which resulted from an episode of severe sigmoid diverticulitis. Our patient was treated medically with antibiotics and anticoagulation and underwent a loop transverse colostomy with full recovery. He was discharged with intravenous antibiotics and long-term anticoagulation. We present this case to highlight a rare complication of an otherwise common pathology and describe our management that led to a positive outcome for this patient.
PubMed: 36185925
DOI: 10.7759/cureus.28524 -
International Journal of Surgery Case... Jun 2021Idiopathic myointimal hyperplasia of the mesenteric veins (IMHMV) is a poorly understood disorder which poses a diagnostic challenge to clinicians and pathologists. Here...
INTRODUCTION AND IMPORTANCE
Idiopathic myointimal hyperplasia of the mesenteric veins (IMHMV) is a poorly understood disorder which poses a diagnostic challenge to clinicians and pathologists. Here we have described the case of a male patient with IMHMV along with a presumed history of ulcerative colitis for 1 year.
CASE PRESENTATION
A 55-year-old male presented to the OPD with history of chronic abdominal pain. Clinical and radiological examination coupled with endoscopic findings resulted in the patient being wrongly diagnosed to be a case of ulcerative colitis and was managed accordingly. Throughout his multiple hospital visits following treatment for ulcerative colitis, the patient was persistently symptomatic. He presented with 10 days history of increasing abdominal pain and constipation following which he developed spontaneous colonic perforation for which he underwent exploratory laparotomy left colectomy and Hartman's procedure. The final pathology of the resected colon found to be consistent of Idiopathic myointimal hyperplasia of the mesenteric veins and ischemic bowel changes.
CLINICAL DISCUSSION
The absence of clear-cut endoscopic biopsy findings of ulcerative colitis made radiological picture to be the mainstay for diagnosis, which was inaccurate and exposed the patient to unnecessary treatment with immuno-modulators thus resulting in poor response to treatment. As the disease progressed, further narrowing of the vessels made the clinical picture to look closer to ischemic bowel pathology as the patient developed a top surgical emergency (i.e. bowel perforation). Such pathological finding (IMHMV) can only be diagnosed in a fully prepared tissue histology, but rather be considered when no other consistent alternative diagnosis was found.
CONCLUSION
The treating physicians must definitely consider the possibility of idiopathic myointimal hyperplasia of mesenteric veins when similar manifestations are encountered in biopsy specimens of old cases with suspected inflammatory bowel disease or non-occlusive ischemia of the distal colorectum.
PubMed: 34082180
DOI: 10.1016/j.ijscr.2021.106022 -
Revista Espanola de Enfermedades... Aug 2021A 41-year-old female patient was under study for abdominal pain located in the epigastrium and mesogastrium with no other associated symptoms. There was no record of...
A 41-year-old female patient was under study for abdominal pain located in the epigastrium and mesogastrium with no other associated symptoms. There was no record of previous episodes of pancreatitis and she denied abdominal trauma and laboratory tests were normal. A computed tomography (CT) scan was performed.
Topics: Abdominal Pain; Adult; Aneurysm; Female; Humans; Mesenteric Veins; Portal Vein; Tomography, X-Ray Computed
PubMed: 33761751
DOI: 10.17235/reed.2021.7932/2021 -
The American Journal of Case Reports Apr 2021BACKGROUND Non-malignant and non-cirrhotic portal and mesenteric vein thrombosis is rare. It has been reported that the hyperthyroid state is associated with increased...
BACKGROUND Non-malignant and non-cirrhotic portal and mesenteric vein thrombosis is rare. It has been reported that the hyperthyroid state is associated with increased risks of venous thrombosis due to increases in levels of various coagulation and anti-fibrinolytic factors. Particularly, changes in levels of these factors are also reported in cases of portal and mesenteric vein thrombosis. Although hyperthyroidism is not known as a risk factor for portal and mesenteric vein thrombosis, it might be an underlying pathogenesis of hyperthyroidism-associated portal and mesenteric vein thrombosis. CASE REPORT A 59-year-old Japanese man with a history of Grave's disease presented with acute portal and mesenteric vein thrombosis and hyperthyroidism. Anticoagulation therapy was initiated and the dose of antithyroid drug was increased. He underwent various tests to identify causes of portal and mesenteric vein thrombosis. However, all test results were within normal range except for hyperthyroidism. Therefore, we discontinued anticoagulation therapy after normalization of thyroid hormone status. After 3 years, he experienced recurrence of portal vein thrombosis concomitant with hyperthyroidism. CONCLUSIONS Hyperthyroidism might be associated with portal vein thrombosis. Thyroid function tests should be performed in cases of portal and mesenteric vein thrombosis in the absence of other risk factors.
