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BMC Surgery May 2023Postoperative pancreatic fistula (POPF) is the most serious complication and the main reason for morbidity and mortality after pancreaticoduodenectomy (PD). Currently,...
BACKGROUND
Postoperative pancreatic fistula (POPF) is the most serious complication and the main reason for morbidity and mortality after pancreaticoduodenectomy (PD). Currently, there exists no flawless pancreaticojejunal anastomosis approach. We presents a new approach called Chen's penetrating-suture technique for pancreaticojejunostomy (PPJ), which involves end-to-side pancreaticojejunostomy by suture penetrating the full-thickness of the pancreas and jejunum, and evaluates its safety and efficacy.
METHODS
To assess this new approach, between May 2006 and July 2018, 193 consecutive patients who accepted the new Chen's Penetrating-Suture technique after a PD were enrolled in this study. Postoperative morbidity and mortality were evaluated.
RESULTS
All cases recovered well after PD. The median operative time was 256 (range 208-352) min, with a median time of 12 (range 8-25) min for performing pancreaticojejunostomy. Postoperative morbidity was 19.7% (38/193) and mortality was zero. The POPF rate was 4.7% (9/193) for Grade A, 1.0% (2/193) for Grade B, and no Grade C cases and one urinary tract infection.
CONCLUSION
PPJ is a simple, safe, and reliable technique with ideal postoperative clinical results.
Topics: Humans; Pancreaticojejunostomy; Pancreaticoduodenectomy; Anastomosis, Surgical; Pancreas; Pancreatic Fistula; Postoperative Complications; Suture Techniques
PubMed: 37248522
DOI: 10.1186/s12893-023-02054-y -
Langenbeck's Archives of Surgery Dec 2022Parenchymal-sparing pancreatectomy (PSP) or pancreas-sparing duodenectomy (PSD) is an alternative method for patients with benign or low-grade malignant tumours at the...
BACKGROUND
Parenchymal-sparing pancreatectomy (PSP) or pancreas-sparing duodenectomy (PSD) is an alternative method for patients with benign or low-grade malignant tumours at the pancreatic head or duodenum. It avoids traumatic pancreaticoduodenectomy (PD) with pancreatic function preservation and improves quality of life. However, few studies have reported on robotic PSP (RPSP) or robotic PSD (RPSD).
METHODS
A retrospective analysis of 17 patients with benign and low-grade malignant pancreatic head and duodenal tumours who underwent RPSP or RPSD from January 2018 to February 2022 was conducted. The demographic, perioperative, and postoperative data of all patients were collected and analysed.
RESULTS
The operations were successful for all seventeen patients without conversion, including 10 cases of RPSP and 7 cases of RPSD. For RPSP, eight patients underwent pancreatic enucleation, and two patients underwent uncinate process resection. For RPSD, five patients underwent local duodenectomy, and two patients underwent segmental duodenectomy, with five simultaneous jejunostomies and two distal gastrectomies. The median OT and EBL were 135 min and 50 mL for RPSP and 220 min and 100 mL for RPSD, respectively. The median LOS was 8 days for RPSP and 19 days for RPSD. The main postoperative complications for RPSP included POPF (grade B, 6 cases), DGE (grade B, 1 case), PPH (1 case), and intra-abdominal infection (1 case). The main postoperative complications for RPSD included DGE (grade B, 1 case, grade C, 3 cases), postoperative haemorrhage (1 case), intra-abdominal infection (1 case), and duodenal fistula (1 case). One patient underwent interventional drain placement after RPSP because of POPF.
CONCLUSION
RPSP or RPSD is feasible for highly selected patients with benign and low-grade malignant pancreatic head and duodenal tumours, avoiding potential pancreaticoduodenectomy.
