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failure-induced model improves Cannabidiol of hepatic liver and brain hepati in a function fulminant



  • failure-induced model improves Cannabidiol of hepatic liver and brain hepati in a function fulminant
  • Liver Disease Information: Liver Disease and Medical Marijuana Treatments
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  • Cannabidiol improves brain and liver function in a fulminant hepatic failure- induced . We adapted the rat model of acute liver failure induced by TAA to mice. and liver function in a fulminant hepatic failure-induced model of hepatic Moreover, CBD restored liver/brain function in a model of hepatic Cannabidiol Rescues Acute Hepatic Toxicity and Seizure Induced by Cocaine Liver Disease in HIV-Hepatitis C Coinfection: A Longitudinal Cohort Analysis. Cannabidiol improves brain and liver function in a fulminant hepatic failure- induced model of hepatic encephalopathy in mice. in amelioration of experimental autoimmune hepatitis following activation of TRPV1 receptors by cannabidiol.

    failure-induced model improves Cannabidiol of hepatic liver and brain hepati in a function fulminant

    Hepatitis A related acute liver failure by consumption of contaminated food. Chi, Heng; Haagsma, Elizabeth B. We present a patient with no medical history admitted for jaundice and dark coloured urine. Further investigations revealed hepatitis A related acute liver failure while the patient had no travel history, nor contact with infected individuals. After admission, the patient deteriorated fulfilling the.

    Fatal acute hepatic failure in a family infected with the hepatitis A virus subgenotype IB: Hepatitis A viral infection is a well-known cause of subclinical or acute self-limited hepatitis.

    To investigate the possible factors that affected the severity of HAV infection, a family cluster infected with the HAV subgenotype IB strain, which is not common in Japan, was described. This family consisted of five members who all were infected with HAV. Four of the five patients hospitalized except for an asymptomatic patient. Two of the five patients, men in their 50s and 60s, developed ALF, and one patient died. Various host factors, including sex male , age, and a high bilirubin level, may affect the outcomes.

    Based on viral factors, HAV RNA was higher in the fatal case compared with others, and it decreased within a short period of time. The similarity of the nucleotide sequences was The rapid clearance of increased HAV and the absence of defective HAV might be closely associated with the onset of liver failure. Full Text Available Chronic hepatitis C is a major cause of chronic liver disease, including liver cirrhosis and hepatocellular carcinoma. The development of direct-acting antivirals DAAs revolutionized hepatitis C virus HCV treatment by offering genuine prospects for the first comprehensive cure of a chronic viral infection in humans.

    While antiviral resistance is a significant limitation for interferon-based therapies, resistance and treatment failure still appear to be present in a small fraction of patients even in state-of-the-art DAA combination therapies. Therefore, treatment failure and resistance still remain a clinical challenge for the management of patients not responding to DAAs.

    In this special issue of Viruses on HCV drug resistance, mechanisms of antiviral resistance for different classes of antiviral drugs are described. Furthermore, the detection and monitoring of resistance in clinical practice, the clinical impact of resistance in different patient groups and strategies to prevent and address resistance and treatment failure using complementary antiviral strategies are reviewed.

    Chronic hepatitis C is a major cause of chronic liver disease, including liver cirrhosis and hepatocellular carcinoma. Full Text Available Among toxic lesions of the liver, an important place belongs to medicinal hepatitis. Among patients with hepatitis , drug disease of the liver occurs in 0. Hepatitis developed after an acute respiratory infection.

    Weakness, nausea, vomiting, jaundice of the skin and sclera, pruritus, multiple increase in serum transaminases and markers of cholestasis are revealed. Viral hepatitis and some hereditary liver diseases were excluded. The drug lesion of the liver was of a mixed nature: Timely administration of therapy detoxification, glucocorticosteroids, ursodeoxycholic acid Ursosan led to a regression of clinical symptoms of the disease and positive dynamics of laboratory indicators.

    Radiation- induced liver disease RILD has been characterized as a veno-occlusive disease with anicteric elevation of alkaline phosphatase ALP. However, HBV reactivation after hepatic irradiation has been reported in only a few studies. Acute on chronic liver failure ACLF is rarely the initial manifestation of a malignant process or precipitated by the initiation of anti-viral treatment with a nucleoside or nucleotide agent. We report an unusual case of ACLF temporally associated with initiation of Entecavir for treatment of chronic hepatitis B.

    To the best of our knowledge, this has not been described in the literature. In reviewing our patients clinical course and liver autopsy, he developed a severe acute exacerbation of his chronic hepatitis B virus coinciding with the institution of antiviral therapy and the underlying HL perhaps modulating the overall degree of hepatic injury. Hodgkin's lymphoma coexisting with liver failure secondary to acute on chronic hepatitis B.

