Monocyte dysregulation: consequences for hepatic infections

Liver disorders due to infections are a substantial health concern in underdeveloped and industrialized countries. This includes not only hepatotropic viruses (e.g., hepatitis B, hepatitis C) but also bacterial and parasitic infections such as amebiasis, leishmaniasis, schistosomiasis, or echinococcosis. Recent studies of the immune mechanisms underlying liver disease show that monocytes play an essential role in determining patient outcomes. Monocytes are derived from the mononuclear phagocyte lineage in the bone marrow and are present in nearly all tissues of the body; these cells function as part of the early innate immune response that reacts to challenge by external pathogens. Due to their special ability to develop into tissue macrophages and dendritic cells and to change from an inflammatory to an anti-inflammatory phenotype, monocytes play a pivotal role in infectious and non-infectious liver diseases: they can maintain inflammation and support resolution of inflammation. Therefore, tight regulation of monocyte recruitment and termination of monocyte-driven immune responses in the liver is prerequisite to appropriate healing of organ damage. In this review, we discuss monocyte-dependent immune mechanisms underlying hepatic infectious disorders. Better understanding of these immune mechanisms may lead to development of new interventions to treat acute liver disease and prevent progression to organ failure.

Fulminant hepatitis B: A case report

Introduction: Fulminant hepatitis is a severe acute liver disease. It occurs due to massive necrosis of hepatocytes. The disease progresses to lethal outcome within a few days. The most common causes of this disease are toxic substances, autoimmune and viral hepatitis. The aim of the study was to present a lethal case of fulminant hepatitis caused by hepatitis B virus in a patient with treated bladder cancer. Case Outline: A 63-year-old patient was admitted for treatment due to weakness, nausea and decreased diuresis. She had surgery to remove her bladder, which was affected by a malignant process, two years earlier. On admission, she had a subicteric, orderly auscultatory finding. The abdomen was palpably painful below the right costal arch, without organomegaly. The ureterostomy was functional. The diagnosis of acute HBV infection was made by evidence of HBsAg, HBeAg and antiHBc IgM antibody titer. Laboratory findings indicated an increase in transaminases, urea, creatinine, total and conjugated bilirubin, decreased albumin values and coagulation disorders. The patient was treated with hepatoprotective therapy, antibiotics and antiviral therapy. Hemodialysis was performed as needed. Encephalopathy developed on the third day with further progression.The disease progressed with gastrointestinal bleeding and cardiac disorders and ended in death on the ninth day. Conclusion: Fulminant liver damage caused by hepatitis B virus is a severe disease that can be complicated by acute renal failure. The prognosis of the disease is often unfavorable, so optimal treatment requires a liver transplant.

Synthesis of a silymarin-gold nanoparticle conjugate and analysis of its liver-protecting activity

Background: The liver disease problem prompts investigators to search for new methods of liver treatment. Introduction: Silymarin (Sil) protects the liver by reducing the concentration of free radicals and the extent of damage to the cell membranes. A particularly interesting method to increase the bioavailability of Sil is to use synthesized gold nanoparticles (AuNPs) as reagents. The study considered whether it was possible to use the silymarin-AuNP conjugate as a potential liver-protecting drug. Method: AuNPs were conjugated to Sil and examine the liver-protecting activity of the conjugate. Experimental hepatitis and hepatocyte cytolysis after carbon tetrachloride actionwere used as a model system, and the experiments were conducted on laboratory animals. Result: For the first time, silymarin was conjugated to colloidal gold nanoparticles (AuNPs). Electron microscopy showed that the resultant preparations were monodisperse and that the mean conjugate diameter was 18–30 nm ± 0.5 nm (mean diameter of the native nanoparticles, 15 ± 0.5 nm). In experimental hepatitis in mice, conjugate administration interfered with glutathione depletion in hepatocytes in response to carbon tetrachloride was conducive to an increase in energy metabolism, and stimulated the monocyte–macrophage function of the liver. The results were confirmed by the high respiratory activity of the hepatocytes in cell culture. Conclusion: We conclude that the silymarin-AuNP conjugate holds promise as a liver-protecting agent in acute liver disease caused by carbon tetrachloride poisoning.

Bidens pilosa L. (Asteraceae) cultivated in Brazil on acute liver disease in dogs

ABSTRACT Bidens pilosa L. is a medicinal plant popularly used for treatment of liver diseases. In this study, the dry extract of aerial parts of Bidens pilosa and Silymarin, a phytocomplex obtained from the Silybum marianum fruits and marketed as hepatoprotective, were tested in dogs experimentally acutely intoxicated with carbon tetrachloride. The liver activity was evaluated by hematological and biochemical profiles, and histological and ultrasound analyzes. It was observed that the lowest serum activities of ALT and serum concentrations of total bilirubin occurred in the groups treated with the dry extract of Bidens pilosa, while only decreased serum concentrations of total bilirubin occurred in the group treated with Silymarin. Best liver recovery was also observed for the dry extract of B. pilosa at a 400mg/Kg dose by ultrasonography. This study showed that the dry extract of Bidens pilosa acted more efficiently in the treatment of acute toxic hepatitis induced in dogs than Silymarin.

