Elevated Serum Transaminase Levels Research Articles

Correlation Between Serum Transaminase Levels and Estimated Glomerular Filtration Rate After Living-Donor Kidney Transplantation

BackgroundThere is a risk of hypoperfusion during kidney transplantation surgery owing to patients’ underlying disease and ischemia-reperfusion injury; further, hypoperfusion may cause injury to major organs. We hypothesized that the decrease in blood pressure after ischemia-reperfusion injury during kidney transplantation may be associated with indicators of liver injury and kidney graft function. MethodsData regarding living-donor kidney transplantations performed at our institution between 2018 and 2022 were retrospectively evaluated. Exclusion criteria included pediatric recipients or donors aged <18 years, multiple organ transplantation, and elevated postoperative serum transaminase levels. Correlations among blood pressure, serum transaminase levels on postoperative days 3 to 5, and estimated glomerular filtration rate (eGFR) on postoperative days 7 and 14 were analyzed. Further, a subgroup analysis was performed based on eGFR. ResultsA total of 276 patients were included in the final analysis. Serum transaminase levels were significantly negatively correlated with eGFR (partial correlation coefficient—0.26, P < .001). The postreperfusion decrease in blood pressure was not correlated with serum transaminase levels. However, the postreperfusion decrease in blood pressure and baseline blood pressure correlated with the eGFR (partial correlation coefficient = −0.18, P = .004). ConclusionThese findings indicate a correlation between intraoperative liver injury and kidney graft function, suggesting the importance of intraoperative management of organ perfusion. Since postreperfusion blood pressure changes did not significantly correlate with liver injury indicators, it is important to consider other causative factors for hypoperfusion in major organs during living-donor kidney transplantation, including microcirculatory failure and organ congestion-related ischemia/reperfusion.

Single-cell transcriptomics reveal the microenvironment landscape of perfluorooctane sulfonate-induced liver injury in female mice

Epidemic and animal studies have reported that perfluoroalkyl and polyfluoroalkyl substances (PFASs) are strongly associated with liver injury; however, to date, the effects of PFASs on the hepatic microenvironment remain largely unknown. In this study, we established perfluorooctane sulfonic acid (PFOS)–induced liver injury models by providing male and female C57BL/6 mice with water containing PFOS at varying doses for 4 weeks. Hematoxylin and eosin staining revealed that PFOS induced liver injury in both sexes. Elevated levels of serum aminotransferases including those of alanine aminotransferase and aspartate transaminase were detected in the serum of mice treated with PFOS. Female mice exhibited more severe liver injury than male mice. We collected the livers from female mice and performed single-cell RNA sequencing. In total, 36,529 cells were included and grouped into 10 major cell types: B cells, granulocytes, T cells, NK cells, monocytes, dendritic cells, macrophages, endothelial cells, fibroblasts, and hepatocytes. Osteoclast differentiation was upregulated and the T cell receptor signaling pathway was significantly downregulated in PFOS-treated livers. Further analyses revealed that among immune cell clusters in PFOS-treated livers, Tcf7+CD4+T cells were predominantly downregulated, whereas conventional dendritic cells and macrophages were upregulated. Among the fibroblast subpopulations, hepatic stellate cells were significantly enriched in PFOS-treated female mice. CellphoneDB analysis suggested that fibroblasts interact closely with endothelial cells. The major ligand–receptor pairs between fibroblasts and endothelial cells in PFOS-treated livers were Dpp4_Cxcl12, Ackr3_Cxcl12, and Flt1_complex_Vegfa. These genes are associated with directing cell migration and angiogenesis. Our study provides a general framework for understanding the microenvironment in the livers of female mice exposed to PFOS at the single-cell level.

RAMP1 Protects Hepatocytes against Ischemia-reperfusion Injury by Inhibiting the ERK/YAP Pathway.