    Prediction of posthepatectomy liver failure using transient elastography in patients with hepatitis B related hepatocellular carcinoma. It is essential to accurately predict Postoperative liver failure PHLF which is a life-threatening complication. Liver hardness measurement LSM is widely used in non-invasive assessment of liver fibrosis. The aims of this study were to explore the application of preoperative liver stiffness measurements LSM by transient elastography in predicting postoperative liver failure PHLF in patients with hepatitis B related hepatocellular carcinoma.

    The study included consecutive patients with hepatitis B related hepatocellular carcinoma who underwent hepatectomy between May and September Detailed preoperative examinations including LSM were performed before hepatectomy. The endpoint was the development of PHLF. PHLF occurred in 37 Paraoxonase activity in patients with chronic renal failure and hepatic insufficiency.

    Paraoxonase PON , a high density lipoprotein HDL associated enzyme, is believed to protect against the oxidation of low density lipoprotein LDL and hence affects the risk of vascular disease.

    PON is sensitive to oxidants and is inactivated by oxidized lipids, and thus it can be postulated that increased oxidative stress may decrease plasma PON activity in patients with chronic renal failure CRF and hepatic insufficiency HI. Moreover, in CRF and HI patients, in contrast to normal individuals, higher levels of plasma biochemical parameters and liver enzymes had an inverse correlation with PON activity. In this study we aimed to investigate PON activity, total bilirubin, creatinine, urea and liver enzymes alanine aminotransferase and alkaline phosphatase that are the index of renal and hepatic insufficiency.

    We have analyzed plasma from pre-dialysis patients and compared the results with the normal individuals. We observed a positive association of PON activity with that of the disease state i. Based on our results we conclude that in CRF and HI, in contrast to normal individuals, higher levels of plasma biochemical parameters and liver enzymes had inverse correlation with PON activity.

    Collectively, these findings may add details to the understanding of the role that PON plays in chronic renal failure and hepatic insufficiency. Drug induced acute toxic hepatitis can be idiosyncratic. Albendazole, a widely used broad spectrum antiparasitic drug is generally accepted as a safe drug. It may cause asymptomatic transient liver enzyme abnormalities but acute toxic hepatitis is very rare.

    Herein, we present the case of 47 year old woman with recurrent acute toxic hepatitis after a single intake of albendazole in and The patient was presented with symptoms and findings of anorexia, vomiting and jaundice. For diagnosis, other acute hepatitis etiologies were excluded. Within 2 months, all pathological findings came to normal. There are a few reported cases of albendazole induced toxic hepatitis , but at adults, there is no known recurrent acute toxic hepatitis due to albendazole at this certainty according to RUCAM score.

    Physicians should be aware of this rare and potentially fatal adverse effect of albendazole. Predictive factors for early failure of transarterial embolization in blunt hepatic injury patients. To evaluate the early success of transarterial embolization TAE in patients with traumatic liver haemorrhage and to determine independent factors for its failure. From January to December , TAE was performed in 48 patients for traumatic liver haemorrhage.

    Their medical charts were reviewed for demographic information, pre-TAE vital signs and laboratory data, injury grade, type of contrast medium extravasation CME at CT, angiography findings, and early failure. Variables were compared between the early success and early failure groups. Variables with univariate significance were also analysed using multivariate logistic regression for predictors of early failure. Among 48 liver TAE cases, nine Major hepatic injury is an important factor in early failure.

    A case of hepatic encephalopathy induced by trotrast. Throtrast in the liver was detected by radiological methods and in vivo measurement of the radioactivity. Hyponatraemia secondary to nivolumab- induced primary adrenal failure. Full Text Available Checkpoint inhibitors, such as ipilimumab and pembrolizumab, have transformed the prognosis for patients with advanced malignant melanoma and squamous non-small-cell lung cancer, and their use will only expand as experience is gained in a variety of other malignancies, for instance, renal and lymphoma.

    As the use of checkpoint inhibitors increases, so too will the incidence of their unique side effects, termed immune-related adverse events irAEs, which can affect dermatological, gastrointestinal, hepatic , endocrine and other systems. Nivolumab is a monoclonal antibody that blocks the human programmed death receptor-1 ligand PD-L1 found on many cancer cells and is licensed for the treatment of advanced malignant melanoma. We describe the first case of nivolumab- induced adrenalitis resulting in primary adrenal failure presenting with hyponatraemia in a year-old man with malignant melanoma.

    The case highlights the potentially life-threatening complications of checkpoint inhibitors and the need for patient education and awareness of irAEs among the wider clinical community because such side effects require prompt recognition and treatment. Prognostic factors for patients with hepatitis B virus-related acute-on-chronic liver failure.

