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Liver disease is one of the most important health problems around the world, and early diagnosis and timely intervention and treatment are the key to preventing liver-related morbidity and mortality rates. The development of endoscopic techniques has provided new diagnostic and intervention methods for liver diseases. This article reviews the application and development of endoscopic techniques in liver diseases from the following aspects: the technical advances and advantages of endoscopic ultrasound-guided liver biopsy; the application and development of endoscopic techniques in the treatment of portal hypertension caused by liver abscess/hepatic cyst and liver diseases, as well as interventional techniques in the treatment of liver tumors; the efficacy and prospects of the endoscopic techniques for weight loss, which are relatively new in China, in the treatment of nonalcoholic fatty liver disease/nonalcoholic steatohepatitis. Endoscopic techniques may hold promise for wide clinical application and exploration in in liver-related diseases in China, so as to provide more options for patients and doctors.
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Liver sinusoidal endothelial cells (LSECs) are crucial to the maintenance of hepatic homeostasis under physiologic conditions, while under the conditions of pathological liver damage, LSEC can respond to the damage by changing their structure through the process called capillarization, thereby aggravating liver damage. In addition, the interaction between LSEC and other cells in the liver plays a certain role in the development and progression of liver fibrosis, especially the interaction between LSEC and hepatic stellate cells, which are the primary effector cells of liver fibrosis. This article mainly elaborates on the role of LSEC in the development and progression of liver fibrosis during chronic liver injury.
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With the rapid increase in the prevalence rate of nonalcoholic fatty liver disease (NAFLD), new treatment methods are needed to prevent disease progression to liver fibrosis, liver cirrhosis, and liver cancer. Although great efforts have been made to clarify the pathological mechanisms of NAFLD disease progression, there are still no effective treatment methods at present. Bile acids (BAs) regulate systemic metabolism by activating nuclear receptors and G protein-coupled receptors and have been identified as important signaling molecules involved in lipid, glucose, and energy metabolism. Dysregulation of BA homeostasis is associated with the severity of NAFLD. This article summarizes the important ligands in BA metabolism and their role in the progression of NAFLD, in order to provide a basis for the treatment of NAFLD by targeting BA messengers.
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Cholestatic liver diseases (CLD) are a series of diseases due to impaired bile flow and accumulation of bile acid in the liver and/or systemic circulation caused by immune, genetic, and environmental factors. The pathogenesis of CLD remains unclear and CLD is difficult to treat. As a substitute for human diseases, animal models can provide a platform for exploring the etiology and pathogenesis of the disease and finding appropriate therapeutic targets. This article reviews the current research advances in the animal models of CLD.
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Background: Unintended intraoperative hypothermia is a common complication of general anesthesia surgery, which can cause pain, coagulation dysfunction, wound infection, delayed recovery, and other adverse consequences. There are few studies related to intraoperative hypothermia during endoscopic retrograde cholangiopancreatography (ERCP). Aims: To analyze the risk factors of intraoperative hypothermia during ERCP under general anesthesia and establish a predictive model. Methods: A total of 121 patients underwent ERCP under general anesthesia from September 2021 to November 2021 at Shanghai General Hospital were recruited, and relevant clinical data were collected. Logistic regression analysis was used to screen risk factors, and a predictive model was constructed. The model was externally validated by independent datasets with ROC curve and Hosmer⁃Lemeshow goodness of fit test. Results: A total of 114 patients were enrolled in modeling group. The incidence of intraoperative hypothermia was 11.40% (13/114). There were more women in the hypothermia group (P<0.05). The temperature of entering the operating room and operating room temperature were relatively lower in the hypothermia group (P<0.05). Gender was an independent risk factor for intraoperative hypothermia in ERCP under general anesthesia (P<0.05). The predictive model constructed by using gender and temperature of entering the operating room screened by Logistic regression analysis had a good discrimination and calibration, area under the ROC curve by external validation was 0.78. Conclusions: Gender and temperature of entering the operating room can effectively predict the occurrence of intraoperative hypothermia and assist perioperative monitoring and management.