Hepatic ischemia-reperfusion injury (HIRI) is a prevalent complication of liver transplantation, partial hepatectomy, and severe infection, necessitating the development of more effective clinical strategies. Receptor activity-modifying protein 1 (RAMP1), a member of the G protein-coupled receptor adapter family, has been implicated in numerous physiological and pathological processes. The study aimed to investigate the pathogenesis of RAMP1 in HIRI. We established a 70% liver ischemia-reperfusion model in RAMP1 knockout (KO) and wild-type mice. Liver and blood samples were collected after 0, 6, and 24 h of hypoxia/reperfusion. Liver histological and serological analyses were performed to evaluate liver damage. We also conducted in-vitro and in-vivo experiments to explore the molecular mechanism underlying RAMP1 function. Liver injury was exacerbated in RAMP1-KO mice compared with the sham group, as evidenced by increased cell death and elevated serum transaminase and inflammation levels. HIRI was promoted in RAMP1-KO mice via the induction of hepatocyte apoptosis and inhibition of proliferation. The absence of RAMP1 led to increased activation of the extracellular signal-regulated kinase (ERK)/mitogen-activated protein kinase (MAPK) pathway and yes-associated protein (YAP) phosphorylation, ultimately promoting apoptosis. SCH772984, an ERK/MAPK phosphorylation inhibitor, and PY-60, a YAP phosphorylation inhibitor, reduced apoptosis in in-vitro and in-vivo experiments. Our findings suggest that RAMP1 protects against HIRI by inhibiting ERK and YAP phosphorylation signal transduction, highlighting its potential as a therapeutic target for HIRI and providing a new avenue for intervention.

Ginsenoside Rk2, a dehydroprotopanaxadiol saponin, alleviates alcoholic liver disease via regulating NLRP3 and NLRP6 inflammasome signaling pathways in mice

Heavy alcohol consumption results in alcoholic liver disease (ALD) with inadequate therapeutic options. Here, we first report the potential beneficial effects of ginsenoside Rk2 (Rk2), a rare dehydroprotopanaxadiol saponin isolated from streamed ginseng, against alcoholic liver injury in mice. Chronic-plus-single-binge ethanol feeding caused severe liver injury, as manifested by significantly elevated serum aminotransferase levels, hepatic histological changes, increased lipid accumulation, oxidative stress, and inflammation in the liver. These deleterious effects were alleviated by the treatment with Rk2 (5 and 30 mg/kg). Acting as an nucleotide-binding oligomerization domain-like receptor family pyrin domain-containing 3 (NLRP3) inhibitor, Rk2 ameliorates alcohol-induced liver inflammation by inhibiting NLRP3 inflammasome signaling in the liver. Meanwhile, the treatment with Rk2 alleviated the alcohol-induced intestinal barrier dysfunction via enhancing NLRP6 inflammasome in the intestine. Our findings indicate that Rk2 is a promising agent for the prevention and treatment of ALD and other NLPR3-driven diseases.

Essential Involvement of Neutrophil Elastase in Acute Acetaminophen Hepatotoxicity Using BALB/c Mice.

Intense neutrophil infiltration into the liver is a characteristic of acetaminophen-induced acute liver injury. Neutrophil elastase is released by neutrophils during inflammation. To elucidate the involvement of neutrophil elastase in acetaminophen-induced liver injury, we investigated the efficacy of a potent and specific neutrophil elastase inhibitor, sivelestat, in mice with acetaminophen-induced acute liver injury. Intraperitoneal administration of 750 mg/kg of acetaminophen caused severe liver damage, such as elevated serum transaminase levels, centrilobular hepatic necrosis, and neutrophil infiltration, with approximately 50% mortality in BALB/c mice within 48 h of administration. However, in mice treated with sivelestat 30 min after the acetaminophen challenge, all mice survived, with reduced serum transaminase elevation and diminished hepatic necrosis. In addition, mice treated with sivelestat had reduced NOS-II expression and hepatic neutrophil infiltration after the acetaminophen challenge. Furthermore, treatment with sivelestat at 3 h after the acetaminophen challenge significantly improved survival. These findings indicate a new clinical application for sivelestat in the treatment of acetaminophen-induced liver failure through mechanisms involving the regulation of neutrophil migration and NO production.