Topics: Humans; Hyperthyroidism; Male; Mesenteric Veins; Middle Aged; Portal Vein; Thrombolytic Therapy; Venous Thrombosis
PubMed: 33819210
DOI: 10.12659/AJCR.929565 -
HPB : the Official Journal of the... Apr 2021Contemporary practice for superior mesenteric/portal vein (SMV-PV) reconstruction during pancreatectomy with vein resection involves biological (autograft, allograft,... (Review)
Review
BACKGROUND
Contemporary practice for superior mesenteric/portal vein (SMV-PV) reconstruction during pancreatectomy with vein resection involves biological (autograft, allograft, xenograft) or synthetic grafts as a conduit or patch. The aim of this study was to systematically review the safety and feasibility of the different grafts used for SMV-PV reconstruction.
METHODS
A systematic search was performed in PubMed and Embase according to the PRISMA guidelines (January 2000-March 2020). Studies reporting on ≥ 5 patients undergoing reconstruction of the SMV-PV with grafts during pancreatectomy were included. Primary outcome was rate of graft thrombosis.
RESULTS
Thirty-four studies with 603 patients were included. Four graft types were identified (autologous vein, autologous parietal peritoneum/falciform ligament, allogeneic cadaveric vein/artery, synthetic grafts). Early and overall graft thrombosis rate was 7.5% and 22.2% for synthetic graft, 5.6% and 11.7% for autologous vein graft, 6.7% and 8.9% for autologous parietal peritoneum/falciform ligament, and 2.5% and 6.2% for allograft. Donor site complications were reported for harvesting of the femoral, saphenous, and external iliac vein. No cases of graft infection were reported for synthetic grafts.
CONCLUSION
In selected patients, autologous, allogenic or synthetic grafts for SMV-PV reconstruction are safe and feasible. Synthetic grafts seems to have a higher incidence of graft thrombosis.
Topics: Humans; Mesenteric Veins; Pancreatectomy; Pancreatic Neoplasms; Pancreaticoduodenectomy; Portal Vein; Treatment Outcome; Vascular Patency
PubMed: 33288403
DOI: 10.1016/j.hpb.2020.11.008 -
The Journal of Emergency Medicine May 2021Patients with coronavirus disease 2019 (COVID-19) commonly present with fever, constitutional symptoms, and respiratory symptoms. However, atypical presentations are...
BACKGROUND
Patients with coronavirus disease 2019 (COVID-19) commonly present with fever, constitutional symptoms, and respiratory symptoms. However, atypical presentations are also well known. Though isolated mesenteric arterial occlusion associated with COVID-19 has been reported in literature, combined superior mesenteric arterial and venous thrombosis is rare. We report a case of combined superior mesenteric arterial and venous occlusion associated with COVID-19 infection.
CASE REPORT
We report a case of a 45-year-old man who was a health care worker who presented to the emergency department with severe abdominal pain. The clinical examination was unremarkable, but imaging revealed acute mesenteric ischemia caused by superior mesenteric artery and superior mesenteric vein occlusion. Imaging of the chest was suggestive of COVID-19 infection, which was later confirmed with reverse transcription polymerase chain reaction of his nasopharyngeal swab. To date, only 1 case of combined superior mesenteric artery and superior mesenteric vein thrombosis caused by COVID-19 has been reported. WHY SHOULD AN EMERGENCY PHYSICIAN BE AWARE OF THIS?: During the COVID-19 pandemic it is important to keep mesenteric ischemia in the differential diagnosis of unexplained abdominal pain. Routinely adding high-resolution computed tomography of the chest to abdominal imaging should be considered in patients with acute abdomen because it can help to identify COVID-19 immediately. © 2020 Elsevier Inc.
Topics: Abdominal Pain; COVID-19; COVID-19 Nucleic Acid Testing; Female; Humans; Intestines; Laparotomy; Male; Mesenteric Arteries; Mesenteric Artery, Superior; Mesenteric Ischemia; Mesenteric Vascular Occlusion; Mesenteric Veins; Middle Aged; Nasopharynx; Pandemics; Radiography, Thoracic; Real-Time Polymerase Chain Reaction; Reverse Transcriptase Polymerase Chain Reaction; SARS-CoV-2; Thrombectomy; Thrombosis; Tomography, X-Ray Computed; Treatment Outcome; Venous Thrombosis
PubMed: 33581991
DOI: 10.1016/j.jemermed.2020.12.016 -
Hamostaseologie Apr 2024Splanchnic or visceral vein thromboses (VVTs) are atypical thrombotic entities and include thrombosis of the portal vein, hepatic veins (Budd-Chiari syndrome),... (Review)
Review
Splanchnic or visceral vein thromboses (VVTs) are atypical thrombotic entities and include thrombosis of the portal vein, hepatic veins (Budd-Chiari syndrome), mesenteric veins, and splenic vein. All VVTs have in common high 30-day mortality up to 20% and it seems to be difficult to diagnose VVT early because of their rarity and their wide spectrum of unspecific symptoms. VVTs are often associated with myeloproliferative neoplasia, thrombophilia, and liver cirrhosis. VVT is primarily diagnosed by sonography and/or computed tomography. In contrast to venous thromboembolism, D-dimer testing is neither established nor helpful. Anticoagulation is the first-line therapy in patients with stable circulation and no evidence of organ complications. Anticoagulation improves significantly recanalization rates and stops the progress of thrombosis. Low-molecular-weight heparin, vitamin K antagonists, as well as direct-acting oral anticoagulants are possible anticoagulants, but it is noteworthy to be aware that all recommendations supporting the off-label use of anticoagulants are based on poor evidence and consist predominantly of case series, observational studies, or studies with small case numbers. When choosing a suitable anticoagulation, the individual risk of bleeding and thrombosis must be weighted very carefully. In cases of bleeding, bowel infarction, or other complications, the optimal therapy should be determined on a case-by-case basis by an experienced multidisciplinary team involving a surgeon. Besides anticoagulation, there are therapeutic options including thrombectomy, balloon angioplasty, stenting, transjugular placement of an intrahepatic portosystemic shunt, liver transplantation, and ischemic bowel resection. This article gives an overview of current diagnostic and therapeutic strategies.
