Evaluation of Preoperative Magnetic Resonance Cholangiopancreatography in Acute Cholecystitis to Predict Technical Difficulties in Laparoscopic Cholecystectomy

Magnetic resonance cholangiopancreatography (MRCP) is a non-invasive imaging technique that provides high-quality visualization of the biliary tree, including the gallbladder. This study aimed to evaluate the useful-ness of preoperative MRCP for acute cholecystitis in predicting technical difficulties during laparoscopic chole-cystectomy (LC). A total of 168 patients who underwent LC with preoperative MRCP were enrolled in this study. Patients were divided into two groups according to preoperative MRCP findings: the visualized group (n = 126), in which the entire gallbladder could be visualized; and the non-visualized group (n = 42), in which the entire gallbladder could not be visualized. The perioperative characteristics and postoperative complica-tions of the two groups were retrospectively analyzed. Operation time was longer in the non-visualized group (median 101.5 vs. 143.5 min; p < 0.001). The non-visualized group had significantly more intraoperative blood loss than the visualized group (median 5 vs. 10 g; p = 0.05). The rate of conversion to open cholecystectomy was significantly higher in the non-visualized group (1.6 vs. 9.5%; p = 0.03). In conclusion, patients in the non- visualized group showed higher difficulty in performance of LC. Our MRCP-based classification is a simple and effective means of predicting difficulties in performing LC for acute cholecystitis

Synergistic effect of interleukin 1 alpha on nontypeable Haemophilus influenzae-induced up-regulation of human beta-defensin 2 in middle ear epithelial cells

BACKGROUND: We recently showed that beta-defensins have antimicrobial activity against nontypeable Haemophilus influenzae (NTHi) and that interleukin 1 alpha (IL-1 alpha) up-regulates the transcription of beta-defensin 2 (DEFB4 according to new nomenclature of the Human Genome Organization) in human middle ear epithelial cells via a Src-dependent Raf-MEK1/2-ERK signaling pathway. Based on these observations, we investigated if human middle ear epithelial cells could release IL-1 alpha upon exposure to a lysate of NTHi and if this cytokine could have a synergistic effect on beta-defensin 2 up-regulation by the bacterial components. METHODS: The studies described herein were carried out using epithelial cell lines as well as a murine model of acute otitis media (OM). Human cytokine macroarray analysis was performed to detect the released cytokines in response to NTHi exposure. Real time quantitative PCR was done to compare the induction of IL-1 alpha or beta-defensin 2 mRNAs and to identify the signaling pathways involved. Direct activation of the beta-defensin 2 promoter was monitored using a beta-defensin 2 promoter-Luciferase construct. An IL-1 alpha blocking antibody was used to demonstrate the direct involvement of this cytokine on DEFB4 induction. RESULTS: Middle ear epithelial cells released IL-1 alpha when stimulated by NTHi components and this cytokine acted in an autocrine/paracrine synergistic manner with NTHi to up-regulate beta-defensin 2. This synergistic effect of IL-1 alpha on NTHi-induced beta-defensin 2 up-regulation appeared to be mediated by the p38 MAP kinase pathway. CONCLUSION: We demonstrate that IL-1 alpha is secreted by middle ear epithelial cells upon exposure to NTHi components and that it can synergistically act with certain of these molecules to up-regulate beta-defensin 2 via the p38 MAP kinase pathway

Fluid collection and pancreatic fistula after pancreaticoduodenectomy

Background: Although postoperative abdominal fluid collection (POFC) is an important predictive factor for clinically relevant postoperative pancreatic fistula (CR-POPF), many patients are asymptomatic and resolve spontaneously. Triple-drug therapy consisting of gabexate mesylate, octreotide, and carbapenem antibiotics has been used at our institution to prevent pancreatic fistula after pancreatectomy. The present study aimed to evaluate the management and outcomes of patients with POFC and to determine the efficacy of triple-drug therapy to prevent CR-POPF after pancreaticoduodenectomy (PD).Methods: From 2016 to 2021, 125 patients who underwent PD were retrospectively analyzed to determine their postoperative fluid collection status. Triple-drug therapy was administered to patients who showed high amylase levels in their drainage (> 10,000 IU/L) on POD 1, 3, or 5, and who had any clinical symptoms associated with POFC.Results: The overall rate of POFC was 26% (n=33). Among these patients, CR-POPF developed in 16 patients (48%). There was no CR-POPF patient in the NO-POFC patient group. Triple-drug therapy was performed for 30 patients according to a preexisting treatment algorithm. Among these 30 patients, there were 23 POFC and 7 No-POFC patients. Twelve (52%) of the POFC patients developed CR-POPF despite treatment with triple-drug therapy. There were no CR-POPF patients in the NoPOFC patient group.Conclusions: Although POFC after PD is an important finding for CR-POPF, it does not necessarily develop into CR-POPF. The administration of triple-drug therapy is effective for the prevention of CR-POPF in cases without POFC fluid drainage aswell as in those with POFC

