Pulmonary embolism and hemorrhage after displacement of angiographic catheter tip to pulmonary artery: A case report and literature review.

Pulmonary embolism and massive hemoptysis caused by intravascular foreign bodies have rarely been reported. We report a case of an end-stage renal disease patient in which the tip of the angiographic catheter fell off into the pulmonary artery during endovascular interventional opening when the patient underwent vascular access occlusion for dialysis. During the operation, the foreign body was displaced repeatedly and finally anchored to the posterior basal segment branch of the right lower pulmonary artery. A pulmonary embolism occurred during the operation, and massive hemoptysis and hemorrhagic shock occurred after anticoagulation and thrombolytic therapy. After receiving anti-shock and symptomatic treatment, the patient gradually recovered. After six months of follow-up, no pulmonary embolism or pulmonary infarction occurred. Our case report presents an alternative approach to extracting a foreign object from the pulmonary artery by locating the foreign object within the vascular terminations, without resorting to forceful removal. This method mitigates the potential risks of pulmonary embolism and bleeding associated with forceful extraction.

Imaging misdiagnosis and clinical analysis of significant hepatic atrophy after bilioenteric anastomosis: A case report.

BACKGROUND: The occurrence of long-term bilioenteric anastomotic stenosis can readily induce liver atrophy and hyperplasia, thereby causing significant alterations in the anatomical and morphological aspects of the liver. This condition significantly hampers the accuracy of preoperative imaging diagnosis, while also exacerbating the complexity of surgical procedures and the likelihood of complications. CASE SUMMARY: A 60-year-old female patient was admitted to the hospital presenting with recurring epigastric pain accompanied by a high fever. The patient had a history of cholecystectomy, although the surgical records were not accessible. Based on preoperative imaging and laboratory examination, the initial diagnosis indicated the presence of intrahepatic calculi, abnormal right liver morphology, and acute cholangitis. However, during the surgical procedure, it was observed that both the left and right liver lobes exhibited evident atrophy and thinness. Additionally, there was a noticeable increase in the volume of the hepatic caudate lobe, and the original bilioenteric anastomosis was narrowed. The anastomosis underwent enlargement subsequent to hepatectomy. As a consequence of the presence of remaining stones in the caudate lobe, the second stage was effectively executed utilizing ultrasound-guided percutaneous transhepatic catheter drainage. Following the puncture, three days elapsed before the drain tip inadvertently perforated the liver, leading to the development of biliary panperitonitis, subsequently followed by pulmonary infection. The patient and her family strongly refused operation, and she died. CONCLUSION: The hepatic atrophy-hypertrophy complex induces notable alterations in the anatomical structure, thereby posing a substantial challenge in terms of imaging diagnosis and surgical procedures. Additionally, the long-term presence of hepatic fibrosis changes heightens the likelihood of complications arising from puncture procedures.

ERCP management of acute cholangitis caused by rupture of Echinococcus hepaticus into the biliary tract.

Background: Hepatic cystic echinococcosis (HCE) rupture into the biliary tract, one of the most common and refractory complications, is treated by laparotomy to remove hydatid lesions. The aim of this article was to investigate the role of endoscopic retrograde cholangiopancreatography (ERCP) in the treatment of this particular disease. Patients and Methods: This was is a retrospective analysis of 40 patients with HCE ruptured into the biliary tract in our hospital from September 2014 to October 2019. They were divided into two groups, ERCP group (group A, n = 14) and conventional surgery group (group B, n = 26). Group A was treated with ERCP first to control infection and improve the general condition before undergoing laparotomy at an optional stage while group B was treated with laparotomy directly. First, the infection parameters and liver, kidney and coagulation functions of group A patients before and after ERCP were compared to evaluate treatment effectiveness. Second, the intraoperative and post-operative parameters during the laparotomy of group A were compared with group B to evaluate the impact of ERCP treatment on laparotomy. Results and Conclusions: White blood cell, NE%, platelet, procalcitonin, C-reactive protein, interleukin-6, Total bilirubin (TBIL), alkaline phosphatase, gamma-glutamyl transpeptidase, aspartate transaminase, alanine transaminase (ALT), ALT and Cr in group A significantly improved by ERCP (P < 0.05); during laparotomy, the bleeding amount and hospital stay in group A were better (P < 0.05); moreover, concerning the post-operative complications, the incidence of acute renal failure and coagulation dysfunction in group A was significantly less (P < 0.05). ERCP, which not only quickly and effectively controls infection and improves the patient's systemic condition but also provides good support for subsequent radical surgery, enjoys good prospects for clinical application.