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Nonalcoholic steatohepatitis (NASH) is a liver disease with a relatively high prevalence worldwide and greatly threatens human health. In recent years, farnesoid X receptor-related drugs have played an important role in regulating the metabolism of bile acid, glucose, and lipids and inhibiting inflammation. This article summarizes the application of farnesoid X receptor agonists in the treatment of NASH, so as to provide a basis for the prevention and treatment of NASH.
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Background: Antibiotic resistance of Helicobacter pylori (Hp) is an important cause of failure of eradication treatment, the latest national and international consensus have recommended a quadruple regimen based on the use of amoxicillin or tetracycline as the first-line treatment for Hp eradication. Minocycline is a semi-synthetic tetracycline easily available clinically and has a low secondary resistance rate, and can be used in penicillin-allergic patients. Aims: To investigate the efficacy and safety of regimen with minocycline combined with metronidazole, rabeprazole and bismuth potassium citrate for eradication of Hp infection. Methods: Patients with Hp infection from August 2020 to January 2021 at Jiangqiao Hospital in Jiading District having the primary treatment for Hp eradication were selected. All the enrolled patients received rabeprazole enteric-coated tablets 10 mg bid + minocycline capsules 100 mg bid + metronidazole tablets 400 mg tid + bismuth potassium citrate capsules 220 mg bid for 14 days. Symptoms and adverse reactions during treatment were recorded. The eradication of Hp was determined by
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Reviewing the history of nonalcoholic fatty liver disease (NAFLD) showed that the definitions, examination methods and treatment approaches have changed greatly. The renaming of NAFLD as metabolic (dysfunction)-associated fatty liver disease (MAFLD) is a new beginning to understand this kind of diseases; the clinical diagnosis and treatment, as well as the related academic research will face new opportunities and challenges. In this editorial, future development of the diagnosis and treatment of MAFLD/NAFLD based on the experiences accumulated in the past years and the latest progresses will be discussed.
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Helicobacter pylori (Hp) can cause a variety of gastric diseases and has a high infection rate. With the widespread use of antibiotics and the influence of geographical, strain and host differences, the failure rate of Hp eradication and reinfection rate are increasing. Therefore, there is a need for individualized precision treatment of refractory Hp infection. This article reviewed the progress of clinical research on individualized precision treatment of Hp infection.
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Objective:To analyze and compare the features of undifferentiated-typed early gastric cancer (UD-EGC) and gastric mucosa-associated lymphoid tissue(MALT) lymphoma under white light endoscopy (WLE) and magnifying endoscopy-narrow band imaging (ME-NBI).Methods:Data of patients with complete endoscopic images of WLE and ME-NBI in Shanghai General Hospital, Shanghai Jiao Tong University from March 2015 to July 2019 were retrospectively analyzed.Twenty-six UD-EGC patients and seven gastric MALT lymphoma patients in ⅠE1 stage were included, and the characteristics of the two diseases under WLE and ME-NBI were compared and summarized.Results:There were no significant differences in age, sex or infiltration depth of lesions between the two groups.Under WLE, UD-EGC was often manifested as a single lesion located in the lower part of the stomach, with unclear lesion boundaries. While MALT lymphoma lesions were mostly multifocal with clear boundaries, located in the middle of the stomach. Under ME-NBI, the microsurface pattern of UD-EGC showed dilation or disappearance of areas between the recesses, and the spiral microvascular pattern. However, the microsurface pattern of MALT lymphomas were characterized by " cross-road traffic sign" , " pebble sign" , and the presentation of residual glandular duct at the lesion was similar to that of Helicobacter pylori ( HP)-related gastritis. Furthermore, the microvascular pattern of MALT lymphomas often showed " tree like appearance (TLA)" . After HP eradication therapy, the morphology of microsurface pattern and microvascular pattern in the original lesion area gradually returned to normal. Conclusion:UD-EGC and gastric MALT lymphoma showed particular features in the number, site and boundary under WLE, and they showed significantly different microsurface pattern and microvascular pattern under ME-NBI. Differentiation of the two diseases will help reduce the risk of missed diagnosis and misdiagnosis.