Synchronous Total Occlusion of the Celiac Axis and Superior Mesenteric Artery: An Autopsy Case

Acute mesenteric ischemia (AMI) is often caused by superior mesenteric artery (SMA) embolization. We report a rare case of synchronous celiac axis and SMA embolization in an elderly woman with initially mild abdominal pain. Ultimately, a second contrast-enhanced computed tomography revealed extensive necrosis from the stomach to the transverse colon together with liver ischemia due to hours of occlusion. Multiorgan failure made palliation the only option, and she died the following evening. Autopsy revealed a fragile atherosclerosis-asso-ciated thrombus. Careful examination and repeat diagnostic tests should be performed in patients with mild abdominal symptoms at risk for AMI

Results of elective laparoscopic cholecystectomy for acute cholecystitis following percutaneous transhepatic gallbladder drainage

The Tokyo Guidelines 2013 (TG13) provides a simple criteria and management strategy for acute cholecystitis. The optimal interval between performing percutaneous transhepatic gallbladder drainage (PTGBD) and delayed elective laparoscopic cholecystectomey (LC) and the suitable period of PTGBD, is controversial. In this study, we evaluate the operative outcome of elective LC with PTGBD for the management of acute cholecystitis. We analyzed 21 patients who underwent elective LC following PTGBD. The diagnosis and severity grading for acute cholecystitis was based on TG13. All patients showed grade II/III acute cholecystitis by TG13. Median time interval from onset of acute cholecystitis to PTGBD was 1.5 days (range 0-6). In all patients, local inflammation of gallbladder was improved by PTGBD. Median time interval from PTGBD to elective LC was 46 days (range 12-74). Only one patient (5%) showed bile leakage, and median postoperative hospital stay was 5 days (range 4-15). In conclusion, delayed elective LC following emergent PTGBD is a safe and effective treatment strategy for patients withcomplicated acute cholecystitis

Results of laparoscopic subtotal cholecystectomy by laparoscopic linear stapler in difficult cases with severe cholecystitis

Laparoscopic subtotal cholecystectomy (LSC) has been recognized as a safe and feasible alternative surgical procedure for a difficult laparoscopic cholecystectomy (LC) with severe inflammation in Calot’s triangle. We compared the surgical outcomesof cholecystectomy for acute cholecystitis between standard LC and LSC using laparoscopic linear stapler. 172 patients were diagnosed as acute cholecystitis, among them, 16 patients who underwent LSC and other 156 patients who underwent standardLC were enrolled in this study. The severity grading of acute cholecystitis in LSC group was significantly higher than LC group. Operation time was longer in the LSC group than LC group. LSC had significantly more intraoperative blood loss compared to LC. However, there was no significant difference in the postoperative complications between two groups. LSC using laparoscopic linear stapler contributes surgeons avoid common bile duct injury in difficult LC

A case of surgical resection for well-differentiated squamous cell carcinoma arising in a ciliated hepatic foregut cyst

Ciliated hepatic foregut cysts (CHFC) are extremely rare, and most are benign cysts of the liver arising from remnants of the embryonic foregut. CHFC is usually found incidentally and as mostly asymptomatic cysts. We report squamous cell carcinoma (SCC) arising in a CHFC in a 50-year-old Japanese woman. She consulted our hospital for upper abdominal pain.A computed tomography and an ultrasound showed a cystic region including calcification and a solid mass in segment 4 of the liver. Left hepatectomy, B6 bile duct resection, and biliary-jejunal anastomosis were performed. Microscopic examination revealed that part of the cyst was lined by a characteristic ciliated pseudostratified columnar epithelium surrounding a connective tissue, a slightly thick fibrotic smooth muscle stromal layer, and an outer fibrous capsule. The cyst wall contained a low-papillary mural nodule showing atypical squamous hyperplasia with high-grade dysplasia. Stromal invasion was identified at the base of the nodule, leading to the diagnosis of well-differentiated SCC arising from a CHFC. We recommend careful clinical follow-up for patients with relatively large CHFCs as potentially malignant lesions and excision if they show any clinical manifestation