Wernicke's encephalopathy after acute pancreatitis with upper gastrointestinal obstruction: A case report and literature review.

A 42-year-old female was admitted with upper abdominal pain. Imaging studies and laboratory tests were performed to consider acute lipogenic pancreatitis. After symptomatic treatment, her abdominal pain was significantly relieved. However, the patient was accompanied by upper gastrointestinal obstruction, which was gradually relieved after long-term fasting, gastrointestinal decompression, and fluid rehydration. The patient developed dizziness and ataxia, which worsened. Cranial magnetic resonance imaging (MRI) indicated patchy abnormal signal shadows in the bilateral thalami and dorsal brainstem and suggested metabolic encephalopathy. Wernicke's encephalopathy (WE) was the initial diagnosis of suspicion, adequate vitamin B1 was immediately replenished until the complete resolution of symptoms, and the patient made a rapid and dramatic recovery.

Massive sympathetic nerve infiltration in advanced hepatic alveolar echinococcosis: a case report and review of the literature.

BACKGROUND: Alveolar echinococcosis is a zoonotic disease that mostly affects the liver, with vascular invasion and a protean clinical symptom. However, no reports of sympathetic nerve infiltration in hepatic alveolar echinococcosis have been reported. Here, we report a case of hepatic alveolar echinococcosis in a 33-year-old man. In this end-stage case, the lesion was heavily involved in the large vessels and biliary tract, and immunohistochemistry also incidentally revealed extensive nerve infiltration in the specimens after surgical treatment. Subsequently, neural classification was identified. CASE PRESENTATION: We herein report a case of advanced hepatic alveolar echinococcosis with macrovascular invasion and sympathetic nerve infiltration. In this case, inferior vena cava (IVC), the portal vein and bile duct were infiltrated. Ultimately, according to our experience, ex vivo liver resection and autotransplantation (ELRA) was the optimal treatment way to perform for this unresectable patient. Samples were collected from normal liver tissue, junction tissue and the lesion. Hematoxylin-eosin (HE) staining was used to confirm the diagnosis. Neural infiltration was observed by immunohistochemical staining with protein gene product 9.5 (PGP9.5). Fluorescence colocalization was determined with PGP9.5 and tyrosine hydroxylase (TH). These results suggest that a large amount of sympathetic nerve infiltration occurred at the junction. CONCLUSION: This study suggests that advanced hepatic alveolar echinococcosis shows infiltrating growth, often invades the large vessels and biliary ducts, and may be accompanied by sympathetic nerve infiltration.

A Novel Hepatectomy Model in Mice Using a Gutta Cutter Tool: A Feasibility Study and Preliminary Results.