LIVER TRANSAMINASES AND PLATELET COUNT CORRELATION IN DENGUE PATIENTS FROM TERTIARY CARE HOSPITAL

Background: Dengue is the arboviral febrile illness, which affects the vascular, muscular, and hematological systems. One of the standards used by WHO recommendations as a possible predictor of the clinical severity of infection is thrombocytopenia. A well-known aspect of dengue illness that is accompanied by hepatomegaly and elevated serum transaminase levels is hepatic dysfunction. This study's objective was to determine the liver's con Objective: tribution to dengue infection during the severity of dengue infection by comparing platelet counts and liver transaminase enzyme levels in a tertiary care facility. Admitted cases of Dengue fever (dengue serology positive –IgM) Method: were divided into 3 groups: DF, DHF, DSS based on the clinical and laboratory finding and relation of aminotransferases level were analyzed. Elevation in LFTs were co-related with DF, DHF, DSS. Result: In DF there was 7% patients having mild platelets and 93% patients having moderate platelets. In DHF, 7.4% patients had mild platelets, 70.4% having moderate and 22.2% had severe platelets. In DSS 79.3% patients had moderate platelets and 20.7% had severe platelets. The association was found significant. Transaminase levels rise in nearly all dengue cases, according t Conclusion: o our study's findings. Since AST and ALT levels are negatively correlated, an increase in dengue severity is accompanied by an increase in AST and ALT levels, and decrease in platelet count.

A Prospective Study on Clinical and Laboratory Predictive Markers of Dengue Fever in Children in Tertiary Care Hospital

Background: Dengue fever is the world's fastest-spreading mosquitoborne viral disease, with a 30-fold increase in global incidence over the last five decades. It is a major public health concern throughout the world's tropical and subtropical regions. 1 Dengue is classified into Dengue +/- warning signs and severe dengue, which includes Dengue shock syndrome, Respiratory distress syndrome, Dengue hemorrhagic fever, and organ failure, according to WHO 2012 guidelines. Material &amp; Methods : Study Design: Prospective Hospital based observational study. Study area: Department of Paediatrics, Siddhartha Medical College, Vijayawada, Andhra Pradesh. Study Period: 1 year. Study population: All children under the age of 13 years who had acute onset high grade fever and were Nonstructural antigen protein 1 [NS1] and/or Immunoglobulin M [IgM] positive were admitted to the paediatric ward. Sample size: study consisted a total of 150 cases. Sampling method: Purposive sampling technique on consecutive cases. The following laboratory test cut-off values are defined: leucopenia (white blood cell count &lt; 4000/mm3), thrombocytopenia (platelet count &lt; 150 103/mm3). Prolonged activated partial thromboplastin time (APTT) (&gt; 38 sec), elevated serum aminotransferase levels (AST or ALT &gt;39 U/L), and low C-reactive protein (CRP) (20 mg/L). The study compared clinical and laboratory parameters in dengue fever, dengue fever with warning signs, and severe dengue. Result: Several laboratory parameters were measured as predictors of laboratory- confirmed dengue infections. The positive predictive value of WBC was 80.6%, and NPV of 50% to differentiate the severity of three dengue groups. Whereas, PPV of platelet count was 90.8%, and NPV of platelet count was 50% to differentiate the severity of dengue groups. Conclusion: Our research discovered that a combination of commonly used blood tests, such as a white blood cell count, platelet count, liver function tests, and CRP and coagulation profiles, can help detect laboratory-confirmed dengue infection. These clinical and laboratory findings could be used as predictive markers to improve the early detection and severity of dengue infection.

Association between COVID-19 and chronic liver disease: Mechanism, diagnosis, damage, and treatment.

