Reticuloendothelial activation and phenotypic alteration of peripheral monocytes with enhanced liver recruitment drive liver injury secondary to yellow phosphorus.

Background And Aim: Monocytes and macrophages play a crucial role in the pathogenesis of acute liver failure (ALF). We aimed to study reticuloendothelial activation and its correlation with disease severity in commonly encountered yellow phosphorus (rodenticide)-induced hepatotoxicity patients. We also studied peripheral monocyte phenotype in a subset of patients.

Improving Transplant-free Survival With Low-volume Plasma Exchange to Treat Children With Rodenticide Induced Hepatotoxicity.

Background: In a prior report, no patient with rodenticidal hepatotoxicity who met Kochi criteria (MELD score ≥36 or baseline INR ≥6 with hepatic encephalopathy) (PMID: 26310868) for urgent liver transplantation survived with medical management alone. Plasma exchange (PLEX) may improve survival in these patients.

Objectives: We describe our experience with low-volume PLEX (PLEX-LV) in treating rodenticide ingestion induced hepatotoxicity in children.

Low Volume Plasma Exchange and Low Dose Steroid Improve Survival in Patients With Alcohol-Related Acute on Chronic Liver Failure and Severe Alcoholic Hepatitis - Preliminary Experience.

Background: Alcohol-related acute on chronic liver failure (A-ACLF) patients have high short-term mortality and are poor candidates for steroid therapy. Plasma exchange (PLEX) improves survival in ACLF patients. We analyzed our experience with low volume PLEX (50% of plasma volume exchanged per session) and low dose steroids to treat A-ACLF patients.

Exocrine Pancreatic Insufficiency Following Gastric Resectional Surgery-is Routine Pancreatic Enzyme Replacement Therapy Necessary?

The data on exocrine pancreatic insufficiency (EPI) following gastric resectional surgery is variable, ranging from 26% to as high as 100%. This study aimed to document symptomatic EPI following gastric resectional surgery and to objectively document EPI, by fecal elastase (FE) testing. This was a cross-sectional study among patients undergoing gastric resection for adenocarcinoma of the stomach, at the Upper Gastrointestinal Surgical Unit at the Christian Medical College Hospital, Vellore, India.

Reticuloendothelial activation correlates with disease severity and predicts mortality in severe alcoholic hepatitis.

Background: Overactivation of reticuloendothelial cells lining liver sinusoids - Kupffer cells (macrophages) and sinusoidal endothelial cells - may narrow the sinusoidal lumen, impair perfusion in liver microcirculation and contribute to disease severity in alcoholic hepatitis.

Aim: The aim of the article was to assess reticuloendothelial activation in patients with severe alcoholic hepatitis (SAH).

Methods: In SAH patients, we prospectively studied baseline reticuloendothelial activation markers [serum ferritin, sCD163 and plasma von Willebrand factor (VWF) antigen] and Macrophage Activation Syndrome (MAS) criteria, correlated them with disease severity scores [model for end-stage liver disease (MELD) and Sequential Organ Failure Assessment (SOFA) scores] and analyzed their ability to predict survival over a 90-day follow-up period.

Clinical Evaluation of a Polyherbal Nutritional Supplement in Dyslipidemic Volunteers.

Ten important plant parts routinely used in South Indian ethnic food preparation as spices and condiments were investigated for their potential antidyslipidemic properties. The aim of the study was to characterize the biochemical properties of the polyherbal formulation (nutritional supplement) and evaluate its use to control dyslipidemia in patients. Phytochemical evaluation, in vitro α-amylase inhibitory assay, and high performance thin layer chromatography (HPTLC) fingerprinting were carried out with alcoholic extracts of all 10 individual plants and with the nutritional supplement.

Plasma hydrogen sulphide does not predict severity of acute pancreatitis in humans.

The primary aim of this study was to assess the usefulness of plasma hydrogen sulphide (HS) level at admission as a predictor of severity of acute pancreatitis. The secondary aims were to examine whether the level of HS after 48 h correlated with severity and whether level of HS correlated with pulmonary, renal or infectious complications. Plasma hydrogen sulphide was measured within 24 h of admission and 48 h later, in patients with acute pancreatitis.