    Full Text Available ObjectiveTo investigate the prognostic factors for patients with hepatitis B virus-related acute-on-chronic liver failure , and to provide a basis for clinical diagnosis and treatment. MethodsA total of patients with hepatitis B virus HBV-related acute-on-chronic liver failure who were admitted to The First Hospital of Jilin University from January 1, to January 1, and had complete medical records and follow-up data were enrolled, and a retrospective analysis was performed for their clinical data and laboratory markers to determine prognostic factors.

    The independent-samples t test was used for comparison of continuous data between groups, the chi-square test was used for comparison of categorical data between groups, and a multivariate logistic regression analysis was performed for the indices determined to be statistically significant by the univariate analysis to screen out independent risk factors for the prognosis of patients with HBV-related acute-on-chronic liver failure.

    The multivariate regression analysis was performed for the complications determined to affect prognosis by the univariate analysis, and the results showed that the complications as risk factors were hepatic encephalopathy, hepatorenal syndrome, and infection.

    Liver failure patients with hepatic. Osteomalacia induced by adefovir in patient with hepatitis B. Osteomalacia is defined as a defect in mineralization of the bone matrix. We describe the case of a patient with chronic hepatitis B infection in whom treatment with adefovir induced renal phosphate loss with intense and sustained hypophosphatemia which derived in symptomatic osteomalacia. Obesity- induced hepatic hypoperfusion primes for hepatic dysfunction after resuscitated hemorrhagic shock.

    Obesity and non-alcoholic fatty liver disease NAFLD produce a low grade systemic inflammatory response syndrome SIRS with compromised hepatic blood flow, which increases with body mass index. We hypothesized that obesity further aggravates liver dysfunction by reduced hepatic perfusion following resuscitated hemorrhagic shock HEM. Hepatic blood flow HBF using galactose clearance, liver enzymes and complete metabolic panel were measured over 4 h after completion of RES.

    The pro-inflammatory state of NAFLD seen in obesity appears to prime the liver for hepatic ischemia after resuscitated hemorrhagic shock, perhaps intensified by insidious and ongoing hepatic hypoperfusion established prior to the traumatic injury or shock. Hepatitis A complicated with acute renal failure and high hepatocyte growth factor: A year-old man was admitted to our hospital. Laboratory data showed severe liver injury and that the patient was positive for immunoglobulin M anti- hepatitis A virus HAV antibodies.

    He was also complicated with severe renal dysfunction and had an extremely high level of serum hepatocyte growth factor HGF. However, liver and renal functions both improved rapidly without intensive treatment, and he was subsequently discharged from our hospital on the 21 st hospital day.

    Although complication with ARF and high levels of serum HGF are both important factors predicting poor prognosis in acute liver failure patients, the present case achieved a favorable outcome. Endogenous HGF might play an important role as a regenerative effector in injured livers and kidneys.

    Corrosion induced failure analysis of subsea pipelines. Pipeline corrosion is one of the main causes of subsea pipeline failure. It is necessary to monitor and analyze pipeline condition to effectively predict likely failure. This paper presents an approach to analyze the observed abnormal events to assess the condition of subsea pipelines. The BN model facilitates the modelling of interdependency of identified corrosion causes, as well as the updating of failure probabilities depending on the arrival of new information.

    Furthermore, an Object-Oriented Bayesian Network OOBN has been developed to better structure the network and to provide an efficient updating algorithm. Based on this OOBN model, probability updating and probability adaptation are performed at regular intervals to estimate the failure probabilities due to corrosion and potential consequences.

    This results in an interval-based condition assessment of subsea pipeline subjected to corrosion. The estimated failure probabilities would help prioritize action to prevent and control failures. Practical application of the developed model is demonstrated using a case study. Full Text Available Ticlopidine hydrochloride has been shown to reduce the risk of first or recurrent stroke in patients who have experienced a transient ischemic attack, reversible ischemic neurological deficit, recurrent stroke or first stroke.

    Severe liver dysfunction is a contraindication for its use. Increase in liver enzymes has been reported with use of this drug, but jaundice is rare.

    A case of severe ticlopidine- induced hepatitis that was associated with a marked increase in antinuclear antibody ANA levels is reported. Physicians prescribing ticlopidine hydrochloride should be aware that a potentially severe acute hepatitis associated with ANA positivity can occur. The drug should be discontinued if signs of liver dysfunction occur. Chronic perfluorooctane sulfonate PFOS exposure induces hepatic steatosis in zebrafish.