As the outbreak evolves, our understanding of the consequences of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection and the resulting coronavirus disease 2019 (COVID-19) on the liver has grown. In this review, we discussed the hepatotropic nature of SARS-CoV-2 and described the distribution of receptors for SARS-CoV-2 (e.g., angiotensin-converting enzyme 2) in the vascular endothelium and cholangiocytes of the liver. Also, we proposed mechanisms for possible viral entry that mediate liver injury, such as liver fibrosis. Due to SARS-CoV-2-induced liver damage, many COVID-19 patients develop liver dysfunction, mainly characterized by moderately elevated serum aminotransferase levels. Patients with chronic liver disease (CLD), such as cirrhosis, hepatocellular carcinoma, nonalcoholic fatty liver disease, and viral hepatitis, are also sensitive to SARS-CoV-2 infection. We discussed the longer disease duration and higher mortality following SARS-CoV-2 infection in CLD patients. Correspondingly, relevant risk factors and possible mechanisms were proposed, including cirrhosis-related immune dysfunction and liver deco-mpensation. Finally, we discussed the potential hepatotoxicity of COVID-19-related vaccines and drugs, which influence the treatment of CLD patients with SARS-CoV-2 infection. In addition, we suggested that COVID-19 vaccines in terms of immunogenicity, duration of protection, and long-term safety for CLD patients need to be further researched. The diagnosis and treatment for liver injury caused by COVID-19 were also analyzed in this review.

New murine model of alcoholic hepatitis in obesity-induced metabolic-associated fatty liver disease.

Metabolic-associated fatty liver disease (MAFLD) and alcoholic hepatitis (AH) are among the most prevalent liver diseases worldwide, and their coexistence is common in clinical practice. However, currently established models of MAFLD-AH coexistence do not fully replicate their pathological characteristics and require sophisticated experimental techniques. Therefore, we aimed to develop an easily replicable model that mimics obesity-induced MAFLD-AH in patients. Our goal was to establish a murine model that replicates MAFLD and AH coexistence, resulting in significant liver injury and inflammation. To this end, we administered a single ethanol gavage dose to ob/ob mice on a chow diet. The administration of a single dose of ethanol led to elevated serum transaminase levels, increased liver steatosis, and apoptosis in ob/ob mice. Furthermore, ethanol binge caused a significant increase in oxidative stress in ob/ob mice, as measured via 4-hydroxynonenal. Importantly, the single dose of ethanol also markedly exacerbated liver neutrophil infiltration and upregulated the hepatic mRNA expression of several chemokines and neutrophil-related proteins, including Cxcl1, Cxcl2, and Lcn2. Whole-liver transcriptomic analysis revealed that ethanol-induced changes in gene expression profile shared similar features with AH and MAFLD. In ob/ob mice, a single dose of ethanol binge caused significant liver injury and neutrophil infiltration. This easy-to-replicate murine model successfully mimics the pathological and clinical features of patients with coexisting MAFLD and AH and closely resembles the transcriptional regulation seen in human disease.

Effect of Intrahepatic Cholestasis of Pregnancy (ICP) on Neonatal Outcome

Intrahepatic cholestasis of pregnancy is a condition unique to pregnancy characterized by pruritus and elevated serum bile acids and/or aminotransferase levels. It usually manifests during second or third trimester of pregnancy and improves after delivery. But neonates are at increased risks of still birth, prematurity, respiratory distress syndrome and metabolic problems. Timely identification and appropriate intervention can reduce the adverse neonatal outcomes.&#x0D; DS (Child) H J 2021; 37(2): 135-139

Hepatic Transaminases in Patients with Type-2 Diabetes Mellitus: Cross-Sectional, Analytic Study