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To investigate the postoperative serum triglyceride (TG) levels in predicting the risk of new-onset diabetes mellitus (NODM) in patients following allogeneic liver transplantation. One hundred and forty three patients undergoing allogeneic liver transplantation in Shanghai General Hospital from July 2007 to July 2014 were enrolled in this study. The NODM developed in 33 patients after liver transplantation. The curve of dynamic TG levels in the early period after liver transplantation was generated. Independent risk factors of NODM were determined by univariate and multivariant logistic regression analyses. The clinical value of TG in predicting NODM was analyzed by area under the ROC curve (AUC). Serum TG levels were gradually rising in the first week and then reached the plateau phase (stable TG, sTG) in patients after surgery. The sTG in NODM group were significantly higher than that in non-NODM group (=-2.31, <0.05). Glucocorticoid therapy (=4.054, <0.01), FK506 drug concentration in the first week after operation (=3.482, <0.05) and sTG (=3.156, <0.05) were independent risk factors of NODM. ROC curve analysis showed that the AUC of sTG in predicting NODM was 0.72. TG shows a gradual recovery process in the early period after liver transplantation, and the higher TG level in stable phase may significantly increase the risk of NODM in patients.
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Humanos , China/epidemiología , Diabetes Mellitus/etiología , Trasplante de Hígado/efectos adversos , Factores de Riesgo , Tacrolimus/efectos adversos , TriglicéridosRESUMEN
Addition to fat digestion and absorption, bile acids also act as signaling molecules through activating bile acid receptors. Increasing evidences have shown that bile acid receptors are closely related to the occurrence of gastrointestinal diseases. TGR5 and FXR play important roles in bile acid metabolism, regulation of glucose utilization, control of energy homeostasis and regulation of immune cell function. Both FXR and TGR5 inhibit gastrointestinal inflammation, however, the former negatively regulates intestinal tumorigenesis, while the latter may be positively related with gastrointestinal tumors. This article reviewed the immune regulatory effects of TGR5 and FXR on gastrointestinal tract.
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Hepatic fat content is an important index for the early diagnosis, disease grading, and outcome evaluation of nonalcoholic fatty liver disease (NAFLD). Various magnetic resonance imaging (MRI) methods have been used to determine hepatic fat content in NAFLD, among which proton density fat fraction obtained by magnetic resonance spectroscopy and chemical-shift-encoded MRI can achieve precise quantification of hepatic fat and therefore, it is considered the imaging gold standard for the diagnosis of fatty liver disease and has been applied in clinical research. This article reviews the research advances in the MRI techniques for quantification of hepatic fat content, in order to provide a reference for clinical application and experiment.
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Hepatorenal syndrome (HRS) is one of the most severe complications of decompensated cirrhosis. Splanchnic arterial vasodilation in patients with advanced liver cirrhosis and the reduction in cardiac output due to cirrhotic cardiomyopathy may trigger the reduction in effective circulating blood volume, the activation of endogenous vasoconstrictor systems, and significant contraction of renal blood vessels; meanwhile, impairment in renal autoregulation of blood flow may finally lead to the reductions in renal blood flow and glomerular filtration rate. Systemic inflammation also plays an important role in the pathogenesis of HRS. The treatment of HRS should start as soon as it is diagnosed. In the past, HRS was considered “functional” renal insufficiency, while at present, it is considered a spectrum of diseases gradually changing from functional renal insufficiency to varying degrees of parenchymal damage. As there are still no suitable animal models of HRS, current investigations of the pathophysiology of HRS and related pharmacological research mainly rely on clinical studies, which brings difficulties in further understanding the natural history and pathophysiology of HRS. This article reviews the recent advances in the basic and clinical research on HRS and related difficulties.