    Perfluorooctane sulfonate PFOS , one persistent organic pollutant, has been widely detected in the environment, wildlife and human. Currently few studies have documented the effects of chronic PFOS exposure on lipid metabolism, especially in aquatic organisms. The underlying mechanisms of hepatotoxicity induced by chronic PFOS exposure are still largely unknown.

    The present study defined the effects of chronic exposure to low level of PFOS on lipid metabolism using zebrafish as a model system. Our findings revealed a severe hepatic steatosis in the liver of males treated with 0. Quantitative PCR assay further indicated that PFOS significantly increase the transcriptional expression of nuclear receptors nr1h3, rara, rxrgb, nr1l2 and the genes associated with fatty acid oxidation acox1, acadm, cpt1a.

    Full Text Available A year-old female who underwent live donor liver transplantation 3 years prior presented after percutaneous liver biopsy with abdominal and shoulder pain, nausea, vomiting, and elevated liver enzymes. Computed tomography CT showed an intrahepatic and subcapsular hematoma. There was a progressive increase in liver enzymes, bilirubin, and INR and a decline in hemoglobin. Subsequent CT imaging revealed flattening of the portal vein consistent with compression by the enlarging hematoma.

    Liver failure ensued and the patient required urgent retransplantation. Full Text Available There are occasional pediatric reports of parvovirus Bassociated transient acute hepatitis and hepatic failure. A case of a year-old immunocompetent woman who developed severe and prolonged but self-limited acute hepatitis and myelosuppression following acute parvovirus B19 infection is reported.

    Parvovirus B19 may be the causative agent in some adult cases of acute non-A-E viral hepatitis and acute liver failure. Regional cerebral blood flow during mechanical hyperventilation in patients with fulminant hepatic failure.

    Hyperventilation is frequently used to prevent or postpone the development of cerebral edema and intracranial hypertension in patients with fulminant hepatic failure FHF.

    The influence of such therapy on regional cerebral blood flow rCBF remains, however, unknown. In this study the CBF Ten consecutive patients median age 48 [range ] years with FHF and 9 healthy controls median age 54 [] years had rCBF determined by single photon There was no significant difference in the rCBF distribution Hepatitis B virus e antigen induces activation of rat hepatic stellate cells.

    Chronic hepatitis B virus infection is a major cause of hepatic fibrosis, leading to liver cirrhosis and hepatocellular carcinoma. Hepatitis B virus e antigen HBeAg is an accessory protein of HBV, not required for viral replication but important for natural infection in vivo. Hepatic stellate cells HSCs are the major producers of excessive extracellular matrix during liver fibrogenesis. A pilot study was conducted to characterize and map the areas susceptible to slope failure using state-wide available data.

    The objective was to determine whether it would be possible to provide slope- failure susceptibility mapping that could be used Necrostatin-1 protects against reactive oxygen species ROS- induced hepatotoxicity in acetaminophen- induced acute liver failure. Various types of cell death in the damaged liver are linked to APAP- induced hepatotoxicity, and, of these, necrotic cell death of hepatocytes has been shown to be involved in disease pathogenesis.

    Until recently, necrosis was commonly considered to be a random and unregulated form of cell death; however, recent studies have identified a previously unknown form of programmed necrosis called receptor-interacting protein kinase RIPK-dependent necrosis or necroptosis, which is controlled by the kinases RIPK1 and RIPK3. Although RIPK-dependent necrosis has been implicated in a variety of disease states, including atherosclerosis, myocardial organ damage, stroke, ischemia—reperfusion injury, pancreatitis, and inflammatory bowel disease.

    However its involvement in APAP- induced hepatocyte necrosis remains elusive. Moreover, a RIPK1 inhibitor ameliorated APAP- induced hepatotoxicity in an animal model, which was underscored by significant suppression of the release of hepatic enzymes and cytokine expression levels. Of note, RIPK1 inhibition also conferred resistance to oxidative stress in hepatocytes. Acute hepatitis is a disorder that goes with liver cell necrosis and liver inflammation. Among the causes of acute hepatitis , the most common reasons are viral hepatitis.

    Epstein-barr virus EBV and cytomegalovirus CMV are from the family of herpes viruses and rare causes of acute hepatitis. Euroasian J Hepato-Gastroenterol ;5 1: Tranilast reduces serum IL-6 and IL and protects against thioacetamide- induced acute liver injury and hepatic encephalopathy. Hepatic encephalopathy is a serious neuropsychiatric disorder usually affecting either acute or chronic hepatic failure patients.

    Hepatic encephalopathy was replicated in a validated rat model to assess the potential protective efficacy of tranilast against experimentally induced hepatic encephalopathy. Most importantly, there was a significant increase in serum ammonia levels with significant astrocytes' swelling and vacuolization; hallmarks of hepatic encephalopathy. Meanwhile, serum ammonia significantly declined with significant reduction in astrocytes' swelling and vacuolization. Several mechanisms can be implicated in the observed hepato- and neuroprotective potentials of tranilast, such as its anti-inflammatory potential, its antioxidant potential as well as its immunomodulatory properties.