Topics: Humans; Anticoagulants; Venous Thrombosis; Practice Guidelines as Topic; Viscera; Budd-Chiari Syndrome; Portal Vein
PubMed: 37992729
DOI: 10.1055/a-2178-6670 -
Arteriosclerosis, Thrombosis, and... May 2022Pulmonary arterial hypertension (PAH) is a life-threatening disease characterized by the hyperproliferation of vascular cells, including smooth muscle and endothelial... (Review)
Review
Pulmonary arterial hypertension (PAH) is a life-threatening disease characterized by the hyperproliferation of vascular cells, including smooth muscle and endothelial cells. Hyperproliferative cells eventually obstruct the lung vasculature, leading to irreversible lesions that collectively drive pulmonary pressure to life-threatening levels. Although the primary cause of PAH is not fully understood, several studies have indicated it results from chronic pulmonary inflammation, such as observed in response to pathogens' infection. Curiously, infection by the intravascular parasite Schistosoma mansoni recapitulates several aspects of the widespread pulmonary inflammation that leads to development of chronic PAH. Globally, >200 million people are currently infected by ., with about 5% developing PAH (Sch-PAH) in response to the parasite egg-induced obliteration and remodeling of the lung vasculature. Before their settling into the lungs, Schistosoma eggs are released inside the mesenteric veins, where they either cross the intestinal wall and disturb the gut microbiome or migrate to other organs, including the lungs and liver, increasing pressure. Spontaneous or surgical liver bypass via collateral circulation alleviates the pressure in the portal system; however, it also allows the translocation of pathogens, toxins, and antigens into the lungs, ultimately causing PAH. This brief review provides an overview of the gut-mesentery-lung axis during PAH, with a particular focus on Sch-PAH, and attempts to delineate the mechanism by which pathogen translocation might contribute to the onset of chronic pulmonary vascular diseases.
Topics: Animals; Disease Models, Animal; Endothelial Cells; Familial Primary Pulmonary Hypertension; Humans; Lung; Mesentery; Pulmonary Arterial Hypertension; Pulmonary Artery; Vascular Remodeling
PubMed: 35296152
DOI: 10.1161/ATVBAHA.121.316236 -
Cells Jun 2019Portal hypertension is a common complication of liver disease, either acute or chronic. Consequently, in chronic liver disease, such as the hypertensive mesenteric... (Review)
Review
Portal hypertension is a common complication of liver disease, either acute or chronic. Consequently, in chronic liver disease, such as the hypertensive mesenteric venous pathology, the coexisting inflammatory response is classically characterized by the splanchnic blood circulation. However, a vascular lymphatic pathology is produced simultaneously with the splanchnic arterio-venous impairments. The pathological increase of the mesenteric venous pressure, by mechanotransduction of the venous endothelium hyperpressure, causes an inflammatory response involving the subendothelial mast cells and the lymphatic endothelium of the intestinal villi lacteal. In portal hypertension, the intestinal lymphatic inflammatory response through the development of mesenteric-systemic lymphatic collateral vessels favors the systemic diffusion of substances with a molecular pattern associated with damage and pathogens of intestinal origin. When the chronic hepatic insufficiency worsens the portal hypertensive inflammatory response, the splanchnic lymphatic system transports the hyperplasied intestinal mast cells to the mesenteric lymphatic complex. Then, an acquired immune response regulating a new hepato-intestinal metabolic scenario is activated. Therefore, reduction of the hepatic metabolism would reduce its key centralized functions, such as the metabolic, detoxifying and antioxidant functions which would try to be substituted by their peroxisome activity, among other functions of the mast cells.
Topics: Humans; Hypertension, Portal; Inflammation; Intestinal Mucosa; Lymphatic Vessels; Mast Cells; Mechanotransduction, Cellular; Mesenteric Veins; Mesentery; Splanchnic Circulation
PubMed: 31261968
DOI: 10.3390/cells8070658