Lysozyme M deficiency leads to an increased susceptibility to Streptococcus pneumoniae-induced otitis media

<p>Abstract</p> <p>Background</p> <p>Lysozyme is an antimicrobial innate immune molecule degrading peptidoglycan of the bacterial cell wall. Lysozyme shows the ubiquitous expression in wide varieties of species and tissues including the tubotympanum of mammals. We aim to investigate the effects of lysozyme depletion on pneumococcal clearance from the middle ear cavity.</p> <p>Methods</p> <p>Immunohistochemistry was performed to localize lysozyme in the Eustachian tube. Lysozyme expression was compared between the wild type and the lysozyme M^-/-mice using real time quantitative RT-PCR and western blotting. Muramidase activity and bactericidal activity of lysozyme was measured using a lysoplate radial diffusion assay and a liquid broth assay, respectively. To determine if depletion of lysozyme M increases a susceptibility to pneumococal otitis media, 50 CFU of <it>S. pneumoniae </it>6B were transtympanically inoculated to the middle ear and viable bacteria were counted at day 3 and 7 with clinical grading of middle ear inflammation.</p> <p>Results</p> <p>Immunolabeling revealed that localization of lysozyme M and lysozyme P is specific to some/particular cell types of the Eustachian tube. Lysozyme P of lysozyme M^-/-mice was mainly expressed in the submucosal gland but not in the tubal epithelium. Although lysozyme M^-/-mice showed compensatory up-regulation of lysozyme P, lysozyme M depletion resulted in a decrease in both muramidase and antimicrobial activities. Deficiency in lysozyme M led to an increased susceptibility to middle ear infection with <it>S. pneumoniae </it>6B and resulted in severe middle ear inflammation, compared to wild type mice.</p> <p>Conclusion</p> <p>The results suggest that lysozyme M plays an important role in protecting the middle ear from invading pathogens, particularly in the early phase. We suggest a possibility of the exogenous lysozyme as an adjuvant therapeutic agent for otitis media, but further studies are necessary.</p

Induction of beta defensin 2 by NTHi requires TLR2 mediated MyD88 and IRAK-TRAF6-p38MAPK signaling pathway in human middle ear epithelial cells

<p>Abstract</p> <p>Background</p> <p>All mucosal epithelia, including those of the tubotympanium, are secreting a variety of antimicrobial innate immune molecules (AIIMs). In our previous study, we showed the bactericidal/bacteriostatic functions of AIIMs against various otitis media pathogens. Among the AIIMs, human β-defensin 2 is the most potent molecule and is inducible by exposure to inflammatory stimuli such as bacterial components or proinflammatory cytokines. Even though the β-defensin 2 is an important AIIM, the induction mechanism of this molecule has not been clearly established. We believe that this report is the first attempt to elucidate NTHi induced β-defensin expression in airway mucosa, which includes the middle ear.</p> <p>Methods</p> <p>Monoclonal antibody blocking method was employed in monitoring the TLR-dependent NTHi response. Two gene knock down methods – dominant negative (DN) plasmid and small interfering RNA (siRNA) – were employed to detect and confirm the involvement of several key genes in the signaling cascade resulting from the NTHi stimulated β-defensin 2 expression in human middle ear epithelial cell (HMEEC-1). The student's <it>t</it>-test was used for the statistical analysis of the data.</p> <p>Results</p> <p>The experimental results showed that the major NTHi-specific receptor in HMEEC-1 is the Toll-like receptor 2 (TLR2). Furthermore, recognition of NTHi component(s)/ligand(s) by TLR2, activated the Toll/IL-1 receptor (TIR)-MyD88-IRAK1-TRAF6-MKK3/6-p38 MAPK signal transduction pathway, ultimately leading to the induction of β-defensin 2.</p> <p>Conclusion</p> <p>This study found that the induction of β-defensin 2 is highest in whole cell lysate (WCL) preparations of NTHi, suggesting that the ligand(s) responsible for this up-regulation may be soluble macromolecule(s). We also found that this induction takes place through the TLR2 dependent MyD88-IRAK1-TRAF6-p38 MAPK pathway, with the primary response occurring within the first hour of stimulation. In combination with our previous studies showing that IL-1α-induced β-defensin 2 expression takes place through a MyD88-independent Raf-MEK1/2-ERK MAPK pathway, we found that both signaling cascades act synergistically to up-regulate β-defensin 2 levels. We propose that this confers an essential evolutionary advantage to the cells in coping with infections and may serve to amplify the innate immune response through paracrine signaling.</p