The risk of chronic liver disease is higher in patient with type 2 diabetes than general population. Raised serum transaminases levels are a sensitive indicator of liver cell injury. This study was performed to estimate the prevalence of elevated serum transaminases levels in type-2 diabetic patients and to identify the associated risk factors. In this cross-sectional type of analytic study, ninety-three purposively selected type-2 diabetic patients and equal number of healthy subjects were studied. Subjects who were taking hepatotoxic drugs and known to have any liver disease were excluded. Demographic data and anthropometric measurements were recorded from all participants. Liver function tests, fasting blood sugar, fasting lipid profile and ultrasonography of the HBS were performed. Raised levels of serum ALT, AST and ALP were found in 22.6%, 14.0% and 4.3% diabetic patients and in 4.3%, 3.2% and 3.2% healthy control. Mean serum ALT, AST and ALP levels were significantly higher in cases than controls (p &lt; 0.05). Significant positive correlation observed between serum ALT level with fasting blood sugar, BMI and waist circumference but significant negative correlation observed between ALT level and age of the patient and duration of the diabetes. Study results were in accordance with previously reported high prevalence rates of abnormal liver enzymes in type-2 diabetic patients. Early detection of liver enzyme abnormality and intervention will help to prevent further progression to chronic liver disease. Screening of type-2 diabetic patients with serum ALT and AST is recommended.

S3240 A Case of Labetalol-Induced Liver Injury

Introduction: Drug induced liver injury (DILI) is a rare but important cause of hepatotoxicity. Presentation varies widely, from mild elevations of serum aminotransferases to fulminant hepatic failure. Here, we present a case of DILI secondary to labetalol use, a rarely cited cause. Case Description/Methods: A 36-year-old woman with a history of hypertension presented to the emergency room with 10 days of progressive painless jaundice. She switched from hydrochlorothiazide to labetalol 9 weeks prior to presentation. Vitals were within normal limits and her exam was remarkable for scleral icterus and jaundice of the skin. Laboratory investigation revealed AST 2,042 IU/L, ALT 1,402 IU/L, total bilirubin 12.1 mg/dL, direct bilirubin 6.9 mg/dL, ANA titer 1:160 and IgG 2,078 g/L. CT abdomen pelvis was unremarkable. Given clinical stability, the patient was discharged with instruction to discontinue labetalol use indefinitely. Her labs and clinical status were closely followed by outpatient GI. Her symptoms and lab abnormalities resolved within two months without further intervention (Figure 1). Discussion: Labetalol has been associated with mild-to-moderate elevations of serum aminotransferase levels in up to 8% of patients, a rate far higher than with other beta-blockers. DILI is a diagnosis of exclusion and may pose a diagnostic challenge, especially in the setting of drugs that are not commonly implicated. Our case is consistent with other reports that describe typical symptom onset between 5 to 90 days after initial exposure to a drug. Our patient first noted symptoms 53 days after labetalol initiation and resolution of symptoms and normalization of labs 66 days after cessation. Additional associated symptoms reported with labetalol mediated DILI include jaundice, abdominal pain, pruritus, nausea and dark urine. Autoantibody formation is rare in labetolol mediated toxicity, however, it is unclear in this case whether autoantibody formation was drug mediated or found incidentally. Our patient improved with drug cessation alone and did not require steroid therapy. Providers must take care to keep a broad differential for liver injury in the absence of a typical history, as a missed diagnosis of DILI without prompt intervention may progress to fulminant liver failure.Figure 1.: Trend of AST, ALT, Direct and Total Bilirubin after labetalol cessation.

Mitochondrial DNA content as a diagnostic marker for antituberculosis drug-induced liver injury

ObjectivesThis study aimed to investigate whether mitochondrial DNA (mtDNA) content, an index of mitochondrial dysfunction, was associated with clinical parameters indicating anti-tuberculosis (TB) drug-induced liver injury (ATDILI) in TB patients and could emerge as an ATDILI biomarker. MethodsLeukocyte mtDNA content in 102 TB patients (49 ATDILI cases and 53 non-ATDILI cases) and 100 age-matched healthy controls was measured using real-time polymerase chain reaction. ResultsCompared with healthy controls, both TB patients with and without ATDILI had significantly decreased mtDNA content. Compared with the patients without ATDILI, mtDNA content was significantly increased in those with ATDILI. Higher mtDNA content was observed to be independently associated with increased susceptibility to ATDILI. Increased mtDNA content measured within 1-7 days of treatment was independently associated with elevated levels of serum aminotransferases assessed within 8-60 days of treatment. After initiating treatment within 1-7 days, mtDNA content was detected to be more sensitive and selective for differentiating TB patients with ATDILI from those without ATDILI than serum aminotransferases. Kaplan-Meier analysis revealed a significant correlation between elevated mtDNA content and increased rate of ATDILI occurrence in TB patients, attested by Cox regression analysis, adjusting for confounders. ConclusionChanges in leukocyte mtDNA content would reflect ATDILI progression and could be used as a potential stratification tool for identifying TB patients at risk of ATDILI.

