FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2917559947> ?p ?o ?g. }

• W2917559947 endingPage "271" @default.
• W2917559947 startingPage "269" @default.
• W2917559947 abstract "1.Answer AVitamin deficiencies in chronic liver disease are due to diminished hepatic reserves, poor dietary intake, or malabsorption. Fat-soluble vitamin deficiencies are commonly seen.1Venu M. Saeian K. Gawrieh S. High prevalence of vitamin A and D deficiency in patients evaluated for liver transplantation.Hepatology. 2012; 56: 938AGoogle Scholar Vitamin A is principally stored in hepatic stellate cells. As quiescent stellate cells become activated, they lose their vitamin A stores.2Bemeur C. Butterworth R.F. Nutrition in the management of cirrhosis and its neurological complications.J Clin Exp Hepatol. 2015; 5: S131-S140Abstract Full Text Full Text PDF PubMed Scopus (10) Google Scholar Vitamin A deficiency is seen in 50% of patients with alcoholic cirrhosis. Patients with chronic alcoholism have been shown to have very low concentrations of hepatic vitamin A at all stages of their disease.3Russell R.M. Vitamin A and zinc metabolism in alcoholism.Am J Clin Nutr. 1980; 33: 2741-2749PubMed Scopus (61) Google Scholar, 4Leo M.A. Lieber C.S. Alcohol, vitamin A, and beta-carotene: adverse interactions, including hepatotoxicity and carcinogenicity.Am J Clin Nutr. 1999; 69: 1071-1085Crossref PubMed Scopus (224) Google Scholar Chronic liver disease commonly results in vitamin D deficiency. Decreased hepatic production of vitamin D binding protein seems to be a key mechanism responsible for the low serum vitamin D levels in patients with liver disease.1Venu M. Saeian K. Gawrieh S. High prevalence of vitamin A and D deficiency in patients evaluated for liver transplantation.Hepatology. 2012; 56: 938AGoogle Scholar, 6Arteh J. Narra S. Nair S. Prevalence of vitamin D deficiency in chronic liver disease.Dig Dis Sci. 2010; 55: 2624-2628Crossref PubMed Scopus (292) Google Scholar, 7Arteel G. Marsano L. Mendez C. Bentley F. McClain C.J. Advances in alcoholic liver disease.Best Pract Res Clin Gastroenterol. 2003; 17: 625-647Abstract Full Text Full Text PDF PubMed Scopus (121) Google Scholar Vitamin E deficiency has been well documented in alcoholic liver disease. However, supplementation has not been shown to cause clinical improvement or reduction in mortality.1Venu M. Saeian K. Gawrieh S. High prevalence of vitamin A and D deficiency in patients evaluated for liver transplantation.Hepatology. 2012; 56: 938AGoogle Scholar, 8de la Maza M.P. Petermann M. Bunout D. Hirsch S. Effects of long term vitamin E supplementation in alcoholics cirrhotics.J Am Coll Nutr. 1995; 14: 192-196Crossref PubMed Scopus (92) Google Scholar, 9Mezey E. Potter J.J. Rennie-Tankersley L. Caballeria J. Pares A. A randomized placebo controlled trial of vitamin E for alcoholic hepatitis.J Hepatol. 2004; 40: 40-46Abstract Full Text Full Text PDF PubMed Scopus (144) Google Scholar Acute and chronic hemorrhagic lesions in thalamus and mammillary bodies that are typical of Wernicke's encephalopathy are seen in thiamine deficiency.2Bemeur C. Butterworth R.F. Nutrition in the management of cirrhosis and its neurological complications.J Clin Exp Hepatol. 2015; 5: S131-S140Abstract Full Text Full Text PDF PubMed Scopus (10) Google Scholar2.Answer A, B, C, D and EMagnesium deficiency is common in chronic liver disease, and is associated with peripheral insulin resistance as well. Supplementation has been shown to improve hepatic enzyme levels.10Poikolainen K. Alho H. Magnesium treatment in alcoholics: a randomized clinical trial.Subst Abuse Treat Prev Policy. 2008; 25: 1Crossref Scopus (31) Google Scholar Selenium is a co-factor for multiple seleno-proteins which have antioxidant functions. Chronic liver disease is associated with decreases in serum, whole blood, and hepatic selenium content.11Czuczejko J. Zachara B.A. Staubach-Topczewska E. Holota W. Kedziora J. Selenium, glutathione and glutathione peroxidases in blood of patients with chronic liver diseases.Acta Biochim Pol. 2003; 50: 1147-1154PubMed Google Scholar Total body manganese stores are increased in cirrhosis, and accumulation of manganese in basal ganglia is common.12Sam J. Nguyen G.C. Protein-calorie malnutrition as a prognostic indicator of mortality among patients hospitalized with cirrhosis and portal hypertension.Liver Int. 2009; 29: 1396-1402Crossref PubMed Scopus (122) Google Scholar Copper and copper-associated protein accumulation may be observed in chronic biliary obstructive processes and cirrhosis.2Bemeur C. Butterworth R.F. Nutrition in the management of cirrhosis and its neurological complications.J Clin Exp Hepatol. 