Topics: Humans; Pancreaticoduodenectomy; Pancreatectomy; Duodenal Neoplasms; Retrospective Studies; Robotic Surgical Procedures; Quality of Life; Pancreas; Postoperative Complications; Intraabdominal Infections; Pancreatic Neoplasms
PubMed: 35980486
DOI: 10.1007/s00423-022-02633-2 -
Gastroenterology Clinics of North... Mar 2023Coronavirus disease 2019 (COVID-19) pulmonary involvement has been extensively reported in the literature. Current data highlight how COVID-19 is a systemic disease,... (Review)
Review
Coronavirus disease 2019 (COVID-19) pulmonary involvement has been extensively reported in the literature. Current data highlight how COVID-19 is a systemic disease, affecting many other organs, including the gastrointestinal, hepatobiliary, and pancreatic organs. Recently, these organs have been investigated using imaging modalities of ultrasound and particularly computed tomography. Radiological findings of the gastrointestinal, hepatic, and pancreatic involvement in patients with COVID-19 are generally nonspecific but are nonetheless helpful to evaluate and manage COVID-19 patients with involvement of these organs.
Topics: Humans; COVID-19; SARS-CoV-2; Radiation Oncology; Gastrointestinal Tract; Liver; Pancreas; COVID-19 Testing
PubMed: 36813425
DOI: 10.1016/j.gtc.2022.10.006 -
Science Advances Mar 2024Coxsackievirus B (CVB) infection of pancreatic β cells is associated with β cell autoimmunity and type 1 diabetes. We investigated how CVB affects human β cells and...
Coxsackievirus B (CVB) infection of pancreatic β cells is associated with β cell autoimmunity and type 1 diabetes. We investigated how CVB affects human β cells and anti-CVB T cell responses. β cells were efficiently infected by CVB in vitro, down-regulated human leukocyte antigen (HLA) class I, and presented few, selected HLA-bound viral peptides. Circulating CD8 T cells from CVB-seropositive individuals recognized a fraction of these peptides; only another subfraction was targeted by effector/memory T cells that expressed exhaustion marker PD-1. T cells recognizing a CVB epitope cross-reacted with β cell antigen GAD. Infected β cells, which formed filopodia to propagate infection, were more efficiently killed by CVB than by CVB-reactive T cells. Our in vitro and ex vivo data highlight limited CD8 T cell responses to CVB, supporting the rationale for CVB vaccination trials for type 1 diabetes prevention. CD8 T cells recognizing structural and nonstructural CVB epitopes provide biomarkers to differentially follow response to infection and vaccination.
Topics: Humans; CD8-Positive T-Lymphocytes; Diabetes Mellitus, Type 1; Insulin-Secreting Cells; Antibodies; Coxsackievirus Infections; Epitopes; Peptides; Antiviral Agents
PubMed: 38446892
DOI: 10.1126/sciadv.adl1122 -
World Journal of Gastroenterology May 2022The coronavirus disease 2019 (COVID-19) is known to cause gastrointestinal symptoms. Recent studies have revealed COVID-19-attributed acute pancreatitis (AP). However,... (Review)
Review
The coronavirus disease 2019 (COVID-19) is known to cause gastrointestinal symptoms. Recent studies have revealed COVID-19-attributed acute pancreatitis (AP). However, clinical characteristics of COVID-19-attributed AP remain unclear. We performed a narrative review to elucidate relation between COVID-19 and AP using the PubMed database. Some basic and pathological reports revealed expression of angiotensin-converting enzyme 2 and transmembrane protease serine 2, key proteins that aid in the entry of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) into the pancreas. The experimental and pathological evaluation suggested that SARS-CoV-2 infects human endocrine and exocrine pancreas cells, and thus, SARS-CoV-2 may have a direct involvement in pancreatic disorders. Additionally, systemic inflammation, especially in children, may cause AP. Levels of immune mediators associated with AP, including interleukin (IL)-1β, IL-10, interferon-γ, monocyte chemotactic protein 1, and tumor necrosis factor-α are higher in the plasma of patients with COVID-19, that suggests an indirect involvement of the pancreas. In real-world settings, some clinical features of AP complicate COVID-19, such as a high complication rate of pancreatic necrosis, severe AP, and high mortality. However, clinical features of COVID-19-attributed AP remain uncertain due to insufficient research on etiologies of AP. Therefore, high-quality clinical studies and case reports that specify methods for differential diagnoses of other etiologies of AP are needed.
