Systemic Review on the Pathogenicity of Plasmodium berghei in the Liver and Spleen of the Experimental Mice

Malaria is still one of the most prevalent tropical and parasitic diseases throughout the world representing a global health concern. Even with all efforts to restrict disease transmission and national malaria control programs, malaria infection continues to cause considerable morbidity and mortality in resource-poor countries. Malaria infection occurs in two stages, the Exoerythrocytic and Erythrocytic stage. The exact biology of malaria parasite in human hosts is likely relatively similar, with the main differences being attributable to the human immune response, the number of previous infections and the exposure profile. The disease severity can be determined by the balance between the pro-inflammatory and anti-inflammatory cytokines. Although, research about the clinical characterization and histology of malaria has shown some information regarding the pathogenesis, the actual mechanisms by which malaria parasites produce severe disease, the immunity defends against infection is remained unknown. Studies in animal models can reveal details about the processes of severe malaria infection and human defense mechanisms. Because of its similarities to the Plasmodium species that cause human malaria, Plasmodium berghei is used as a model organism for the experimental research. In addition, of affecting the central nervous system, Plasmodium berghei infection in the Swiss Webster mouse causes systemic damage, and affects numerous organs including the liver and lymphoid organs. The infected spleen demonstrations includethe splenomegaly, re-modelling and other basic changes consist of the red pulp’s expansion, marginal zone’s slight damage, enlarged vasculature and the barrier cells activities. Moreover, the liver shows hyperplastic Kupffer cells, fatty change, portal tract inflammation, cholestasis, liver cell necrosis, sequestration of Parasitized Red Blood Cells (PRBCs) and deposition of hemozoin pigments.

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.

Mercury Kushta Induced Histopathological Changes in Liver of Wister Rats

Background: Heavy metals are the natural constituents of the earth's crust but the indiscriminate human activities have drastically effected their biochemical balance and geochemical cycles. Heavy metals and their compounds have pharmacological importance. These are being used in south Asian countries as component of different medicines. These medicines may have serious side effects on liver. Objectives: To see the histological changes of Kushta which contains mercury, on liver of wister rats. Material and Methods: It was an animal experimental study in which a total of 42 Wistar rats were included and divided into five exposed and one control groups. Morphological changes were observed in liver of rats by using indigenous as well as patent mercury preparations. Results: Morphological changes in liver of exposed rats included hepatocyte swelling, hepatocyte necrosis, hepatocyte apoptosis, disarray of hepatic architecture, development of portal tract inflammation, central vein congestion, sinusoidal congestion and dilatation, development of fatty change and damage to hepatic vascular and liver capsule were seen at the end of 8 weeks. Conclusions: Indigenous herbo-mineral preparation (Kushta) of mercury produces deleterious morphological effects on liver of wister rats. Keywords: Mercury Kushta, Liver, Histopathology

A real-world study evaluating ultrasound guided percutaneous non-targeted liver biopsy needle failures and pathology sample quality assessment in both end-cut and side-notch needles

Objectives: To determine biopsy device failures, causative factors, complications and sample quality of the 16G end-cut Biopince™ and side-notch Bard™ needles. Methods: All ultrasound-guided non-targeted liver biopsies between 01/01/2016 to 31/12/2018 were included. Operator, device, number of failures, complications and repeat biopsies were recorded. Histopathology samples were reviewed for all cases of needle failure and a group with no failures, and graded “yes/no” for presence of steatosis, inflammation and fibrosis. The pathology slides from these cases were reviewed to assess biopsy sample quality (length and portal tract number). The failure and no-failure groups were compared in terms of device type/ histology and sample quality was compared between the needle types. Results: 1004 patients were included. 93.8% (n = 942) required one needle pass to obtain a sample and 6.2% (n = 62) required >1 pass due to needle failure. Total of 76 needle failures, more with end-cut than side-notch needles (8.7% vs 2.9%) (p < 0.001). No needle failures resulted in complication. The presence of liver fibrosis was associated with fewer needle failures (p = 0.036). The major complication rate was 0.4% (4/1044). A biopsy with >10 portal tracts was obtained in 90.2% of specimens > 20 mm long, compared with 66% of 16–20 mm biopsies and 21% of <16 mm biopsies. The target of >10 portal tracts was achieved in 10/26 (38.5%) of side-notch biopsies and 64/90 (71.1%) of end-cut biopsies (p = 0.004). Conclusion: Ultrasound-guided liver biopsy is safe and sample quality is consistently good when a core >20 mm long is obtained. The end-cut biopsy device generated reliably good quality biopsy samples, however the needle failure rate was significantly higher than the side-cut needle. Advances in knowledge: Ultrasound guided liver biopsy specimen quality is consistently good when a core >20 mm long is obtained which can be achieved with a single pass using the 16G BiopinceTM end-cut needle, although the needle failure rate is significantly higher than the 16G Max-Core™ Bard™ side-notch needle.

