Sirs at Admission is a Predictor of AKI Development and Mortality in Hospitalized Patients with...
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Results: Feeding alcohol significantly elevated the activ- ities of serum aspartate transaminase (AST), alanine transaminase (ALT), alkaline phosphatases (ALP) and gamma-glutamyl transpeptidase (GGT) and altered the liver and brain fatty acid composition compared with control rats. Subsequently, glycine supplementation to alcohol-fed rats significantly lowered the activities of serum AST, ALT, ALP, GGT and normalized the liver fatty acid composition compared with untreated alcohol-fed rats. Conclusion: The present study demonstrates that oral administration of glycine confers a significant protective effect against alcohol-induced hepatotoxicity by virtue of its ability to optimize the activities of serum AST, ALT, ALP and GGT, as well as the tissue fatty acid compo- sition. Corresponding author: Senthilkumar Rajagopal. Email: [email protected] NATURAL HISTORY OF DECOMPENSATED ALCOHOLIC LIVER DISEASE IN A TERTIARY CARE HOSPITAL OF NORTH INDIA Amit Jindal, Ashok Dalal, Alok Sangam, Geeta Mutreja, Nitin Gupta, Sanjeev Sachdeva, Amarender S. Puri Department of Gastroenterology, G B Pant Hospital, New Delhi, India Background and Objectives: Alcoholic liver disease (ALD) is a major cause of morbidity and mortality among people who regularly abuse alcohol. Our aim was to study the drinking patterns and natural history of patients of de- compensated alcoholic liver disease hospitalized in a ter- tiary care hospital. Methods: Sixty-two patients were enrolled between March 2013 and December 2013 and were prospectively evalu- ated. We recorded all information including age of onset of drinking alcohol, pattern of drinking, socioeconomic status, clinical presentations and in hospital complications and outcome in these patients. Results: Of total 62 patients enrolled, 61 patients were male. Mean age of onset of starting alcohol intake was 24.4 years (95% CI 23.1–25.7) and mean duration of alcohol intake was 19.4 years (95% CI 16.6–22.1); mean amount of alcohol intake was 133.1 grams/day (95% CI 117.5–148.6) and majority of patients (51; 82%) consumed IMFL, while rest consumed country made li- quor (11; 17%). Mean interval between onset of drinking and 1st symptom was 20.5 years (95% CI 18.2–22.7). Ma- jority of patients presented with jaundice (73%) followed by upper GI bleed (9.7%), hepatic encephalopathy (19%), anasarca (15%) and sepsis (2.4%). Mean MELD, CTP and DF scores at admission were 25.5 (95% CI 22.5–28.4), 11.1 (95% CI 10.6–11.5) and 69.1 (95% CI 57.1–80.1) respectively. Out of 62 patients, 15 patients (24%) expired during follow up and of these (n = 15), 6 pa- tients (40%) expired within 7 days and rest 9 (60%) expired within 7–30 days of admission. The causes of death were multiorgan failure, hepatorenal syndrome and upper GI bleed in 6 (40%), 3 (20%) and 3 (20%) pa- tients, respectively. Conclusions: Our study group from urban Delhi shows higher age at initiation of alcohol versus other studies from urban slums. Liver disease manifests after a mean duration of 20 years of prolonged drinking. Jaundice is the initial manifestation in majority of the cases. ALD has high short term mortality (24%) at 30 days. Corresponding author: Amit Jindal. Email: [email protected] SIRS AT ADMISSION IS A PREDICTOR OF AKI DEVELOPMENT AND MORTALITY IN HOSPITALIZED PATIENTS WITH SEVERE ALCOHOLIC HEPATITIS Rakhi Maiwall, Zeeshan Wani, Manoj Sharma, Chitranshu Vashishtha, Shiv Sarin Department of Hepatology, Institute of Liver and Biliary Sciences, New Delhi, India Background: Systemic Inflammatory response syndrome (SIRS) is associated with an increased risk of hepatic en- cephalopathy (HE), renal failure and poor outcome in pa- tients with acute liver failure; however this is not reported for severe alcoholic hepatitis (SAH). Aim: To look at SIRS at baseline as a predictor of develop- ment of acute kidney injury and its progression including mortality in patients with SAH. Methods: Consecutive in-patients with SAH (Discrimi- nant Function=32) without AKI at baseline were included and followed for the development and progression of AKI (defined by AKIN criteria). Results: Of