BACKGROUND: A simple and reproducible model of hepatectomy provides an essential basis for the study of liver regeneration. However, current rodent models of hepatectomy involve lobectomy, which cannot simulate clinical liver resection with surgical margins. The main purpose of this study was to evaluate a novel murine modeling technique for hepatectomy using a gutta cutter. METHODS: Seventy-five C57BL/6 mice were randomly divided into 3 groups (n = 25 mice per group). Group 1 (control) underwent single ligature of the left lobe. Group 2 underwent left lobe local (5-mm diameter) hepatectomy by gutta cutter. Group 3 underwent partial left lobe resection (1.5 cm) by gutta cutter. Postoperative complications were analyzed. Serum aspartate transaminase, alanine aminotransferase, alkaline phosphatase, urea nitrogen, interleukin 6, and tumor necrosis factor-α were detected using an automatic biochemical analyzer. Hematoxylin-eosin and immunohistochemical staining was used to examine pathology, proliferating cell nuclear antigen, caspase-3, CD34, signal transducer and activator of transcription 3 (STAT-3), and phosphorylated STAT-3 (p-STAT-3). RESULTS: Major postoperative complications, hepatic enzymes, kidney function, interleukin 6, and tumor necrosis factor-α were similar among the groups (all P > .05). Histology showed little necrosis and a clear surgical boundary in groups 2 and 3. Groups 1 and 3 had higher positive cell levels (proliferating cell nuclear antigen, CD34, p-STAT-3) than group 2 (P < .05). There were no significant differences in caspase-3 and STAT-3 positive cells. CONCLUSIONS: Hepatectomy in mice using a gutta cutter to better mimic human liver resection shows potential as an alternative and safe animal model. This model may be useful in investigating methods of promoting liver regeneration.

Reconstruction of hepatic venous outflow and management of its complications using ex vivo liver resection and autotransplantation: a single-center experience.

BACKGROUND: This study was designed to investigate the techniques of hepatic venous outflow reconstruction and the management of its complications using ex vivo liver resection and autotransplantation (ELRA). METHODS: Being a retrospective case series covering 84 patients who underwent hepatic venous outflow reconstruction during ELRA from January 2016 to October 2020, 11 cases of postoperative hepatic venous outflow obstruction (HVOO), whose surgery details were described and survival rates analyzed. RESULTS: A total of the 84 alveolar Echinococcosis (AE) series was no intraoperative death. The 30-day mortality was 5.95% (5 /84). The most common postoperative complication was pleural effusion in 21 cases (25%). HVOO occurred in 11 cases, one of them died of liver failure, and the other 10 patients underwent interventional revascularization with good results. There was no significant difference in survival between patients with successful interventional revascularization due to HVOO and patients without HVOO (P > 0.05). CONCLUSIONS: Individualized and well design reconstruction of hepatic vein can be considered as a key procedure to reduce the complications of HVOO in ELRA. Once HVOO occurs, emergent management must be performed immediately before liver dysfunction. Interventional revascularization showed an effective approach, though the more clinical cases need to be evaluated.

Netrin-1 promotes liver regeneration possibly by facilitating vagal nerve repair after partial hepatectomy in mice.

Hepatic regeneration after hepatectomy is a great concern in clinical practice. Recently, the neuronal guidance protein netrin-1 has been reported to enhance regeneration after nerve injury. The goal of this study was to preliminarily investigate whether netrin-1 stimulates vagus nerve regeneration to promote liver regeneration after partial hepatectomy in mice. The expression of netrin-1 in murine remnant livers after partial hepatectomy (PHx) was evaluated in initial studies. C57BL/6 mice that received exogenous netrin-1 after PHx were used to examine liver regeneration. PHx was performed in wild-type mice after adeno-associated virus injection (Ntn1 gene silencing) to detect the impact of endogenous netrin-1. After PHx and hepatic branch vagotomy (HV), the mice were injected with or without netrin-1 to evaluate the effects on hepatic regeneration and vagal nerve recovery. Significant reductions in netrin-1 at the transcript and protein levels in murine liver tissue after hepatectomy were observed. Subsequent studies of netrin-1 administration revealed the promotion of hepatocyte proliferation and specific growth factors contributing to liver repair and a decrease in hepatic-specific injury enzymes. Furthermore, the opposite results were observed in the netrin-1 knockdown group. HV delayed liver regeneration after PHx. However, this retardation was reversed by exogenous netrin-1 supplementation. In addition, the results of nerve growth and vagal nerve repair in the remnant liver suggested that netrin-1 promoted vagal nerve regeneration after hepatectomy. Netrin-1 accelerates liver regeneration after partial hepatectomy in mice, and the potential mechanism is related to the promotion of vagus nerve repair and regeneration.

Insomnia Promotes Hepatic Steatosis in Rats Possibly by Mediating Sympathetic Overactivation.

