Liver Involvement in SARS-CoV-2 Vertically Infected Newborn: A Case Report

Neonatal SARS-CoV-2 infection can occur antenatally, peripartum, or postnatally. In the newborn, clinical manifestations may vary including fever and respiratory, gastrointestinal and neurological symptoms. Most commonly, they are subclinical. We herein present a case of vertical transmission of SARS-CoV-2 presenting with liver injury, characterized by an increase in serum transaminases.

Hepatotoxicity of methoxychlor and camel milk restoration

Purpose The purpose of this paper is to investigate the restoration effect of camel's milk against methoxychlor induced liver toxicity. Design/methodology/approach The present study was carried out to investigate the restoration effect of camel's milk against methoxychlor induced liver toxicity. Findings Methoxychlor (MXC) caused a significant increase in serum transaminases (aspartate transaminase and alanine transaminase) and alkaline phosphatase, while MXC induced a significant reduction in total protein and albumin levels. MXC significantly inhibited lipid peroxidation and markedly enhanced glutathione in liver homogenate. Pathological damages as degeneration and coagulative necrosis of hepatocytes were established in liver. Newly formed bile ducteules denotes neoplastic changes in the portal tract with abnormal mitotic pattern were associated with the long-term exposure. Originality/value The present study concluded that camel milk treatment may play a protective role against methoxychlor-induced liver damage in rats.

Exploring evidence-based innovative therapy for the treatment of chronic HBV infection: experimental and clinical

With the advent of various vaccines and antimicrobial agents during the 20th century, the control and containment of infectious diseases appeared to be a matter of time. However, studies unveiled the diverse natures of microbes, their lifestyle, and pathogenetic potentials. Since the ground-breaking discovery of the hepatitis B virus (HBV) by Baruch Blumberg and the subsequent development of a vaccine in the early 1980s, the main task of the scientific community has been to develop a proper management strategy for HBV-induced chronic liver diseases. In the early 1980’s, standard interferon (IFN) induced a reduction of HBV DNA levels, followed by the normalization of serum transaminases (alanine aminotransferase, ALT), in some chronic hepatitis B (CHB) patients. However, in the course of time, the limitations of standard IFN became evident, and the search for an alternative began. In the late 1980’s, nucleoside analogs entered the arena of CHB treatment as oral drugs with potent antiviral capacities. At the beginning of the 21st century, insights were developed into the scope and limitations of standard IFN, pegylated-IFN as well as nucleoside analogs for treating CHB. Considering the non-cytopathic nature of the HBV, the presence of covalently closed circular DNA (cccDNA) in the nucleus of the infected hepatocytes and HBV-induced immune-mediated liver damages, a new field of CHB management was initiated by modulating the hosts’ immune system through immune therapy. This review will discuss the nature and design of innovative immune therapy for CHB.

Fat: Quality, or Quantity? What Matters Most for the Progression of Metabolic Associated Fatty Liver Disease (MAFLD)

Objectives: Lately, many countries have restricted or even banned transfat, and palm oil has become a preferred replacement for food manufacturers. Whether palm oil is potentially an unhealthy food mainly due to its high content of saturated Palmitic Acid (PA) is a matter of debate. The aim of this study was to test whether qualitative aspects of diet such as levels of PA and the fat source are risk factors for Metabolic Syndrome (MS) and Metabolic Associated Fatty Liver Disease (MAFLD). Methods: C57BL/6 male mice were fed for 14 weeks with three types of Western diet (WD): 1. LP-WD—low concentration of PA (main fat source—corn and soybean oils); 2. HP-WD—high concentration of PA (main fat source—palm oil); 3. HP-Trans-WD—high concentration of PA (mainly transfat). Results: All types of WD caused weight gain, adipocyte enlargement, hepatomegaly, lipid metabolism alterations, and steatohepatitis. Feeding with HP diets led to more prominent obesity, hypercholesterolemia, stronger hepatic injury, and fibrosis. Only the feeding with HP-Trans-WD resulted in glucose intolerance and elevation of serum transaminases. Brief withdrawal of WDs reversed MS and signs of MAFLD. However, mild hepatic inflammation was still detectable in HP groups. Conclusions: HP and HP-Trans-WD play a crucial role in the genesis of MS and MAFLD.

The Levels of Inhibitory Cytokines in the Serum of Patients with Hepatitis B and C

Hepatitis B and C Viruses (HBV dan HCV) can cause acute or chronic hepatitis that may develop into fibrosis, cirrhosis, and hepatocarcinoma. Previous studies have reported that hepatocyte damage is mainly due to overactive immune responses rather than viral infection. Cytokines are essential mediators in the immune response. This study aimed to determine the correlation between the levels of serum inhibitory cytokines, i.e., IL-4, IL-10, and TGF-β, and the development of liver disease in patients with hepatitis B and C. The levels of serum IL-4, IL-10, and TGF-β from 58 patients with hepatitis B or hepatitis C were determined by ELISA. The progression of liver disease is inferred from the levels of serum transaminases and the degree of liver fibrosis. Data were analyzed using the Spearman correlation test with a p-value of < 0.05 is considered statistically significant. This study showed no correlation between the levels of serum IL-4, IL-10, and TGF-β and the development of liver disease in patients with hepatitis B and C (p > 0.05). Therefore, cytokine testing using ELISA was unable to replace liver biopsy to assess liver disease progression in patients with hepatitis B and C.