Congenital hepatic fibrosis with novel mutations in PKD1 gene masquerading as early cryptogenic cirrhosis: a rare case report

Background Congenital hepatic fibrosis (CHF) is a rare disorder of the porto-biliary system occurring due to the defective remodeling of ductal architecture leading to progressive fibrosis of the portal tract. Though classically, CHF has been reported to be associated with autosomal recessive polycystic kidney disease (ARPKD), there have been only a few reports associating CHF with autosomal dominant polycystic kidney disease (ADPKD). Also, there is a lack of proper sequencing panels and gene database covering CHF-related genes in the medical literature. CHF often presents with features of portal hypertension without overt signs or symptoms of liver disease. However, often due to lack of awareness among radiologists and physicians, such cases might get labeled as early stage of cryptogenic cirrhosis. Case presentation Here, we report a 17-year-old boy who presented with a portal hypertensive bleed. Though initially an early phase of cirrhosis was suspected, no identifiable cause was found. Though he had grade IV esophageal varices, the liver function was absolutely normal with no signs of liver failure. This further leads to subsequent cross-sectional imagings which lead to the diagnosis of CHF. Further genetic analysis revealed it to be a rare case of CHF associated with ADPKD, with some novel mutations in the PKD1 gene. Conclusion CHF is a rare disorder needing a high index of suspicion and awareness. The presence of classic radiological morphological features of left lobe hypertrophy and right lobe atrophy with the tell-tale histopathological findings, fibrous enlargement of the portal tract, and irregularly shaped proliferating bile ducts often clinches the diagnosis.

Effects of samin yogurt on the liver of adult wistar rats

Background: Yogurt is basically fermented milk that is heated and mixed with two types of body friendly bacteria. It is very nutritious and therefore, it is being eaten by all and sundry. Purpose: The study was designed to determine the effect of yogurt on the liver of adult Wister rats. Method: A total of twenty four adzult Wister rats bred and harboured at the animal house of Anatomy and Neurobiology department, Imo State University Owerri were used for the study. The rats which weighed between 180 and 220 grammes were separated and housed in four different cages marked A, B, C and D. Each cage contained four rats. The group A served as control group and so received only the normal rat feed and water. Group B rats were administered 2500mg/kg body weight of yogurt; group C received 5000mg/kg body weight of yogurt why group D was given 10000mg/kg body weight of yogurt, all through oral intubation for four weeks. At the end of the four week treatment, the rats were anesthetized in chloroform vapour and the liver was dissected out for histological investigations. Results: On examining the processed liver tissue, it was observed that there was a mild (for group B), moderate (for group C), and serve (for group D) lymphocyte infiltration on the liver portal tract when compared to the control group which showed very little presence of haepatocytes around a central venule. The effect observed could be described to be dose dependent.

Intrahepatic distribution of nerve fibers and alterations due to fibrosis in diseased liver

Autonomic nerve fibers in the liver are distributed along the portal tract, being involved in the regulation of blood flow, bile secretion and hepatic metabolism, thus contributing to systemic homeostasis. The present study investigated changes in hepatic nerve fibers in liver biopsy specimens from patients with normal liver, viral hepatitis and non-alcoholic steatohepatitis, in relation to clinical background. The areal ratio of nerve fibers to the total portal area was automatically calculated for each sample. The nerve fiber areal ratios (NFAR) for total nerve fibers and sympathetic nerve fibers were significantly lower in liver affected by chronic hepatitis, particularly viral hepatitis, and this was also the case for advanced liver fibrosis. However, the degree of inflammatory activity did not affect NFAR for either whole nerves or sympathetic nerves. Comparison of samples obtained before and after antiviral treatment for HCV demonstrated recovery of NFAR along with improvement of liver fibrosis.

Bile Acids and GPBAR-1: Dynamic Interaction Involving Genes, Environment and Gut Microbiome

Bile acids (BA) are amphiphilic molecules synthesized in the liver from cholesterol. BA undergo continuous enterohepatic recycling through intestinal biotransformation by gut microbiome and reabsorption into the portal tract for uptake by hepatocytes. BA are detergent molecules aiding the digestion and absorption of dietary fat and fat-soluble vitamins, but also act as important signaling molecules via the nuclear receptor, farnesoid X receptor (FXR), and the membrane-associated G protein-coupled bile acid receptor 1 (GPBAR-1) in the distal intestine, liver and extra hepatic tissues. The hydrophilic-hydrophobic balance of the BA pool is finely regulated to prevent BA overload and liver injury. By contrast, hydrophilic BA can be hepatoprotective. The ultimate effects of BA-mediated activation of GPBAR-1 is poorly understood, but this receptor may play a role in protecting the remnant liver and in maintaining biliary homeostasis. In addition, GPBAR-1 acts on pathways involved in inflammation, biliary epithelial barrier permeability, BA pool hydrophobicity, and sinusoidal blood flow. Recent evidence suggests that environmental factors influence GPBAR-1 gene expression. Thus, targeting GPBAR-1 might improve liver protection, facilitating beneficial metabolic effects through primary prevention measures. Here, we discuss the complex pathways linked to BA effects, signaling properties of the GPBAR-1, mechanisms of liver damage, gene-environment interactions, and therapeutic aspects.