Background: Insomnia is a widespread problem that can lead to the occurrence of other diseases and correlates closely with sympathetic nerve hyperactivation. Obesity-induced hepatic steatosis is mediated by sympathetic overactivation. However, it remains unclear whether insomnia may cause hepatic steatosis. The goal of this study was to preliminarily investigate whether insomnia caused hepatic steatosis in rats via sympathetic hyperactivation. Methods: A total of 32 Sprague-Dawley male rats were divided randomly into four groups: model, sympathetic denervation (Sd), estazolam, and control (eight rats/group). Model group received sustained sleep deprivation using the modified multiple platform method. In the Sd group, rats underwent sleep deprivation after receiving Sd by 6-hydroxydopamine (6-OHDA). Estazolam group: the rats concurrently received sleep deprivation and treatment with estazolam. The other eight rats housed in cages and kept in a comfortable environment were used as control. Blood samples were obtained for analysis of plasma lipids and hepatic function. Sympathetic hyperactivation-related indexes and hepatic steatosis in liver tissues were tested. Results: Liver enzymes, plasma lipid levels, and hepatic steatosis were elevated in insomnia rats, and sympathetic hyperactivation was found. Insomnia-induced hepatic steatosis was effectively lowered with pharmacological ablation of the hepatic sympathetic nerves. Furthermore, the treatment of insomnia with estazolam inhibited sympathetic activation and reduced hepatic steatosis. Conclusion: Sustained sleep deprivation-induced insomnia promotes hepatic steatosis in rats possibly by mediating sympathetic overactivation.

Single-Cell RNA Sequencing Reveals the Heterogeneity of Infiltrating Immune Cell Profiles in the Hepatic Cystic Echinococcosis Microenvironment.

Human cystic echinococcosis, caused by the larval stage of Echinococcus granulosus sensu lato, has been reported a near-cosmopolitan zoonotic disease. Various infiltrating immune cells gather around the lesion and produce a lesion microenvironment; however, cellular composition and heterogeneity in hepatic cystic echinococcosis lesion microenvironments are incompletely understood. Here, 81,865 immune cells isolated from peripheral blood, perilesion liver tissue, and adjacent normal liver tissue from four cystic echinococcosis patients were profiled using single-cell RNA sequencing. We identified 23 discrete cell populations and found distinct differences in infiltrating immune cells between tissue environments. Despite the significant similarity between perilesion and adjacent normal liver tissue-resident immune cells, the cellular proportions of type 2 innate lymphoid cells (ILC2s) and plasmacytoid dendritic cells (pDCs) were higher in perilesion liver tissue. Interestingly, the immunosuppressive gene NFKBIA was upregulated in these cells. Seven subsets of CD4+ T cell populations were found, and there were more regulatory-CD4+ T cells (Treg-CD4+) and Th2-CD4+ T cells in perilesion tissue than in adjacent normal tissue. There was close contact between CD4+ T cells and ILC2s and pDCs, which caused upregulation of genes related to positive immune activity in adjacent normal liver tissue. However, expression of genes related to immunosuppression, especially the immune inhibitory checkpoint gene NKG2A/HLA-E, was obviously higher in perilesion tissue, suggesting that cellular interaction resulted in an inhibitory microenvironment in the cystic echinococcosis (CE) lesion. This work offers new insights into the transcriptional heterogeneity of infiltrating immune cells in hepatic cystic echinococcosis lesion microenvironments at a single-cell level and provides potential target signatures for diagnosis and immunotherapies.

Contrast enhanced ultrasound in diagnosing liver lesion that spontaneously disappeared: A case report.

BACKGROUND: Focal liver lesions (FLLs) are abnormal masses that are distinguishable from the surrounding liver parenchyma, solid or cystic and may be benign or malignant. They are usually detected incidentally on abdominal examinations. The classification of FLLs is very important as it directly determines the diagnosis and treatment of patients. CASE SUMMARY: A 46-year-old male patient was admitted into the hospital with tarry stool, during the investigation of this issue an incidental FLL was detected. Upon further investigation of this "incidentaloma" computerized tomography and magnetic resonance imaging reached contradictory conclusions. The lesion was then further investigated using contrast-enhanced ultrasound (CEUS) with an initial diagnosis of idiopathic FLL was acquired and observation of the FLL over time need for final diagnosis, however in the follow up the FLL disappeared spontaneously. CONCLUSION: CEUSs value for characterization of FLLs is undeniable, especially when other methods produce inconsistent results, is undeniable but with its limitations. Why and how the FLL disappeared is not known, and can be only hypothesized it was a pseudolesion.