    Hepatitis C virus induces a prediabetic state by directly impairing hepatic glucose metabolism in mice. Virus-related type 2 diabetes is commonly observed in individuals infected with the hepatitis C virus HCV ; however, the underlying molecular mechanisms remain unknown.

    We observed that these mice displayed glucose intolerance and insulin resistance. Higher hepatic glucose production was observed in the HCV mice, despite higher fasting insulinemia, concomitant with decreased expression of hepatic gluconeogenic genes.

    Akt kinase activity was higher in HCV mice than in WT mice, but Akt-dependent phosphorylation of the forkhead transcription factor FoxO1 at serine , which triggers its nuclear exclusion, was lower in HCV mouse livers.

    Thus, the expression of HCV proteins in the liver is sufficient to induce insulin resistance by impairing insulin signaling and glucose uptake.

    In conclusion, we observed a complete set of events leading to a prediabetic state in HCV-transgenic mice, providing a valuable mechanistic explanation for HCV- induced diabetes in humans. What Is Hepatitis A? For kids, hep A is the most common Can Hepatitis A Be Prevented? The following will help keep people We present a review of software- induced failures in commercial nuclear power plants NPPs and in several non-nuclear industries.

    We discuss the approach used for connecting operational events related to these failures and the insights gained from this review. In particular, we elaborate on insights that can be used to model this kind of failure in a probabilistic risk assessment PRA model. We present the conclusions reached in these areas. An overview of animal models for investigating the pathogenesis and therapeutic strategies in acute hepatic failure.

    Acute hepatic failure AHF is a severe liver injury accompanied by hepatic encephalopathy which causes multiorgan failure with an extremely high mortality rate, even if intensive care is provided. Management of severe AHF continues to be one of the most challenging problems in clinical medicine. Liver transplantation has been shown to be the most effective therapy, but the procedure is limited by shortage of donor organs.

    Although a number of clinical trials testing different liver assist devices are under way, these systems alone have no significant effect on patient survival and are only regarded as a useful approach to bridge patients with AHF to liver transplantation.

    As a result, reproducible experimental animal models resembling the clinical conditions are still needed. The three main approaches used to create an animal model for AHF are: We have recently developed a viral model of AHF by meansof the inoculation of rabbits with the virus of rabbit hemorrhagic disease.

    This model displays biochemical and histological characteristics, and clinical features that resemble those in human AHF. In the present article an overview is given of the most widely used animal models of AHF, and their main advantages and disadvantages are reviewed.

    It is prevalent in most countries. Alcohol is an independent cofactor that accelerates the development of HCC in chronic hepatitis C patients. The purpose of the current study was to evaluate ethanol- induced hepatic changes in HCV core-Tg mice and mutant core Tg mice. To observe liver morphological changes, we performed histopathological and immunohistochemical examinations. Histopathologically, NTG, TG-K and TG mice showed moderate centrilobular necrosis, while severe centrilobular necrosis and hepatocyte dissociation were observed in TG mice with increasing lymphocyte infiltration and piecemeal necrosis.

    In all groups, a small amount of collagen fiber was found, principally in portal areas. CYP2E1-positive cells were clearly detected in the centrilobular area in all groups. Data from this study will be useful for elucidating the association between alcohol intake and HCV infection. L-Carnitine Ameliorates Immunological- induced Hepatitis in rats. Immunological mediated hepatitis can be initiated by bacterial product; Lipopolysaccharide LPS.

    The later is increased during severe infection, bacterial overgrowth or translocation. LPS stimulates Kupffer cells. Activation of the kupffer cells contributes to the onset of liver injuries by producing and releasing cytotoxic agents, inflammatory cytokines and reactive oxygen species. In the present study, L-carnitine, a natural antioxidant and immunoprotective agent, is used to protect against LPS- induced hepatitis.

    Moreover, liver histopathological changes are determined. It also increased serum IL2 and activity of all the estimated liver enzyme markers indicating massive hepatic cellular damage as also shown as a necrotic damage in liver histological sections. These data suggest that LCr could be used as an adjuvant therapy in severely infected and specific patients to counteract LPS- induced liver hepatitis.

    Crizotinib- induced fatal fulminant liver failure. Herein we describe a case of a year-old female in good clinical condition with non-small-cell lung cancer who was treated with crizotinib. After 24 days of crizotinib therapy she presented with acute liver failure.