Liver Involvement in Congenital Disorders of Glycosylation and Deglycosylation

Background: Congenital disorders of glycosylation (CDG) and NGLY1-CDDG (NGLY1-congenital disorder of deglycosylation) usually represent multisystem (especially neurovisceral) diseases with liver involvement reported in some of them. The aim of the study was to characterize the liver phenotype in CDG and NGLY1-CDDG patients hospitalized in our Institute, and to find the most specific features of liver disease among them.Material and Methods: The study involved 39 patients (from 35 families) with CDG, and two patients (from two families) with NGLY1-CDDG, confirmed molecularly, for whom detailed characteristics of liver involvement were available. They were enrolled based on the retrospective analysis of their medical records.Results: At the time of the first consultation, 13/32 patients were diagnosed with hepatomegaly; none of them with splenomegaly. As many as 23/32 persons had elevated serum transaminases, including 16 (70%) who had mildly elevated levels. During the long-term follow-up (available for 19 patients), serum transaminases normalized in 15/19 (79%) of them, including a spontaneous normalization in 12/15 (80%) of them. The GGT activity was observed to be normal in all study cases. Protein C, protein S and antithrombin activities in plasma were observed in 16 patients, and they were decreased in all of them.Conclusions: It is necessary to conduct a long-term follow-up of liver disease in CDG to obtain comprehensive data.

Hepatotoxic Manifestations of Arsenic Trioxide Loaded Poly (Lactide-co-Glycolide) Nanoparticles in Wistar Rat

Present study reports on the hepatotoxic manifestations of arsenic trioxide loaded poly lactide-co-glycolide nanoparticles (As2O3-PLGA- NPs) in rats. As2O3-PLGA- NPs enhances the activity of serum transaminases. As2O3-PLGA-NPs are potential inducer of lipid peroxidation in mitochondria as well as microsomes. Mitochondrial lipid peroxidation was higher than the microsomal lipid peroxidation. CYP450 2E1 was lower in the liver of As2O3-PLGA- NPs treated rats in comparison to arsenic trioxide treated rats. GSH showed lower values than control rats and arsenic trioxide treated rats. Glutathione-S-transferase inhibited by arsenic trioxide, non significant increase was recorded in the liver of As2O3-PLGA- NPs treated rats. As2O3-PLGA- NPs readily accumulates in liver and induces peculiar histopathological changes viz. intracytoplasmic/intranuclear inclusions and apoptosis. Since As2O3-PLGA- NPs are being considered as a suitable chemo-preventive agent against different types of cancer, its toxicological properties are of prime concern from bio-safety point of view. Thus, present observations seem to be important from human health risk assessment point of view.

Hepatotoxic manifestations of arsenic trioxide loaded poly (lactide-co-glycolide) nanoparticles in wistar rat

Present study reports on the hepatotoxic manifestations of arsenic trioxide loaded poly lactide-co-glycolide nanoparticles (As2O3-PLGA- NPs) in rats. As2O3-PLGA- NPs enhances the activity of serum transaminases. As2O3-PLGA-NPs are potential inducer of lipid peroxidation in mitochondria as well as microsomes. Mitochondrial lipid peroxidation was higher than the microsomal lipid peroxidation. CYP450 2E1 was lower in the liver of As2O3-PLGA- NPs treated rats in comparison to arsenic trioxide treated rats. GSH showed lower values than control rats and arsenic trioxide treated rats. Glutathione-S-transferase inhibited by arsenic trioxide, non significant increase was recorded in the liver of As2O3-PLGA- NPs treated rats. As2O3-PLGA- NPs readily accumulates in liver and induces peculiar histopathological changes viz. intracytoplasmic/intranuclear inclusions and apoptosis. Since As2O3-PLGA- NPs are being considered as a suitable chemo-preventive agent against different types of cancer, its toxicological properties are of prime concern from bio-safety point of view. Thus, present observations seem to be important from human health risk assessment point of view.

Hepatic Presentation of Late-Onset Multiple Acyl-CoA Dehydrogenase Deficiency (MADD): Case Report and Systematic Review

Diagnosis of pediatric steatohepatitis is a challenging issue due to a vast number of established and novel causes. Here, we report a child with Multiple Acyl-CoA Dehydrogenase Deficiency (MADD) presenting with an underrated muscle weakness, exercise intolerance and an atypically severe steatotic liver involvement. A systematic literature review of liver involvement in MADD was performed as well. Our patient is a 11-year-old otherwise healthy, non-obese, male child admitted for some weakness/asthenia, vomiting and recurrent severe hypertransaminasemia (aspartate and alanine aminotransferases up to ×20 times upper limit of normal). Hepatic ultrasound showed a bright liver. MRI detected mild lipid storage of thighs muscles. A liver biopsy showed a micro-macrovacuolar steatohepatitis with minimal fibrosis. Main causes of hypertransaminasemia were ruled out. Serum aminoacids (increased proline), acylcarnitines (increased C4-C18) and a large excretion of urinary glutaric acid, ethylmalonic, butyric, isobutyric, 2-methyl-butyric and isovaleric acids suggested a diagnosis of MADD. Serum acylcarnitines and urinary organic acids fluctuated overtime paralleling serum transaminases during periods of illness/catabolic stress, confirming their recurrent nature. Genetic testing confirmed the diagnosis [homozygous c.1658A &gt; G (p.Tyr553Cys) in exon 12 of the ETFDH gene]. Lipid-restricted diet and riboflavin treatment rapidly ameliorated symptoms, hepatic ultrasonography/enzymes, and metabolic profiles. Literature review (37 retrieved eligible studies, 283 patients) showed that liver is an extramuscular organ rarely involved in late-onset MADD (70 patients), and that amongst 45 patients who had fatty liver only nine had severe presentation.Conclusion: MADD is a disorder with a clinically heterogeneous phenotype. Our study suggests that MADD warrants consideration in the work-up of obesity-unrelated severe steatohepatitis.