Autonomic Nervous System Diseases ; physiopathology ; Humans ; Liver Cirrhosis ; physiopathology

Intestinal failure (IF) is defined as the critical reduction of functional intestines below the minimum needed to absorb nutrients and fluids, so that intravenous supplementation with parenteral nutrition (PN) is required to maintain health and/or growth. Although the benefits are evident, patients receiving PN can suffer from serious cholestasis due to lack of enteral feeding and small intestinal bacterial overgrowth (SIBO). One such complication that may arise is intestinal failure-associated liver disease (IFALD). Evidences from recent studies suggest that alterations in the intestinal microbiota, as well as intraluminal bile acid driven signaling, may play a critical role in both hepatic and intestinal injury. Since Marshall first proposed the concept of the gut-liver axis in 1998, the role of gut-liver axis disorders in the development of IFALD has received considerable attention. The conversation between gut and liver is the key to maintain liver metabolism and intestinal homeostasis, which influences each other and is reciprocal causation. However, as a "forgotten organ" , intestinal microbiota on the pathogenesis of IFALD has not been well reflected. As such, we propose, for the first time, the concept of gut-microbiota-liver axis to emphasize the importance of intestinal microbiota in the interaction of gut-liver axis. Analysis and research on gut-microbiota-liver axis will be of great significance for understanding the pathogenesis of IFALD and improving the prevention and treatment measures.
Bacterial Infections/physiopathology* ; Bile Acids and Salts/physiology* ; Cholestasis/physiopathology* ; Enteral Nutrition ; Gastrointestinal Microbiome/physiology* ; Humans ; Intestinal Diseases/physiopathology* ; Intestines/physiopathology* ; Liver/physiopathology* ; Liver Diseases/physiopathology* ; Parenteral Nutrition/adverse effects* ; Short Bowel Syndrome/physiopathology* ; Signal Transduction

BACKGROUND/AIMS: Increased intestinal permeability has been possible contributing factors to the pathogenesis of alcoholic liver disease. Moreover, it can contribute to the development of bacterial infection and intestinal endotoxemia in patients with liver cirrhosis. This study aimed to examine the difference of intestinal barrier dysfunction between alcoholic and viral liver disease patients through the comparison of the intestinal permeabilities of patients with clinical characteristics. METHODS: Intestinal permeabilities were measured in 18 healthy controls, 41 patients with alcoholic liver disease (17 cases of alcoholic liver disease without cirrhosis and 24 cases of alcoholic liver cirrhosis) and 46 patients with viral liver disease (14 cases of chronic viral hepatitis and 32 cases of viral liver cirrhosis) by measuring 24 hour urine excretion of 51Cr-EDTA. RESULTS: The intestinal permeability was significantly increased in the patients with alcoholic liver disease without cirrhosis (5.62 +/- 2.80%), alcoholic liver cirrhosis (5.29 +/- 2.48%) and viral liver cirrhosis (3.15 +/- 1.39%) compared with that in control subjects (1.99 +/- 0.53%). On the contrary, it was not increased in the patients with chronic viral hepatitis (2.05 +/- 0.57%) versus controls. The significant correlation was not found between intestinal permeability and clinical and laboratory findings. CONCLUSIONS: The intestinal permeability was elevated in patients with alcoholic liver disease compared to those with viral liver cirrhosis. The pathophysiology of liver injury secondary to intestinal epithelial damage may be different between alcoholic and viral liver diseases.
Aged ; Chronic Disease ; English Abstract ; Female ; Hepatitis, Viral, Human/*physiopathology ; Humans ; Intestines/*physiopathology ; Liver Cirrhosis, Alcoholic/physiopathology ; Liver Diseases, Alcoholic/*physiopathology ; Male ; Middle Aged ; Permeability

Adult ; Chemical and Drug Induced Liver Injury ; Dimethylformamide ; adverse effects ; Formamides ; analysis ; Humans ; Kidney ; physiopathology ; Kidney Diseases ; chemically induced ; physiopathology ; urine ; Kidney Function Tests ; Liver ; physiopathology ; Liver Diseases ; physiopathology ; urine ; Liver Function Tests ; Male ; Middle Aged ; Occupational Exposure

Acute Disease ; Child ; Cytomegalovirus Infections ; drug therapy ; physiopathology ; Humans ; Liver ; physiopathology ; Liver Diseases ; drug therapy ; physiopathology ; Measles ; drug therapy ; physiopathology ; Prognosis ; Rotavirus Infections ; drug therapy ; physiopathology ; Virus Diseases ; drug therapy ; physiopathology