    Serum aspartate aminotransferase and alanine aminotransferase levels had increased. Single Event Effects are a very significant failure mode in modern semiconductor devices that may limit their reliability. Accelerated testing is important for semiconductor industry. Considerable more work is needed in this field to mitigate the problem. Mitigation of this problem will probably come from Physicists and Electrical Engineers working together.

    Pharmacogenetics of ribavirin- induced anemia in hepatitis C. Pharmacogenetics assesses inherited genetic differences in drug metabolic pathways and its role in medicine is growing.

    Ribavirin RBV and peginterferon were the standard of care therapy in hepatitis C virus infection during 15 years, with the addition of first-generation protease inhibitors at the beginning of s. New direct-acting agents are the new standard of care, but RBV remains important in some scenarios.

    The main adverse effect of RBV is anemia, which requires dose reduction and even stopping treatment in some patients. The routine evaluation of these genes could help to identify those patients at risk of developing anemia during the hepatitis C virus treatment. Acute liver failure caused by hepatitis E virus genotype 3 and 4: A systematic review and pooled analysis. Acute liver failure caused by hepatitis E virus genotype 3 and 4 has been rarely described.

    Because of the presence of a short golden therapeutic window in patients with viral acute liver failure from other causes, it is possible that early recognition and treatment might reduce the morbidity and mortality.

    We performed a systematic review and pooled analysis of acute liver failure caused by hepatitis E virus genotype 3 and 4. Two reviewers appraised studies after searching multiple databases on June 12th, Appropriate tests were used to compare hepatitis E virus genotype 3 vs 4, suspected vs confirmed genotypes, hepatitis E virus-RNA positive vs negative, and to discern important mortality risk factors.

    The median bilirubin, ALT, AST and alkaline phosphatase expressed by multiplication of the upper limit of normal levels were Age was a predictor of poor prognosis in multivariate analysis. Age is predictive of poor prognosis in multivariate analysis. Edaravone prevents lung injury induced by hepatic ischemia-reperfusion. We also measured malondialdehyde MDA , an indicator of oxidative stress, in the liver and the lung, as well as cytokine messenger RNA expressions in the reperfused liver and plasma cytokine concentrations.

    Moreover, a significant increase in lung wet-to-dry ratio was observed. MDA concentration increased in the reperfused liver, but not in the lungs. Edaravone administration attenuated the lung injury and the increase of MDA in the reperfused liver. Edaravone also suppressed the reperfusion- induced increase of interleukin-6 messenger RNA expressions in the liver and plasma interleukin-6 concentrations. Edaravone administration before reperfusion of the ischemic liver attenuates oxidative stress in the reperfused liver and the subsequent lung injury.

    Clinical and biochemical parameters and outcomes of death, spontaneous recovery, or liver transplantation were compared between groups. Ameliorative effects of rutin on hepatic encephalopathy- induced by thioacetamide or gamma irradiation. Hepatic encephalopathy HE is a syndrome resulting from acute or chronic liver failure. At the end of experiment, blood, liver and brain samples were collected to assess biochemical and biophysical markers as well histopathological investigations.

    Also an alteration in relative permeability and conductivity of erythrocytes was observed. Furthermore, cytokines levels and AChE activity were induced whereas the activities of HO-1 and neurotransmitters contents were depleted.

    Treatment with rutin resulted in improvement in liver function by the decline in serum AST and ALT activities and reduction in serum ammonia level. In addition, the administration of rutin significantly modulated the alteration in cytokines levels and neurotransmitters content. Histopathological examinations of liver and brain tissues showed that administration of rutin has attenuate TAA or radiation- induced damage and improve tissue architecture.

    Consequently, rutin has been a powerful hepatoprotective effect to combat hepatic encephalopathy associated hyperammonemia and its consequential damage in liver and brain. Full Text Available We report a case of fulminant liver failure resulting in emergent liver transplantation following 3 weeks of nausea, vomiting, and malaise from Jamaican Vomiting Sickness.

    Jamaican Vomiting Sickness is caused by ingestion of the unripe arils of the Ackee fruit, its seeds and husks. It is characterized by acute gastrointestinal illness and hypoglycemia. In severe cases, central nervous system depression can occur. We highlight macroscopic and microscopic changes in the liver secondary to hepatoxicity of Ackee fruit versus those caused by a previously unknown sickle cell trait. We discuss the clinical variables and the synergistic hepatotoxic effect of Ackee fruit and ischemic injury from sickled red blood cells, causing massive hepatic necrosis in this patient.

    Acute liver failure during treatment of interferon alpha 2a chronic hepatitis B and coinfection of parvovirus B Parvovirus B19 infection is associated with a broad spectrum of clinical manifestations among which some are well known but others remain controversial. The role of this infection as a cause of acute hepatitis or exacerbation of chronic liver disease requires discussion regarding its significance in a strategy of prevention and treatment of patients with chronic hepatitis.