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Hepatorenal syndrome is one of the major complications of decompensated cirrhosis secondary to the reduction in effective blood volume, imbalance of endogenous vasoactive substances, and the reduction in renal blood flow, with renal insufficiency as the main manifestation. In clinical practice, hepatorenal syndrome mainly manifests as the reduction in renal blood flow and glomerular filtration rate, with no marked changes in renal histology. The treatment of hepatorenal syndrome should start as soon as it is diagnosed. Current therapeutic modalities include the following: (1) general supportive therapies for primary diseases and predisposing factors; (2) pharmacotherapy, including albumin and vasoactive agents; (3) renal replacement therapy; (4) molecular adsorbent recirculating system; (5) transjugular intrahepatic portosystemic shunt; (6) liver transplantation. Liver transplantation is the optimal regimen for the treatment of hepatorenal syndrome, and the other methods including pharmacotherapy and renal replacement therapy are often used as transitional therapies before liver transplantation. Albumin combined with terlipressin is currently the preferred regimen of pharmacotherapy for hepatorenal syndrome. This article reviews the new concepts and advances in the treatment of hepatorenal syndrome.
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Hepatorenal syndrome (HRS) is a common complication of decompensated cirrhosis and is traditionally defined as progressive oliguria or anuria, azotemia, dilutional hyponatremia, and hyponatremia, while renal insufficiency without marked organic lesions in the kidney is the typical manifestation of HRS. Recent studies have found that besides the abnormalities in hemodynamics, inflammatory response, oxidative stress, and direct renal tubular toxicity of bile salts are jointly involved in the development and progression of HRS. HRS is not the only renal complication in patients with liver cirrhosis, and it is only a functional form of acute kidney injury (AKI). HRS meeting the criteria for AKI is called HRS-AKI, which is formerly known as HRS-Ⅰ type. For cirrhotic patients with acute kidney disease or chronic kidney disease, if they meet the criteria for HRS, they can be diagnosed with HRS-NAKI, which is formerly known as HRS-Ⅱ type. The most common risk factors for HRS are infection, digestive bleeding, and large-volume paracentesis without transfusion of human serum albumin for volume expansion.
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With the changes in people’s lifestyle and dietary structure, the incidence rate of nonalcoholic fatty liver disease (NAFLD) has been increasing year by year, and NAFLD has become a serious threat to human health. The treatment of NAFLD has always been a hot topic of basic and clinical research on liver diseases. In recent years, many studies have revealed that omega-3 polyunsaturated fatty acids (ω3-PUFA) can promote fatty acid oxidation, improve intestinal homeostasis, and thus improve lipid metabolism and liver inflammation, and therefore, more and more clinical studies have applied ω3-PUFA in the treatment of NAFLD. However, the mechanism of ω3-PUFA in the treatment of NAFLD is still unclear, and there are certain limitations in related clinical studies. This article mainly introduces the role of ω3-PUFA in NAFLD and the results of related clinical studies and further discusses the problems that need to be solved in ω3-PUFA for the treatment of NAFLD.