OBJECTIVE: To explore the effects of hydrogen on liver injury in chronic intermittent hypoxia rats and the related oxidative stress mechanism. METHODS: Twenty-four male adult SD rats were randomly divided into 3 groups(=8):the normoxia group (Norm), the chronic intermittent hypoxia group (CIH), the chronic intermittent hypoxia and hydrogen group (H + CIH). Rats in Norm group were exposed in air, those in the other 2 groups suffered from chronic intermittent hypoxia conditions for 5 weeks. Before the CIH treatment, rats in H+CIH group inhaled hydrogen gas at 67% concentration for 1 hour. The serum biochemical indicators of oxidative stress, pro-inflammatory cytokine, liver enzyme and blood lipid were inspected after five weeks treatment, the pathological changes of liver tissue were also observed in the transmission electron microscope. RESULTS: Compared with Norm group, the microstructure of liver cells was severely injured, and the serum levels of glutamic-pyruvic transaminase(ALT),glutamic-oxalacetic transaminase (AST) were significantly higher in CIH group (<0.05); the serum level of 8-hydroxy-2 deoxyguanosine(8-OHdG) and interleukin-6(IL-6) was significantly higher, the serum level of superoxide dismutase (SOD) was significantly lower. Compared with CIH group, the pathology of liver microstructure were significantly improved and the serum levels of ALT, AST were significantly lower in H+CIH group (<0.05); the serum levels of 8-OHdG and IL-6 were significantly lower, the serum level of SOD was significantly higher. Compared with Norm group, the serum level of IL-1 was higher, the serum level of TC, TG, and low density lipoprotein(LDL) were lower, but there was no statistical difference with those in CIH group. There was no statistical difference in the serum level of high density lipoprotein (HDL)among the three groups. CONCLUSIONS Pre-treatment with hydrogen could improve the liver injury caused by chronic intermittent hypoxia, and reducing oxidative stress level for protecting the liver cells damage.
Animals ; Hydrogen ; pharmacology ; Hypoxia ; physiopathology ; Liver ; physiopathology ; Liver Diseases ; therapy ; Male ; Oxidative Stress ; Random Allocation ; Rats ; Rats, Sprague-Dawley

As the most abundant liver-specific microRNA, microRNA-122 (miR-122) is involved in various physiological processes in hepatic function as well as in liver pathology. There is now compelling evidence that miR-122, as a regulator of gene networks and pathways in hepatocytes, plays a central role in diverse aspects of hepatic function and in the progress of liver diseases. This liver-enriched transcription factors-regulated miRNA promotes differentiation of hepatocytes and regulates lipid metabolism. With regard to liver diseases, miR-122 was shown to stimulate hepatitis C virus (HCV) replication through a unique and unusual interaction with two binding sites in the 5'-UTR of HCV genome to mediate the stability of the viral RNA, whereas inhibit the expression and replication of hepatitis B virus (HBV) by a miR-122-cylin G1/p53-HBV enhancer regulatory pathway. In addition, miR-122 acts as a suppressor of cell proliferation and malignant transformation of hepatocytes with remarkable tumor inhibition activity. Notably, a clinical trial targeting miR-122 with the anti-miR-122 oligonucleotides miravirsen, the first miRNA targeted drug, has been initiated for treatment of HCV infection. With further understanding of the comprehensive roles of miR-122 in hepatic functions and the mechanisms involved in miR-122 down-regulation in chronic hepatitis or hepatocellular carcinoma, miR-122 appears to be a promising candidate for effective therapeutic approaches against tumor and infectious diseases.
Humans ; Lipid Metabolism ; genetics ; Liver ; growth & development ; metabolism ; physiopathology ; Liver Diseases ; genetics ; physiopathology ; MicroRNAs ; genetics ; metabolism ; Models, Biological

Acetamides ; Aminopyrine ; Animals ; Breath Tests ; methods ; Carbon Isotopes ; Chemical and Drug Induced Liver Injury ; diagnosis ; pathology ; physiopathology ; Humans ; Liver ; injuries ; pathology ; physiopathology ; Liver Cirrhosis ; diagnosis ; pathology ; physiopathology ; Liver Diseases ; diagnosis ; pathology ; physiopathology ; Liver Function Tests ; Phenylalanine ; Prognosis

Adult ; Autonomic Nervous System Diseases ; etiology ; physiopathology ; Biopsy ; adverse effects ; Hepatitis B, Chronic ; pathology ; physiopathology ; Humans ; Liver ; pathology ; physiopathology ; Male ; Vagus Nerve ; physiopathology ; Vasomotor System ; physiopathology

The aim of this study was to investigate the clinical features of acquired hemophagocytic lymphohistiocytosis (HLH) complicated with hepatic dysfunction. 18 cases of acquired HLH were analyzed. The characteristics of hepatic dysfunction, the relationship between hepatic dysfunction and the cause, as well as prognosis of the acquired HLH were preliminarily analysed. The results indicated that characteristics of hepatic dysfunction in acquired HLH patients were hypoproteinemia, jaundice and increase of L-aspirate aminotransferase (AST) and lactate dehydrogenase (LDH) levels. The level of AST and direct bilirubin (DBil) in the non-malignancy associated hemophagocytic lymphohistiocytosis group were higher than that in malignancy-associated hemophagocytic lymphohistiocytosis group (p<0.05). And the increase of LDH and AST levels indicated poor prognosis (p<0.05). In conclusion, liver damage is a common organ functional disorder in patients with acquired HLH, which may be correlated to the cause and the prognosis of acquired HLH.
Adolescent ; Adult ; Aged ; Aged, 80 and over ; Female ; Humans ; Liver ; physiopathology ; Liver Diseases ; complications ; physiopathology ; Lymphohistiocytosis, Hemophagocytic ; complications ; etiology ; physiopathology ; Male ; Middle Aged ; Young Adult