Clinical and epidemiological aspects of an outbreak of viral hepatitis E in a training centre

Background: HEV infection is responsible for half of all outbreaks of acute liver disease in endemic areas. The present study deals with eighty eight cases of faeces orally transmitted Hepatitis E virus (HEV) in a regimental training center in South India in October 2016 to November 2016.Methods: Methodology and case definitions which were used for confirmed case and presumptive case of viral hepatitis were same as those which were used by Singh et al in their study. Surveillance data for all the cases was reviewed. The outbreak was described in terms of person, place and time. A sanitary survey carried out to detect the likely sources of contamination of water and to study the methods of sewage disposal with regards to septic tanks/soak pits.Results: Out of eighty-eight cases, two persons were HBsAg +ve, five were positive for both Hepatitis A and E, sixty-eight were positive for hepatitis E, five were positive for Hepatitis A, 8 persons were found negative for all the above hepatitis viruses. Overflow of sewage with foul smell and leaking water pipeline in 2 places were observed in the unit area. The overall attack rate was 27.69%.Conclusions: The present outbreak was due to faecal contamination of drinking water supplied to the regimental centre, which occurred due to old and corroded leaking pipelines in close proximity to old sewage lines having leakage through their walls. Medical authorities should maintain surveillance for all water and food borne diseases.

Possible Pathways of Hepatotoxicity Caused by Chemical Agents

Background: Liver injury induced by drugs has become a primary reason for acute liver disease and therefore posed a potential regulatory and clinical challenge over the past few decades and has gained much attention. It also remains the most common cause of failure of drugs during clinical trials. In 50% of all acute liver failure cases, drug-induced hepatoxicity is the primary factor and 5% of all hospital admissions. Methods: The various hepatotoxins used to induce hepatotoxicity in experimental animals include paracetamol, CCl4, isoniazid, thioacetamide, erythromycin, diclofenac, alcohol, etc. Among the various models used to induce hepatotoxicity in rats, every hepatotoxin causes toxicity by different mechanisms. Results: The drug-induced hepatotoxicity caused by paracetamol accounts for 39% of the cases and 13% hepatotoxicity is triggered by other hepatotoxic inducing agents. Conclusion: Research carried out and the published papers revealed that hepatotoxins such as paracetamol and carbon- tetrachloride are widely used for experimental induction of hepatotoxicity in rats.

Assessment the Epidemiological Status of Patients with Acute Liver Hepatitis Referred to Shahid Sadoughi Hospital of Yazd From 2015 to 2018

Introduction: Acute hepatitis has several causes. Transfusion of non-infected blood to the virus and avoidance of undesirable social contacts have reduced the prevalence of hepatitis B and C transmission. Improved socioeconomic status and access to healthy food and water have also reduced the prevalence of hepatitis E and A. The transition from Hyper Endimicity to Intermediate or Low Endimicity has increased the incidence of acute Hepatitis A especially in adults. The aim of this study was to determine the epidemiological status of patients with acute liver hepatitis referred to the Shahid Sadoughi Hospital of Yazd from 2015 to 2018 Methods: This cross-sectional study was performed on the patients referring to the gastrointestinal clinic of Shahid Sadoughi Hospital from 2015 to 2018. The sampling method was that after rule out chronic liver disease according to medical history and patient lab data, the patients imported to the category of acute liver disease. SPSS Inc, Chicago, IL; version 16 was used to determine the prevalence of each type of acute hepatitis. Results: 23 patients were diagnosed with acute hepatitis, 14 were male and 9 were female. Hepatitis A was found in 15 patients, 2 patients had acute hepatitis B, 2 patients had autoimmune hepatitis, and 4 patients had other causes for hepatitis. Conclusion: 65% of patients in this study had acute hepatitis A. Therefore, acute hepatitis A is one of the important factors in the development of acute liver disease study and is therefore one of the important factors in the development of acute liver disease.

Thioacetamide-induced liver damage and thrombocytopenia is associated with induction of antiplatelet autoantibody in mice

Thrombocytopenia is usually associated with liver injury, elevated plasma aspartate aminotransferase and alanine aminotransferase levels, and high antiplatelet immunoglobulin (Ig) titers, although the mechanism behind these effects remains elusive. Deciphering the mechanism behind acute liver disease–associated thrombocytopenia may help solve difficulties in routine patient care, such as liver biopsy, antiviral therapy, and surgery. To determine whether liver damage is sufficient per se to elicit thrombocytopenia, thioacetamide (TAA)-induced hepatitis rodent models were employed. The analysis results indicated that TAA treatment transiently induced an elevation of antiplatelet antibody titer in both rats and mice. B-cell-deficient (BCD) mice, which have loss of antibody expression, exhibited markedly less thrombocytopenia and liver damage than wild-type controls. Because TAA still induces liver damage in BCD mice, this suggests that antiplatelet Ig is one of the pathogenic factors, which play exacerbating role in the acute phase of TAA-induced hepatitis. TNF-α was differentially regulated in wild-type versus BCD mice during TAA treatment, and anti-TNF treatment drastically ameliorated antiplatelet Ig induction, thrombocytopenia, and liver injury, suggesting that the TNF pathway plays a critical role in the disease progression.

Cardiovascular and Metabolic Consequences of Liver Transplantation: A Review

Liver transplantation (LT) is considered the curative treatment option for selected patients who suffer from end-stage or acute liver disease or hepatic malignancy (primary). After LT, patients should be carefully monitored for complications that may appear, partially due to immunosuppressive therapy, but not entirely. Cardiovascular diseases are frequently encountered in patients with LT, being responsible for high morbidity and mortality. Patients with underlying cardiovascular and metabolic pathologies are prone to complications after the transplant, but these complications can also appear de novo, mostly associated with immunosuppressants. Metabolic syndrome, defined by obesity, hypertension, dyslipidemia, and hyperglycemia, is diagnosed among LT recipients and is aggravated after LT, influencing the long-term survival. In this review, our purpose was to summarize the current knowledge regarding cardiovascular (CV) diseases and the metabolic syndrome associated with LT and to assess their impact on short and long-term morbidity and mortality.