Topics: Acute Disease; COVID-19; Child; Humans; Pancreas; Pancreatitis; SARS-CoV-2
PubMed: 35664035
DOI: 10.3748/wjg.v28.i19.2034 -
Cell Reports Mar 2022Concerns that infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the etiological agent of coronavirus disease 2019 (COVID-19), may cause...
Concerns that infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the etiological agent of coronavirus disease 2019 (COVID-19), may cause new-onset diabetes persist in an evolving research landscape, and precise risk assessment is hampered by, at times, conflicting evidence. Here, leveraging comprehensive single-cell analyses of in vitro SARS-CoV-2-infected human pancreatic islets, we demonstrate that productive infection is strictly dependent on the SARS-CoV-2 entry receptor ACE2 and targets practically all pancreatic cell types. Importantly, the infection remains highly circumscribed and largely non-cytopathic and, despite a high viral burden in infected subsets, promotes only modest cellular perturbations and inflammatory responses. Similar experimental outcomes are also observed after islet infection with endemic coronaviruses. Thus, the limits of pancreatic SARS-CoV-2 infection, even under in vitro conditions of enhanced virus exposure, challenge the proposition that in vivo targeting of β cells by SARS-CoV-2 precipitates new-onset diabetes. Whether restricted pancreatic damage and immunological alterations accrued by COVID-19 increase cumulative diabetes risk, however, remains to be evaluated.
Topics: COVID-19; Diabetes Mellitus; Humans; Insulin-Secreting Cells; Pancreas; SARS-CoV-2
PubMed: 35247306
DOI: 10.1016/j.celrep.2022.110508 -
Frontiers in Immunology 2022Neutrophil extracellular traps (NETs) are produced in large quantities at the site of inflammation, and they locally capture and eliminate various pathogens. Thus, NETs... (Review)
Review
Neutrophil extracellular traps (NETs) are produced in large quantities at the site of inflammation, and they locally capture and eliminate various pathogens. Thus, NETs quickly control the infection of pathogens in the body and play vital roles in immunity and antibacterial effects. However, evidence is accumulating that NET formation can exacerbate pancreatic tissue damage during acute pancreatitis (AP). In this review, we describe the research progress on NETs in AP and discuss the possibility of NETs as potential therapeutic targets. In addition, since the current detection and visualization methods of NET formation are not uniform and the selection of markers is still controversial, a synopsis of these issues is provided in this review.
Topics: Acute Disease; Extracellular Traps; Humans; Neutrophils; Pancreas; Pancreatitis
PubMed: 36032164
DOI: 10.3389/fimmu.2022.974821 -
Khirurgiia 2022Ascaris lumbricoides is nematode localized in human small bowel in most cases. This nematode is capable for migration. Pancreatitis is one of the most common surgical...
Ascaris lumbricoides is nematode localized in human small bowel in most cases. This nematode is capable for migration. Pancreatitis is one of the most common surgical diseases. One of the causes of this pancreatitis may be migration of Ascaris lumbricoides from small bowel through the major duodenal papilla to the pancreatic ducts. This migration is provided by complex of morphological and functional disorders of digestive system associated with this helminthiasis, as well as certain risk factors. These are previous cholecystectomy, sphincterotomy, living in endemic areas, massive Ascaris lumbricoides invasion, pregnancy. Damage of the pancreas develops due to direct mechanical effect of nematodes and allergic reactions, papillitis and functional disorders of digestive tract. Pancreatitis is usually mild, but severe course of disease is also possible. A typical symptom of pancreatitis caused by Ascaris lumbricoides is helminths in vomit and/or feces.