Non-hepatotropic viral hepatitis and its causative pathogens: The ongoing need for monitoring in children with severe acute hepatitis of unknown etiology.

Non-hepatotropic viral hepatitis and its causative pathogens: The ongoing need for monitoring in children with severe acute hepatitis of unknown etiology.

Fufang Zhenzhu Tiaozhi Capsule Prevents Intestinal Inflammation and Barrier Disruption in Mice With Non-Alcoholic Steatohepatitis.

Nonalcoholic steatohepatitis (NASH) has become a major cause of liver transplantation and liver-associated death. Targeting the gut–liver axis is a potential therapy for NASH. The Fufang Zhenzhu Tiaozhi (FTZ) capsule, a traditional Chinese medicine commonly used in clinical practice, has recently emerged as a promising drug candidate for metabolic diseases such as NASH. The present study aimed to investigate whether FTZ exerts an anti-NASH effect by targeting the gut–liver axis. Mice were fed with a high-fat diet (HFD) for 20 weeks to induce NASH. HFD-fed mice were daily intragastrically administrated with FTZ at 10 weeks after tbe initiation of HFD feeding. The mRNA levels of genes associated with the intestinal tight junction, lipid metabolism, and inflammation were determined by the q-PCR assay. Hepatic pathology was evaluated by H&E staining. The gut microbiota was analyzed by 16S rRNA gene sequencing. FTZ attenuated HFD-induced obesity, insulin resistance, and hepatic steatosis in mice. FTZ treatment decreased the elevated levels of serum aminotransferases and liver triglyceride in NASH mice. Furthermore, FTZ treatment reduced hepatic inflammatory cell infiltration and fibrosis in mice. In addition, FTZ attenuated the intestinal inflammatory response and improved intestinal barrier function. Mechanistically, FTZ-treated mice showed a different gut microbiota composition compared with that in HFD-fed mice. Finally, we identified eight differential metabolites that may contribute to the improvement of NASH with FTZ treatment. In summary, FTZ ameliorates NASH by inhibiting gut inflammation, improving intestinal barrier function, and modulating intestinal microbiota composition.

Evaluation of liver injury in multiple sclerosis patients receiving pulsed steroid therapy

ObjectivesThere is a paucity of literature about the methylprednisolone induced liver injury in multiple sclerosis (MS) patients. In this study, we intended to investigate the incidence, severity, and risk factors for liver injury in MS patients treated with pulsed methylprednisolone therapy. MethodsThis is a prospective observational study on MS patients treated with methylprednisolone pulses. All MS subjects with relapses who were referred to Sina Hospital between May 2020 to May 2021 were included in the study. They were evaluated for the demographic, clinical characteristics, and liver function tests. Liver injury was diagnosed if there was an elevation of serum aminotransferase levels above the upper normal limit (45 IU/L). ResultsA total of 314 individuals participated in the study. The prevalence of liver injury after treatment with pulsed methylprednisolone therapy was 2.86%. None of the cases with liver injury were severe. Univariate regression analysis demonstrated that the patients with liver injury had a significantly higher frequency of hyperlipidemia (p: 0.002), alcohol abuse (p: 0.021), and non-alcoholic fatty liver disease (NAFLD) (p: 0.005) compared to those without liver injury. Multivariate regression analysis showed that hyperlipidemia (p: 0.04, odds ratio (OR): 6.31), and history of alcohol abuse (p: 0.007, OR: 36.71) were significantly associated with liver injury. ConclusionsOur study highlights the importance of a close follow-up of the liver function tests in MS patients following pulsed methylprednisolone therapy, particularly in patients with NAFLD, hyperlipidemia, and history of alcohol-abusing.