Pregnancy-related liver disorders.

Pregnancy-related liver disorders accounted for 8% of all maternal deaths at our center from 1999 to 2011. Of the three pregnancy-related liver disorders (acute fatty liver of pregnancy (AFLP), HELLP (Hemolysis, elevated liver enzymes, low platelets) syndrome and pre-eclamptic liver dysfunction, which can lead to adverse maternal and fetal outcome, AFLP is most typically under - diagnosed. Risk of maternal death can be minimised by timely recognition and early/aggressive multi-specialty management of these conditions.

Retinoid metabolism in the small intestine during development of liver cirrhosis.

Background And Aims: Retinoids are important mediators of cellular differentiation and proliferation in various epithelia of the body including the small intestine. Though alterations in intestinal epithelial cell proliferation have been noted in liver cirrhosis, mechanisms involved in the process are not well understood. This study examined the levels of various retinoids and retinoid-metabolizing enzymes in the small intestine during development of liver cirrhosis.

Curcumin attenuates indomethacin-induced oxidative stress and mitochondrial dysfunction.

Oxidative stress and mitochondrial dysfunction have been implicated in the pathogenesis of indomethacin-induced enteropathy. We evaluated the potential of curcumin, a known cytoprotectant, as an agent to protect against such effects. Rats were pretreated with curcumin (40 mg/kg by intra-peritoneal injection) before administration of indomethacin (20 mg/kg by gavage).

Spontaneous bacterial peritonitis results in oxidative and nitrosative stress in ascitic fluid.

Background And Aim: Spontaneous bacterial peritonitis (SBP) is a major complication of liver cirrhosis and accounts for significant mortality. Although oxygen free radicals and nitric oxide been implicated in the pathophysiology of liver cirrhosis, information on their role during the development of SBP is scarce. This study examined these active species in ascitic fluid from patients with SBP, and in response to treatment.

Oxidative stress in experimental liver microvesicular steatosis: role of mitochondria and peroxisomes.

Background: Hepatic microvesicular steatosis is a clinical manifestation seen in a number of liver diseases. Although the role of mitochondrial beta-oxidation in the development of the disease has been well studied, information on lipid peroxidative damage in liver subcellular organelles is scarce. The present study looked at oxidative stress in hepatic peroxisomes and microsomes in microvesicular steatosis, using an animal model of the disease.

Renal damage in experimentally-induced cirrhosis in rats: Role of oxygen free radicals.

Cirrhosis with ascites is associated with impaired renal function accompanied by sodium and water retention. Although it has been suggested that mediators such as nitric oxide play a role in the development of renal failure in this situation, other mechanisms underlying the process are not well understood. This study examined the role of oxidative stress in mediating renal damage during the development of cirrhosis in order to understand mechanisms involved in the process.

Oxidative stress in the development of liver cirrhosis: a comparison of two different experimental models.

Background/aims: Oxidative stress has been implicated in liver cirrhosis. Carbon tetrachloride and thioacetamide are the most widely used models to develop cirrhosis in rats and the present study compares oxidative stress in the liver induced by these compounds at different stages of cirrhosis development.

Methods: Twice-weekly intragastric or intraperitoneal administration of carbon tetrachloride or thioacetamide, respectively, produced liver cirrhosis after 3 months.

Mild whole-body heat stress alters retinoid metabolism in the rat small intestine.

Mild heat treatment can modulate metabolism and prevent stress-induced alterations in cells and tissues. Retinoids are known to influence cellular metabolism and are essential for growth and differentiation, particularly of epithelial tissue. This study examines the effect of mild heat treatment on retinoid alterations in enterocytes in the rat small intestine.

Alterations in the intestinal glycocalyx and bacterial flora in response to oral indomethacin.