    Clinical importance of this infection in patients with chronic hepatitis B treated with pegylated interferon alpha 2a is still unclear but exactly in this population significant complications during treatment may arise. Parvovirus B19 infection is not rare among persons with chronic hepatitis B, therefore searching for co-infection should be placed in standard diagnostic procedures especially in case of exacerbation of chronic hepatitis , pancytopaenia or anaemia of unknown origin.

    Pegylated interferon alpha 2a still remains a gold standard of therapy of patients with chronic hepatitis B according to European EASL and Polish guidelines. We present a case of 35 years old woman treated with pegylated interferon alpha 2a who developed acute liver failure in 23rd week of chronic hepatitis B therapy. An exacerbation of hepatitis with encephalopathy and pancytopaenia have been observed. Parvovirus B19 and HBV co-infection does not increase the frequency of liver function abnormalities in patients with chronic hepatitis B.

    Further investigations should be done to describe the natural course of co-infection with parvovirus B19 and HBV and to establish possible association between parvovirus B19 infection and chronic hepatitis B and also the influence of interferon alpha 2a on the infections course.

    Hyperbilirubinemia and rapid fatal hepatic failure in severe combined immunodeficiency caused by adenosine deaminase deficiency ADA-SCID. Thyroid storm complicated by fulminant hepatic failure: Fulminant hepatic failure FHF entails encephalopathy with severe coagulopathy in the setting of liver disease.

    Fulminant hepatic failure is a rare but serious complication of thyroid storm. There have been only 6 previously reported cases of FHF with thyroid storm. We present a patient from our institution with thyroid storm and FHF. A literature review was performed to analyze the outcomes of the 6 additional cases of concomitant thyroid storm and FHF. Our patient underwent thyroidectomy followed by OLT. Over the course of follow-up, persons There were no differences in the crude rates between marijuana users and nonusers for any of the outcomes assessed.

    Tables 3 and 4 present the results of the multivariate models for the association between marijuana smoking and progression to liver diseases. No significant association could be found between marijuana use and development of significant fibrosis or cirrhosis measured with the APRI score. Lagging the exposure variable by one visit had no impact on these conclusions. Neither current nor lagged marijuana smoking accelerated progression to ESLD.

    Models are adjusted for baseline: Models adjusted for same variables, with the exception of binary indicator of marijuana smoking relating to 6—12 mo before outcome assessment.

    Smoking marijuana seemed to accelerate progression to a clinical diagnosis of cirrhosis HR, 1. However, lagging the exposure attenuated this association HR, 1. Marijuana smoking was also associated with a slightly increased risk of progression to clinically diagnosed cirrhosis and ESLD combined: This association was no longer significant when marijuana exposure was lagged HR, 1.

    There was no evidence of a dose-response relationship between marijuana and APRI scores in follow-up. The linear spline regression model did not provide a better fit to the data over a simple linear regression. There was no difference in the slope of ln APRI observed with increasing marijuana use. The ln APRI score would increase by 0.

    APRI, aspartate aminotransferase-to-platelet ratio. In this first longitudinal study to our knowledge of marijuana smoking and risk of liver disease among HIV-HCV coinfected persons without significant fibrosis at baseline, we found no evidence that cannabis smoking increases the risk of progression to significant liver fibrosis or cirrhosis as measured by the standard APRI cutoffs.

    Furthermore, there was no evidence of any dose-response relationship with increasing cannabis use on APRI score. In addition, we did not observe any effect of marijuana use on the development of ESLD.

    However, this association disappeared after lagging the exposure, suggesting that previous cross-sectional studies reporting an association between marijuana smoking and liver fibrosis may be biased by reverse causation due to self-medication with marijuana for relief of symptoms related to significant liver fibrosis.

    The 2 principal studies implicating marijuana as an independent risk factor for liver fibrosis were cross-sectional in design. They found a strong association between daily cannabis use and moderate to severe fibrosis OR, 6. They concluded that cannabis may have little or no influence on the initiation of fibrosis, but once fibrosis is present, it may be an important cofactor in fibrosis progression.

    They found an OR of 0. Reported use for symptom relief was very prevalent suggesting that the association of daily cannabis use and more advanced fibrosis may, in fact, be related to an increased use for symptom management as disease advances. The cannabinoid system consists of 2 receptors CB1 and CB2 to which cannabinoids can bind [ 11 ].