Evaluation of Visual Examination of Stool as A Screening Test for Infant with Prolonged Neonatal Cholestasis Namely Biliary Atresia

Introduction: Neonatal cholestasis is a hepatobiliay disease characterized by biliary obstruction in the neonatal period. Biochemically it is evidenced by prolonged elevation of serum conjugated bilirubin beyond the first 14 days of life.1 Most common causes are biliary atresia and idiopathic neonatal hepatitis.3, 4 Objective: To evaluate stool color as a screening test by visual inspection in infants with prolonged neonatal cholestasis. Methodology: This was a cross-sectional analytic study, conducted in Pediatric Gastroenterology and Nutrition Department,BSMMU, Dhaka, from 3 September 2012 to 3 February 2013 about 6 month duration. Statistically calculated 38 infants with prolonged neonatal direct hyperbilirubinaemia beyond their 14 days of age were included in this study. Results: The mean age of the subjects was 62.3 days with a standard deviation (SD) ±13.7 days. Male to female ratio was 1.2:1. All (100%) the subjects were icteric and hepatomegaly was found in 94.7% subjects. Dark urine (84.2%), pale stool (78.5%), bleeding manifestations (31.8%) and infection (29%) were also observed. Thirty (78.5%) subjects had pale colored stool. Mean (± SD) albumin and conjugated bilirubin levels were 3.68 (±1.88)gm/dl and 5.29 (±1.31)mg/dl respectively. ALT and GGT level of the study subjects were 346.19±124.28 u/dl and 315±198.91 u/l respectively. Common ultrasonographic findings of the patients were non visualization of gallbladder 60.5%, non-visualization of common bileduct 50%, hepatomegaly 92.1%, and triangular cord sign in portahepatis 7.9%. Scintigraphy revealed impaired excretion into intestine 88.9% in majority of the subjects. Liver biopsy revealed liver architecture was preseved 65.8% bile duct proliferation 52.6%, regenarating nodule was absent 65.8% gaint cell was present 52.6% portal tract inflammation was found in 47.4%. Sensitivity of stool color in the diagnosis of neonatal cholestasis was found 90.6%, specificity 83.3%, accuracy 89.5%, positive predictive value 96.7% and negative predictive value 62.5%. Conclusion: It can be concluded that stool color might be reliable indicator for screening of prolonged neonatal cholestasis namely biliary atresia. J Bangladesh Coll Phys Surg 2021; 39(1): 46-52

Interobserver study on histologic features of idiopathic non-cirrhotic portal hypertension

Background Histologic features of idiopathic non-cirrhotic portal hypertension (INCPH) may overlap with those without INCPH. Recently, these features have been recognized as part of the larger spectrum of porto-sinusoidal vascular disease (PSVD). We assessed interobserver agreement on histologic features that are commonly associated with INCPH and studied whether a provision of relevant clinical history improves interobserver agreement. Methods The examined histologic features include lobular (such as anisocytosis, nodular regeneration, sinusoidal dilatation, increased parenchymal draining veins, and incomplete fibrous septa) and portal tract changes (such as paraportal shunting vessel(s), portal tract remnant, increased number of portal vessels, and obliterative portal venopathy). Thirty-four archived liver samples from patients with (group A) and without (group B) INCPH were retrieved. A total of 90 representative images of lobules (L) and portal tracts (P) were distributed among 9 liver pathologists blinded to true clinical history. Each pathologist answered multiple choice questions based on the absence (Q1) or presence (Q2) of clinical history of portal hypertension. Fleiss’ kappa coefficient analysis (unweighted) was performed to assess interobserver agreement on normal versus abnormal diagnosis, in L and P, based on Q1 and Q2. Results The kappa values regarding normal versus abnormal diagnosis were 0.24, 0.24, 0.18 and 0.18 for L-Q1, L-Q2, P-Q1, and P-Q2, respectively. With true clinical history provided, the kappa values were L- 0.32, P-0.17 for group A and L-0.12, P-0.14 for group B. Four pathologists changed their assessments based on the provided history. Interobserver agreement on the interpretation of L and P as normal versus abnormal was slight to fair regardless of provision of clinical history. Conclusions Our findings indicate that the histologic features of INCPH/PSVD are not limited to patients with portal hypertension and are subject to significant interobserver variation.