Topics: Animals; Ascariasis; Ascaris lumbricoides; Female; Humans; Pancreas; Pancreatic Neoplasms; Pancreatitis; Pregnancy
PubMed: 35775847
DOI: 10.17116/hirurgia202207171 -
Frontiers in Cellular and Infection... 2020Pancreatic cancer is considered a lethal disease with a low survival rate due to its late-stage diagnosis, few opportunities for resection and lack of effective... (Review)
Review
Pancreatic cancer is considered a lethal disease with a low survival rate due to its late-stage diagnosis, few opportunities for resection and lack of effective therapeutic strategies. Multiple, highly complex effects of gut microbiota on pancreatic cancer have been recognized as potential strategies for targeting tumorigenesis, development and treatment in recent decades; some of the treatments include antibiotics, probiotics, and fecal microbiota transplantation. Several bacterial species are associated with carcinogenesis of the pancreas, while some bacterial metabolites contribute to tumor-associated low-grade inflammation and immune responses via several proinflammatory factors and signaling pathways. Given the limited evidence on the interplay between gut microbiota and pancreatic cancer, risk factors associated with pancreatic cancer, such as diabetes, chronic pancreatitis and obesity, should also be taken into consideration. In terms of treatment of pancreatic cancer, gut microbiota has exhibited multiple effects on both traditional chemotherapy and the recently successful immunotherapy. Therefore, in this review, we summarize the latest developments and advancements in gut microbiota in relation to pancreatic cancer to elucidate its potential value.
Topics: Fecal Microbiota Transplantation; Gastrointestinal Microbiome; Humans; Pancreas; Pancreatic Neoplasms; Probiotics
PubMed: 33117731
DOI: 10.3389/fcimb.2020.572492 -
The Journal of Hospital Infection Oct 2022Among hospital-acquired infections, surgical site infections (SSIs) are frequent. SSI in the early post-transplant course poses a relevant threat to transplant...
BACKGROUND
Among hospital-acquired infections, surgical site infections (SSIs) are frequent. SSI in the early post-transplant course poses a relevant threat to transplant recipients.
AIM
To determine incidence, risk factors for SSI and its association with post-transplant outcomes and pancreas transplant (P-Tx) recipients.
METHODS
Adult simultaneous kidney-pancreas transplantation (SPK-T) and P-Tx recipients with a follow-up of at least 90 days were identified in the Swiss Transplant Cohort Study (STCS) dataset. Except for the categorization of SSIs according to Centers for Disease Control and Prevention (CDC) criteria, all other data were prospectively collected. Risk factors for SSI were investigated with logistic regression. A Weibull accelerated failure-time model was applied to address the impact of SSI on length of stay, correcting for transplant-related complications and delayed graft function.
FINDINGS
Of 130 transplant recipients, 108 SPK-Tx and 22 P-Tx, 18 (14%) individuals developed SSI within the first 90 days after transplantation. Deep incisional (seven, 38.9%) and organ/space infections (eight, 44.4%) predominated. In the majority of SSIs (11, 61.1%; two SSIs with simultaneous identification of fungal pathogens) bacteria were detected with Enterococcus spp. being most frequent. The median duration of hospitalization after transplantation was significantly longer in recipients with SSI (median: 26 days; interquartile range (IQR): 19-44) than in patients without SSI (median: 17 days; IQR: 12-25; P = 0.002). In multivariate analysis, SSI was significantly associated with increased length of stay and prolonged the duration of hospitalization by 36% (95% confidence interval: 4-79).
CONCLUSION
SSI after SPK-Tx and P-Tx occurred at a frequency of 14%. Among pathogens, Enterococcus spp. predominated. SSI was independently associated with a longer hospitalization after transplantation.
Topics: Adult; Cohort Studies; Humans; Kidney; Kidney Transplantation; Pancreas; Pancreas Transplantation; Risk Factors; Surgical Wound Infection; Switzerland
PubMed: 35840001
DOI: 10.1016/j.jhin.2022.07.009