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Mitochondrion-localized retinol dehydrogenase 13 (Rdh13) is a short-chain dehydrogenase/reductase involved in vitamin A metabolism in both humans and mice. We previously generated Rdh13 knockout mice and showed that Rdh13 deficiency causes severe acute retinal light damage. In this study, considering that Rdh13 is highly expressed in mouse liver, we further evaluated the potential effect of Rdh13 on liver injury induced by carbon tetrachloride (CCl). Although Rdh13 deficiency showed no significant effect on liver histology and physiological functions under regular culture, the Rdh13 mice displayed an attenuated response to CCl-induced liver injury. Their livers also exhibited less histological changes and contained lower levels of liver-related metabolism enzymes compared with the livers of wild-type (WT) mice. Furthermore, the Rdh13 mice had Rdh13 deficiency and thus their liver cells were protected from apoptosis, and the quantity of their proliferative cells became lower than that in WTafter CCl exposure. The ablation of Rdh13 gene decreased the expression levels of thyroid hormone-inducible nuclear protein 14 (Spot14) and cytochrome P450 (Cyp2e1) in the liver, especially after CCl treatment for 48 h. These data suggested that the alleviated liver damage induced by CCl in Rdh13 mice was caused by Cyp2e1 enzymes, which promoted reductive CCl metabolism by altering the status of thyroxine metabolism. This result further implicated Rdh13 as a potential drug target in preventing chemically induced liver injury.
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Animales , Femenino , Masculino , Ratones , Oxidorreductasas de Alcohol , Genética , Intoxicación por Tetracloruro de Carbono , Enfermedad Hepática Inducida por Sustancias y Drogas , Patología , Citocromo P-450 CYP2E1 , Metabolismo , Inmunohistoquímica , Hígado , Patología , Ratones de la Cepa 129 , Ratones Endogámicos C57BL , Ratones Noqueados , Proteínas Nucleares , Metabolismo , Factores de Transcripción , MetabolismoRESUMEN
OBJECTIVE@#To study the expression of PSMA7 and its effect on proliferation, invasion and migration of gastric cancer and subcutaneous tumorigenesis in nude mice. >and subcutaneous tumorigenesis in nude mice.@*METHODS@#Specimens of tumor tissues and paired adjacent tissues were collected from 60 patients with gastric cancer for detecting the expression levels of PSMA7 using immunohistochemical method. Gastric cancer cell line SGC7901 was transfected with a lentiviral vector to inhibit PSMA7 expression, and the changes in cell proliferation and invasion were observed using cell counting kit-8 (CCK-8), clone formation assay and Transwell assay. A BALB/c mouse model bearing subcutaneous gastric cancer xenograft was established using SGC7901 cells with stable PSMA7 knockdown to assess the effect of low expression of PSMA7 on xenograft growth.@*RESULTS@#Gastric cancer tissues expressed significantly higher levels of PSMA7 than the paired adjacent tissues ( < 0.05). In SGC7901 cells, interference of PSMA7 expression significantly inhibited the cell proliferation and invasion ( < 0.05). In the tumor-bearing BALB/c mice, the xenografts derived from SGC7901 cells with PSMA7 expression interference showed significant growth suppression as compared with the control xenografts ( < 0.05).@*CONCLUSIONS@#PPSMA 7 is overexpressed in gastric cancer tissues, and PSMA7 knockdown inhibits the proliferation, invasion, migration and subcutaneous tumorigenesis of gastric cancer cells in nude mice.
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Animales , Humanos , Ratones , Línea Celular Tumoral , Movimiento Celular , Proliferación Celular , Ratones Endogámicos BALB C , Ratones Desnudos , Invasividad Neoplásica , Complejo de la Endopetidasa Proteasomal , Metabolismo , Neoplasias GástricasRESUMEN
Intrahepatic cholestasis is a pathological condition in which the synthesis, secretion, and excretion of bile are blocked, and thus the bile does not flow normally into the duodenum and bloodstream. According to cytological damage site, it can be divided into hepatocellular cholestasis, biliary duct cell cholestasis and mixed cell cholestasis. The two kinds of pathophysiological models [ascending or upstream (damage begins with cholangiocytes and then extends to the hepatocytes) and descending or downstream (the damage starts from the liver cells and then extends to the bile duct cells)] has distinct features in the process of disease occurrence and development. This article mainly elaborates the "descending" pathophysiological model of cholestatic liver disease (hepatocytic damage progresses to biliary duct cell), and further explores its etiology, pathogenesis and treatment methods.