the 427 patients (mean age 45.5 9.5, 416 males), SIRS at baseline was present in 312 (73%). AKI developed in 143 (33.5%) of which 62 (14.5%) had progres- sion of AKI. Presence of SIRS significantly correlated with serum creatinine (P = 0.001), serum sodium (P = 0.01), serum bilirubin (P = 0.003) and DF score (P = 0.001). SIRS, presence of hepatic encephalopathy, and serum creatinine at baseline were significant predictors on univar- iate analysis for AKI development. On multivariate anal- ysis, SIRS predicted both AKI development (P < 0.001, OR 2.7, 95% CI–1.54.6) and AKI progression (P = 0.05, HR 2.1, 95% CI 1.1–4.6). Resolution of AKI also had a sig- nificant inverse association with SIRS (P = 0.05). High MELD score (=18) (P = 0.008, HR 2.1, 95% CI 1.2–3.6), JOURNAL OF CLINICAL AND EXPERIMENTAL HEPATOLOGY Journal of Clinical and Experimental Hepatology | March 2014 | Vol. 4 | No. S2 | S30–S38 S31 AFLD and NAFLD
Transcript of Sirs at Admission is a Predictor of AKI Development and Mortality in Hospitalized Patients with...
JOURNAL OF CLINICAL AND EXPERIMENTAL HEPATOLOGY
AFL
Dand
NAFL
D
Results: Feeding alcohol significantly elevated the activ-ities of serum aspartate transaminase (AST), alaninetransaminase (ALT), alkaline phosphatases (ALP) andgamma-glutamyl transpeptidase (GGT) and altered theliver and brain fatty acid composition compared withcontrol rats. Subsequently, glycine supplementation toalcohol-fed rats significantly lowered the activities ofserum AST, ALT, ALP, GGT and normalized the liverfatty acid composition compared with untreatedalcohol-fed rats.Conclusion: The present study demonstrates that oraladministration of glycine confers a significant protectiveeffect against alcohol-induced hepatotoxicity by virtueof its ability to optimize the activities of serum AST,ALT, ALP and GGT, as well as the tissue fatty acid compo-sition.
Corresponding author: Senthilkumar Rajagopal.Email: [email protected]
NATURAL HISTORY OF DECOMPENSATEDALCOHOLIC LIVER DISEASE IN A TERTIARYCARE HOSPITAL OF NORTH INDIA
Amit Jindal, Ashok Dalal, Alok Sangam, Geeta Mutreja,Nitin Gupta, Sanjeev Sachdeva, Amarender S. Puri
Department of Gastroenterology, G B Pant Hospital, New Delhi,India
Background and Objectives: Alcoholic liver disease(ALD) is a major cause of morbidity and mortality amongpeople who regularly abuse alcohol. Our aim was to studythe drinking patterns and natural history of patients of de-compensated alcoholic liver disease hospitalized in a ter-tiary care hospital.Methods: Sixty-two patients were enrolled between March2013 and December 2013 and were prospectively evalu-ated. We recorded all information including age of onsetof drinking alcohol, pattern of drinking, socioeconomicstatus, clinical presentations and in hospital complicationsand outcome in these patients.Results: Of total 62 patients enrolled, 61 patients weremale. Mean age of onset of starting alcohol intake was24.4 years (95% CI 23.1–25.7) and mean duration ofalcohol intake was 19.4 years (95% CI 16.6–22.1); meanamount of alcohol intake was 133.1 grams/day (95%CI 117.5–148.6) and majority of patients (51; 82%)consumed IMFL, while rest consumed country made li-quor (11; 17%). Mean interval between onset of drinkingand 1st symptom was 20.5 years (95% CI 18.2–22.7). Ma-jority of patients presented with jaundice (73%) followedby upper GI bleed (9.7%), hepatic encephalopathy (19%),anasarca (15%) and sepsis (2.4%). Mean MELD, CTP andDF scores at admission were 25.5 (95% CI 22.5–28.4),
Journal of Clinical and Experimental Hepatology | March 2014 | Vol. 4 | No
11.1 (95% CI 10.6–11.5) and 69.1 (95% CI 57.1–80.1)respectively. Out of 62 patients, 15 patients (24%)expired during follow up and of these (n = 15), 6 pa-tients (40%) expired within 7 days and rest 9 (60%)expired within 7–30 days of admission. The causes ofdeath were multiorgan failure, hepatorenal syndromeand upper GI bleed in 6 (40%), 3 (20%) and 3 (20%) pa-tients, respectively.Conclusions: Our study group from urban Delhi showshigher age at initiation of alcohol versus other studiesfrom urban slums. Liver disease manifests after a meanduration of 20 years of prolonged drinking. Jaundice isthe initial manifestation in majority of the cases. ALDhas high short term mortality (24%) at 30 days.