Bicyclol alleviates high-fat diet-induced hepatic ER stress- and autophagy-associated non-alcoholic fatty liver disease/non-alcoholic steatohepatitis in mice

Background and objective Non-alcoholic fatty liver disease (NAFLD) is a manifestation of the metabolic syndrome in the liver, and non-alcoholic steatohepatitis (NASH) represents its advanced stage. Bicyclol has protective activity against NAFLD in mice; however, the effect of bicyclol on high-fat diet (HFD)-induced NASH and its underlying molecular mechanism remains unknown particularly anti-endoplasmic reticulum (ER) stress and autophagic machinery potentials. Therefore, the present study was performed to investigate the protective effect and underlying mechanisms of bicyclol action on NAFLD/NASH. Methods Mice were fed an HFD to induce NAFLD/NASH, and bicyclol was administered as a treatment. Biochemistry and histopathological assays were performed to evaluate the effects of bicyclol on NAFLD/NASH. Moreover, the levels of hepatic ER stress- and autophagy-related markers were determined by western blotting. Results The present results revealed that bicyclol exerted significant protective effects against HFD-induced NAFLD/NASH. This activity was evidenced by the decrease in elevated serum transaminase and hepatic triglyceride levels, and the attenuation of negative histopathological changes. Bicyclol considerably alleviated hepatic inflammation and apoptosis. The protein expression of ER stress-related markers, including C/EBP homologous protein (CHOP) and glucose-regulated protein 78 (GRP78), was downregulated by the bicyclol treatment in HFD-induced mice. However, the protein expression of autophagy-related markers (LC3 and Beclin 1) was upregulated by the treatment with bicyclol. Conclusion Bicyclol protected HFD-induced NASH, and partly due to its ability of reducing ER stress and promoting autophagy.

Clinical Evaluation of efficacy of Rasarakta pachak Ghanavati in Hyperlipidaemia (Rasagat sneha vriddhi)

Hyperlipidaemia is one such lifestyle disorder which is identified as an impending risk factor for many diseases like hypertension, metabolic syndrome, coronary artery disease (CAD) and cerebrovascular diseases (CVD). In Hyperlipidaemia levels of lipoproteins i.e. (cholesterol, triglycerides, or both) are raised in the plasma, which can be co-related to elevated Sneha or Meda Dhatu in the body. As drugs used in modern medicine viz. statins, fibrates etc. to treat hyperlipidaemia has several adverse effects such as myopathy, potential elevation in serum transaminase levels leading to hepatic damage, nausea or vomiting, bowel upset, multiple joint pain etc. Hence, it is very much necessary to have definite and harmless solution to this problem. Apatarpan is the treatment advocated in ayurved for Santarpanjanya Vyadhis and Hyperlipidaemia is one among this group of disease. Taking into consideration all the treatment modalities in Ayurveda, Rasarakta Pachak Ghanavati was given as a line of treatment in Hyperlipidaemia. Methods - 60 patients of Hyperlipidaemia as per the objective criteria of range for lipid profile mentioned in American Journal of Lifestyle Medicine were randomly selected from OPD and IPD of Dr. D. Y. Patil College of Ayurved and Research centre, Pimpri, Pune. Group A (n=30) patients were treated with Rasarakta Pachak Ghanavati (500mg) 2 tabs twice in a day after food for 30 days and Group B (n=30) patients were treated with Tab Atorvastatin (10mg) 1 tab once in a day after food for 30 days. Result- Rasarakta Pachak Ghanavati group showed marked improvement on Serum Total Cholesterol and Serum LDL – Cholesterol and moderate improvement on Serum Triglycerides and Serum HDL – Cholesterol parameters of lipid profile. While Tab Atorvastatin group showed marked improvement on almost all the parameters of lipid profile.