Nonsteroidal anti-inflammatory drugs (NSAIDs), used extensively in clinical medicine, tend to cause adverse effects in the gastrointestinal tract. Earlier work has shown that oral administration of indomethacin produced oxidative damage in the small intestine and attenuation of the glycocalyx layer of the mucosa. The present study assessed, in greater detail, the alterations produced in the glycocalyx of rat small intestinal mucosa in response to indomethacin, with specific reference to surfactant-like particles (SLP) and brush border membranes (BBM).

Retinoid metabolism in the rat small intestine.

Vitamin A (retinol) is essential for epithelial cell growth, differentiation and proliferation. The absorption of retinol occurs in the small intestine, and the metabolism of this vitamin is not well studied in this organ. The intestinal epithelium has a high rate of cell proliferation and differentiation, and the present study looked at the level of retinoids and metabolizing enzymes involved in their interconversion along the villus-crypt axis under normal conditions.

Surgical manipulation of the intestine results in quantitative and qualitative alterations in luminal Escherichia coli.

Objectives: To look at the qualitative and quantitative changes in the luminal bacterial flora in response to surgical manipulation of the small intestine.

Summary Background Data: The barrier function of the intestine is compromised in pathologic conditions, such as shock, trauma, or surgical stress. Our earlier work has shown that surgical manipulation results in oxidative stress in the intestinal mucosa leading to permeability alterations.

Oral glutamine attenuates indomethacin-induced small intestinal damage.

The use of NSAIDs (non-steroidal anti-inflammatory drugs), although of great therapeutic value clinically, is limited by their tendency to cause mucosal damage in the gastrointestinal tract. In the small intestine, the effects these drugs have been shown to produce include inhibition of cyclo-oxygenase, mitochondrial dysfunction and free radical-induced oxidative changes, all of which contribute to the mucosal damage seen. Glutamine is a fuel preferentially used by enterocytes and is known to contribute to maintaining the integrity of these cells.

Indomethacin-induced renal damage: role of oxygen free radicals.

Nonsteroidal anti-inflammatory drugs are used extensively in clinical medicine. In spite of their therapeutic utility, however, they are known to cause significant gastrointestinal and renal toxicities, circumstances that limit their use. The side effects produced in these organs have been attributed mainly to the inhibitory effect of these drugs on the activity of cyclooxygenase, a key enzyme in prostaglandin synthesis.

Role of intestine in postsurgical complications: involvement of free radicals.

Surgery at any location in the body leads to surgical stress response and alterations in normal body homeostasis. The intestine is extremely sensitive to surgical stress even at remote locations and the gastrointestinal tract plays an important role in the development of postsurgical complications such as sepsis, the systemic immune response syndrome (SIRS), and multiple organ failure syndrome (MOFS). The generation of free radicals and subsequent biochemical alterations at the cellular and subcellular level in the intestine has been suggested to play an important role in this process.

Indomethacin-induced free radical-mediated changes in the intestinal brush border membranes.

Nonsteroidal anti-inflammatory drugs (NSAIDs) cause small intestinal damage but the pathogenesis of this toxicity is not well established. Our earlier work has shown that villus enterocytes are most susceptible to the effects of indomethacin, a commonly used NSAID. This study looked at the acute effect of indomethacin on brush border membranes (BBM), which are present mainly in the villus cells and are in immediate contact with the contents of the small intestinal lumen.

Indomethacin-induced mitochondrial dysfunction and oxidative stress in villus enterocytes.

Nonsteroidal anti-inflammatory drugs (NSAIDs) are known to cause small intestinal damage but the pathogenesis of this toxicity is not well established. Intestinal epithelial cells are thought to be affected by these drugs in the course of their absorption. These cells are of different types, viz.

Intestinal mucosal alterations in experimental cirrhosis in the rat: role of oxygen free radicals.

Cirrhosis is associated with altered gastrointestinal function, and bacterial translocation from the gut plays an important role in the etiology of spontaneous bacterial peritonitis (SBP) seen in this condition. Although alterations in gut motility and intestinal permeability are recognized in cirrhosis, the intestinal damage at the cellular and subcellular levels is not well understood. This study looked at the mucosal alterations in experimental cirrhosis and the role of oxygen free radicals in this process.