    Depending on which receptor is expressed, cannabinoids could have opposite effects on the liver. Antifibrogenic and antiinflammatory effects of CB2 receptor have been observed in mice [ 10 , 21—23 ]. However, expression of the CB1 receptor seems to have pro-fibrogenic properties [ 10 , 26 ]. In cell culture, cannabidiol induces death of hepatic stellate cells, activation of which contributes to development of fibrosis [ 7 ].

    However, levels of CB1 are 6 times higher in chronic HCV patients than in controls, and twice higher in cirrhotic patients than in those at a low fibrosis stage [ 27—29 ]. In this study, we selected a population with evidence of chronic HCV infection, thus more likely to express high levels of profibrogenic CB1 receptors.

    It is also possible that we favored the inclusion of those with higher CB2 expression by selecting a population free of significant fibrosis and ESLD. However, this is unlikely to have biased our results because we were interested in studying progression to liver disease. Our study has several strengths. In previous studies, patients were only selected based on having undergone liver biopsy, which potentially introduces selection bias. Indeed, excluded patients in the Ishida study were significantly less likely to use marijuana.

    We assessed marijuana use and other potential confounders such as alcohol use and HIV disease stage concurrently at each study visit and exposures were updated longitudinally, thus limiting the potential for reverse causality. In addition to using a noninvasive surrogate for significant fibrosis and cirrhosis, we corroborated our results with clinical outcomes.

    There are several limitations worth noting. We used APRI as a noninvasive surrogate for significant liver fibrosis, which may underestimate the degree of fibrosis present and may be influenced by factors other than fibrosis that affect AST and platelet values. However, the reference standard for the diagnosis of significant hepatic fibrosis, liver biopsy, is invasive, costly and prone to sampling error and therefore not amenable to be used repeatedly [ 33 ].

    Given the 18 years median duration of HCV infection, it is expected that many participants would have some degree of fibrosis at baseline. For this reason we also adjusted for baseline APRI in multivariate models, itself a strong predictor of liver fibrosis progression. Although the relatively short follow-up time and the lack of information on duration of smoking before cohort entry do not allow us to make inference about long-term use of marijuana, the results of this study could still be valuable to clinicians who need to provide advice to their patients about immediate risks of marijuana smoking.

    Longer follow-up would be very valuable, however, to confirm our findings for extended exposure. Clinical outcomes were relatively rare over the course of this study so it remains possible that we have missed a true effect type II error that may have been present if follow-up were extended so as to capture more events.

    Thus, if there is any effect of marijuana exposure it is likely to be quite small and only in more advanced disease. Transient receptor potential vanilloid 1 gene deficiency ameliorates hepatic injury in a mouse model of chronic binge alcohol-induced alcoholic liver disease. Cannabidiol improves brain and liver function in a fulminant hepatic failure-induced model of hepatic encephalopathy in mice.

    Endocannabinoids in liver disease. Is lipid signaling through cannabinoid 2 receptors part of a protective system? References Publications referenced by this paper. Showing of 32 references. Pharmacology of cannabinoid CB1 and CB2 receptors.

    Capsaicin administration inhibits the abducent branch but excites the thyroarytenoid branch of the recurrent laryngeal nerves in the rat.

    Liver Disease Information: Liver Disease and Medical Marijuana Treatments

    Furthermore, CBD improved alcohol-induced hepatic metabolic dysregulation and steatosis by restoring changes in hepatic mRNA or protein. autoimmune hepatitis following activation of TRPV1 receptors by cannabidiol improves brain and liver function in a fulminant hepatic failure-induced model. system abnormalities (autoimmune hepatitis, primary biliary cirrhosis, or primary treatment diverges based on calculated Model for End-stage Liver Disease1 scores; patients blockade can improve neurologic function in mice with induced liver failure Cannabidiol improves brain and liver function in a fulminant hepatic.

    Associated Data



    Furthermore, CBD improved alcohol-induced hepatic metabolic dysregulation and steatosis by restoring changes in hepatic mRNA or protein.


    autoimmune hepatitis following activation of TRPV1 receptors by cannabidiol improves brain and liver function in a fulminant hepatic failure-induced model.


    system abnormalities (autoimmune hepatitis, primary biliary cirrhosis, or primary treatment diverges based on calculated Model for End-stage Liver Disease1 scores; patients blockade can improve neurologic function in mice with induced liver failure Cannabidiol improves brain and liver function in a fulminant hepatic.


    Cannabidiol Improves Brain and Liver Function in a Fulminant Hepatic Failure- induced models with induced hepatic encephalopathy associated with caused by acute or chronic liver failure, usually observed in patients.


    Cannabidiol improves brain and liver function in a fulminant hepatic .. Results: Hepatitis A in 4 patients, non-A, non-E hepatitis in 4; mushroom poisoning in 3; .. [Discussion of Chinese syndrome typing in acute hepatic failure model].

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