Corresponding author: Amit Jindal.Email: [email protected]
SIRS AT ADMISSION IS A PREDICTOROF AKIDEVELOPMENT AND MORTALITY INHOSPITALIZED PATIENTS WITH SEVEREALCOHOLIC HEPATITIS
Rakhi Maiwall, Zeeshan Wani, Manoj Sharma,Chitranshu Vashishtha, Shiv Sarin
Department of Hepatology, Institute of Liver and Biliary Sciences,New Delhi, India
Background: Systemic Inflammatory response syndrome(SIRS) is associated with an increased risk of hepatic en-cephalopathy (HE), renal failure and poor outcome in pa-tients with acute liver failure; however this is not reportedfor severe alcoholic hepatitis (SAH).Aim: To look at SIRS at baseline as a predictor of develop-ment of acute kidney injury and its progression includingmortality in patients with SAH.Methods: Consecutive in-patients with SAH (Discrimi-nant Function=32) without AKI at baseline were includedand followed for the development and progression of AKI(defined by AKIN criteria).Results: Of the 427 patients (mean age 45.5 � 9.5, 416males), SIRS at baseline was present in 312 (73%). AKIdeveloped in 143 (33.5%) of which 62 (14.5%) had progres-sion of AKI. Presence of SIRS significantly correlated withserum creatinine (P = 0.001), serum sodium (P = 0.01),serum bilirubin (P = 0.003) and DF score (P = 0.001).SIRS, presence of hepatic encephalopathy, and serumcreatinine at baseline were significant predictors on univar-iate analysis for AKI development. On multivariate anal-ysis, SIRS predicted both AKI development (P < 0.001,OR 2.7, 95% CI–1.54.6) and AKI progression (P = 0.05,HR 2.1, 95% CI 1.1–4.6). Resolution of AKI also had a sig-nificant inverse association with SIRS (P = 0.05). HighMELD score (=18) (P = 0.008, HR 2.1, 95% CI 1.2–3.6),
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ABSTRACTS 22ND ANNUAL CONFERENCE–2014
AFLD
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NAFLD
in-hospital progression of AKI (P = 0.01, HR 1.8, 95% CI1.1–2.9) and SIRS (P = 0.001, HR 2.9, 95% CI 1.5–5.7)were significant predictors of short-term mortality at 1and 3 months.Conclusion: SIRS at admission predicts both develop-ment and in-hospital progression of AKI as well as short-term mortality in patients with SAH. This could definitelyhave a therapeutic and prognostic implication.