The effectiveness of small heterodimer partner and FGF 19 levels in prediction of perinatal morbidity in intrahepatic cholestasis of pregnancy

Fibroblast growth factor 19 (FGF19) and small heterodimer partner (SHP) are molecules responsible for controlling serum bile acid levels. We designed this study for evaluating the effects of FGF 19 and SHP in intrahepatic cholestasis of pregnancy (ICP). Fifty-six pregnant women having ICP and 20 healthy pregnant women were included in the study. The patients were followed up until delivery in terms of pregnancy-related morbidity/mortality. Serum FGF 19 and SHP levels were determined by enzyme-linked immunosorbent assay (ELISA). Serum FGF 19 and SHP levels were significantly higher in the patient group compared to the control group (p: .04, p: .003, respectively). In ROC analysis, SHP level above 1995 ng/L was found effective in predicting the need for neonatal intensive care unit (ICU) follow-up with 53.8% sensitivity and 77.8% specificity. High SHP levels were correlated with perinatal morbidity, mortality and neonatal ICU hospitalisation. Impact Statement What is already known on this subject? Itching, elevated serum transaminase and serum total bile acid (TBA) levels are the most important clinical and biochemical findings of intrahepatic cholestasis of pregnancy (ICP). Fibroblast growth factor 19 (FGF19) and small heterodimer partner (SHP) are molecules – responsible for controlling serum bile acid levels. ICP is associated with preterm labour, asphyxia, foetal distress, stillbirth and preeclampsia. What do the results of this study add? Serum FGF 19 and SHP levels were significantly higher in the patient group compared to the control group. High SHP level was found effective in predicting the need for neonatal intensive care unit and showed a negative correlation with birth week and birth weight. What are the implications of these findings for clinical practice and/or further research? Checking SHP levels can help to predict perinatal mortality and morbidity. Treatments to be developed through the mechanism of action of FGF 19 and SHP can be promising in the treatment of ICP and other cholestatic liver diseases.

An evaluation of liver function tests in severe acute respiratory syndrome - Corona virus 2 (SARS-CoV-2) infection in the backdrop of chronic kidney disease.

Background:The SARS-CoV-2 pandemic has emerged as the most challenging global health problem of this century. The concomitant presence of co-morbidities like chronic kidney disease (CKD), diabetes, CHD, further complicates the problem.Aim:To assess the patterns of LFT abnormalities in patients of SARS-CoV-2 infection with and without CKD and evaluate the probable outcomes.Materials and Methods:A cross-sectional retrospective observational study done on 600 patient samples (Group 1: SARS-CoV-2 without CKD, Group 2: SARS-CoV-2 with CKD and Group 3: CKD uninfected with SARS-CoV-2) which were processed for LFT and KFT.Results:AST and ALT were significantly higher in all SARS-CoV-2 infected; Group 1 mean ± 2SD, (63.63 ± 42.89U/L & 50.25 ± 46.53U/L), group 2 (90.59 ± 62.51U/L & 72.09 ± 67.24 U/L) as compared to Group 3 (25.24 ± 7.47U/L & 24.93 ± 11.44U/L). A statistically significant elevation is seen in these two parameters in Group 2 as compared to Group 1. There was a negative significant correlation between eGFR and AST/ALT levels in Group 1 (p < 0.05). In Group 2, a weak positive correlation was seen with ALT. Group 3, eGFR’s showed strong correlations with AST and ALT levels; reduction in kidney function correlated well with increase in serum ALP levels.Conclusions:This study establishes that SARS-CoV-2 infected, with CKD, show higher elevations in serum aminotransferase levels in comparison to those without CKD. In contrast, the CKD group not infected, shows a decline in serum aminotransferase levels. Serum ALT values in SARS-CoV-2 show significant correlation with eGFR. Also, elevated ALP values in CKD patients may be used as an indicator of declining kidney function.