Identification of infiltrating immune cell subsets and heterogeneous macrophages in the lesion microenvironment of hepatic cystic echinococcosis patients with different cyst viability.

Human cystic echinococcosis (CE) is characterized by lesion microenvironment formation through gathering various immune cells, including macrophages. However, immune cell subsets and heterogeneous macrophages in CE lesion microenvironment are poorly defined. Massive infiltrating immune cells formed lesion microenvironment, among which CD4+T cells and CD19+B cells were predominant and CD68+ macrophages were more evident in patients with active cysts. Different degrees of liver fibrosis was observed in Peri-Lesion (PL) liver samples, which was more evident in patients with active cysts. Expression of both M1 and M2 macrophage markers was significantly increased in PL liver samples. Importantly, elevation of M1 macrophage markers was more obvious in patients with inactive cysts, whereas M2 macrophage markers represented dominant macrophage phenotype in patients with active cysts. Additionally, macrophage-derived MIF, TGF-ß1 and ECM1 were also expressed at higher level in CE lesion microenvironment of patients with active cysts. Moreover, MIF was evidently enhanced in the serum of hepatic CE patients, which was also predominant in patients with active cysts. Correlation analysis demonstrated positive correlation between expression of macrophage-derived cytokines and liver fibrosis degree. Heterogeneous macrophages may play significant roles in liver fibrosis of CE lesion microenvironment through producing pro-fibrogenic cytokines.

Dihydroartemisinin/miR-29b combination therapy increases the pro-apoptotic effect of dihydroartemisinin on cholangiocarcinoma cell lines by regulating Mcl-1 expression.

BACKGROUND: Cholangiocarcinoma is a malignant tumor that originates from the neoplastic transformation of bile duct epithelial cells. OBJECTIVES: To investigate the role of DHA and miR-29b on the proliferation and apoptosis of cholangiocarcinoma cells, and to explore whether DHA exerted its role through the miR-29b/Mcl-1 signaling pathway. MATERIAL AND METHODS: Human cholangiocarcinoma cell lines HUCCT-1 and FRH0201 were treated with dihydroartemisinin (DHA) and DHA+miR-29b. The inhibitory effects of DHA and miR-29b on proliferation were detected using MTT assay. The effects of DHA and miR-29b on apoptosis were detected using flow cytometry (FCM). The mRNA and protein expressions of Mcl-1L and Mcl-1S were evaluated with reverse transcriptase polymerase chain reaction (RT-PCR) and western blotting, respectively. RESULTS: The DHA increased miR-29b expression in HUCCT-1 and FRH201 cells. The MTT assay showed that DHA+miR-29b combination therapy promoted the inhibition effects on the proliferation of HUCCT-1 and FRH201 cells. The FCM results revealed that DHA and miR-29b combination therapy increased the apoptosis of HUCCT-1 and FRH201 cells. The RT-PCR and western blotting analysis found that DHA+miR-29b combination therapy significantly decreased Mcl-1L expression and increased Mcl-1S expression in both HUCCT-1 and FRH201 cells. The Mcl-1S:Mcl-1L ratio was notably higher in the DHA+miR-29b combination therapy group than in the control group and DHA therapy group, in both HUCCT-1 and FRH201 cells. CONCLUSIONS: The DHA and miR-29b have a pro-apoptotic effect on cholangiocarcinoma cells through the DHA/miR-29b/Mcl-1 pathway, possibly by upregulating the expression of the pro-apoptotic protein Mcl-1S and thus increasing the proportion of Mcl-1S protein among the total amount of Mcl-1 protein.