Corresponding author: Rakhi Maiwall.Email: [email protected]
INTERLEUKIN-15 IN THE REGULATION OFOBESITY AND FATTY LIVER DISEASE
Sheela Ramanathan*, Gregory Lacraz*,Yuneivy Cepar Donates*, Marian Mayhue*,Marie France Langoisy, Marek Rola Pleszczynski*,Subburaj Ilangumaran*
*Departments of Immunology/Pediatrics and yDepartments ofMedicine, University of Sherbrooke, Canada
Background and objectives: Inflammatory cytokines areimplicated in the pathogenesis of obesity and fatty liverdisease. IL-15 is an inflammatory cytokine secreted bymany cell types. IL-15 is also produced during physical ex-ercise by skeletal muscle and has been reported to reduceweight gain in mice. Contrarily, our findings on IL-15knockout mice indicated that IL-15 promotes obesity.The aim of this study is to investigate the role of IL-15 inobesity and fatty liver disease.Methods: C57BL/6 wildtype, IL-15 knockout (IL15-KO)and mice were maintained on high fat diet (HFD) ornormal control diet. After 16 weeks, body weight, livermass, fat accumulation in the liver, serum lipid levelsand gene expression in the liver were evaluated. Primary he-patocytes were stimulated with IL-15 and signalling andgene expressions were studied.Results: IL-15 deficiency prevents weight gain and accu-mulation of lipids in the liver. Circulating levels of choles-terol and non-esterified fatty acids were elevated inwildtype mice but not in IL-15-KO mice. The adiposeand liver tissues of IL-15 KO mice showed decreasedexpression of TNF a and iNOS, chemokines CCl2, CCL5and CXCL10, and macrophage markers CD68 and F4/80. The brown adipose tissue of IL-15 KO mice showedincreased thermogenic activity.Conclusions: IL-15 inhibits the thermogenic activity in-creases the accumulation of lipids in the white adipose tis-sues. The increased inflammatory response in the liver inthe absence of IL-15 may promote the accumulation offat in the liver. Our results suggest that IL-15 can promoteobesity and fatty liver disease.
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Corresponding author: Sheela Ramanathan.Emails: [email protected],[email protected]
IMPACT OF ETHANOL EXPOSURE ON THEPRODUCTION OF REACTIVE OXYGENSPECIES, MALONDIALDEHYDE, ANDADIPOKINES (LEPTIN & RESISTIN) IN3T3L1 CELLS
Palash Mandal, Nishank Reddy, Raghava Jagadeesh,Imran Khan
Department of Biological Sciences, Birla Institute of Technologyand Science Pilani, Hyderabad Campus, Hyderabad, AndhraPradesh, India
Background and Objectives: Chronic consumption ofalcohol impacts the health of the drinker via alcohol depen-dence, cirrhosis of liver, liver cancers and injuries. Adiposetissue which has long been considered as an energy storagedepot is now being identified to also function as an endo-crine organ secreting a variety of cytokines, termed as adipo-kines or adipocytokines that have important roles at theinterface between the metabolic and immune systems. Thelevels of these adipokines are found to be altered on ethanolconsumption. So an understanding of the effect of ethanolconsumptionon the oxidative stress, endoplasmic reticulum(ER) stress in adipose tissue and the subsequent effect ofthese in the regulation of adipokine expression will aid inidentification of new integrative approaches as it relates toalcoholic liver injury and provides potential new directionsto develop therapeutic target intervention.Methods: In order to study the effect of ethanol treatmenton 3T3L1 adipocyte cells, the cells were first cultured anddifferentiated into mature adipocytes using 3T3L1 differ-entiation medium. Differentiation was confirmed by Oilred O staining. The differentiated 3T3L1 cells were thentreated with different concentrations of ethanol addedDulbecco's Modified Eagle's medium (DMEM) for up to48 hours. Oxidative stress markers like reactive oxygen spe-cies (ROS) and malondialdehyde (MDA) were measured bydichlorofluorescein diacetate (DCFDA) method and thio-barbituric acid (TBARS) assay respectively. RNA was iso-lated from cells, reverse transcribed and the expressionlevels of proinflammatory cytokines like leptin and resistinwere quantified by qRT-PCR.Results: Ethanol exposure in increasing concentrationsresulted in increased production of ROS and MDA levels asestimated by DCFDA (Figure 1) and TBARS (Figure 2) assaymethods. Treatment of cells with CYP2E1 inhibitor like dailysulphide (DAS) was found to reduce oxidative stress inducedby ethanol. qRT-PCRof adipokine genes showedan increasedlevel of leptin and resistin when compared to control.
© 2014, INASL