2015; 5: S131-S140Abstract Full Text Full Text PDF PubMed Scopus (10) Google Scholar3.Answer A, B and EPatients with cirrhosis are usually malnourished and require careful nutritional management to prevent energy and nutrient depletion and correction of macro- and micronutrient deficiencies. Carbohydrate content should constitute 45–75% of caloric intake divided in 4–6 carbohydrate rich meals. A late evening or nighttime snack prevents gluconeogenesis, reduce protein utilization and favor a positive nitrogen balance. Protein intake of 1.2–1.5 g/kg should be maintained even in patients with hepatic encephalopathy. Vegetable and dairy protein is preferable.2Bemeur C. Butterworth R.F. Nutrition in the management of cirrhosis and its neurological complications.J Clin Exp Hepatol. 2015; 5: S131-S140Abstract Full Text Full Text PDF PubMed Scopus (10) Google Scholar Branched chain amino acid supplementation may be considered as they are not metabolized by the liver, providing an alternative source of proteins.13Mendenhall C.L. Tosch T. Weesner R.E. et al.VA cooperative study on alcoholic hepatitis. Prognostic significance of protein-calorie malnutrition.Am J Clin Nutr. 1986; 43: 213-218PubMed Scopus (190) Google Scholar Total body manganese stores are increased in patients with liver disease and its supplementation is not recommended.14Versieck J. Barbier F. Speecke A. Hoste J. Manganese, copper, and zinc concentrations in serum and packed blood cells during acute hepatitis, chronic hepatitis, and posthepatitic cirrhosis.Clin Chem. 1974; 20: 1141-1145PubMed Google Scholar4.Answers A and DThe spectrum of nonalcoholic fatty liver disease (NAFLD) ranges from simple steatosis to nonalcoholic steatohepatitis (NASH). The physiological level of fat in the hepatocytes is <5%, and accumulation of fat more than this is required for development of NASH. NAFLD is a polygenic disease with involvement of multiple loci, environmental and nutrient interactions. The major locus among these is 22q13.31, which harbors the PNPLA3 gene.15Speliotes E.K. Yerges-Armstrong L.M. Wu J. et al.Genome-wide association analysis identifies variants associated with nonalcoholic fatty liver disease that have distinct effects on metabolic traits.PLoS Genet. 2011; 7: e1001324Crossref PubMed Scopus (693) Google Scholar Single nucleotide polymorphisms in the PNPLA 3 gene are strongly associated with progression of NAFLD to NASH. Polyunsaturated fatty acids (PUFAs) are of 2 types – n3 and n6. n-6 PUFAs which includes linoleic acid and arachadonic acid and have the capability of producing proinflammatory eicosanoids, thereby aggrevating the lipotoxicity in NASH.16Feldstein A.E. Lopez R. Tamimi T.A. et al.Mass spectrometric profiling of oxidized lipid products in human nonalcoholic fatty liver disease and nonalcoholic steatohepatitis.J Lipid Res. 2010; 51: 3046-3054Crossref PubMed Scopus (212) Google Scholar Although raised aspartate aminotransferase and alanine aminotransferase levels are very common, they may even be normal in biopsy proven NASH.17Mofrad P. Contos M.J. Haque M. et al.Clinical and histological spectrum of non-alcoholic fatty liver disease associated with normal ALT values.Hepatology. 2003; 37: 1286-1292Crossref PubMed Scopus (889) Google Scholar5.Answers A, C, D and EHepatitis may be commonly seen with coeliac disease. Upto 10% patients with unexplained transaminitis have been found to have coeliac disease.18Volta U. De Franceschi L. Lari F. Molinaro N. Zoli M. Bianchi F.B. Coeliac disease hidden by cryptogenic hypertransaminasaemia.Lancet. 1998; 352: 26-29Abstract Full Text Full Text PDF PubMed Scopus (205) Google Scholar Transaminitis may be seen in 50% of coeliac disease at presentation.19Bardella M.T. Fraquelli M. Quatrini M. Molteni N. Bianchi P. Conte D. Prevalence of hypertransaminasemia in adult celiac patients and effect of gluten-free diet.Hepatology. 1995; 22: 833-836Crossref PubMed Google Scholar Although usually subclinical, the liver injury can occasionally progress to cirrhosis and liver failure. Thus, it is recommended to screen coeliac disease patients for liver disease at presentation, and follow-up with periodic liver function tests.20Rubio-Tapia A. Hill I.D. Kelly C.P. Calderwood A.H. Murray J.A. ACG clinical guidelines: diagnosis and management of celiac disease.Am J Gastroenterol. 2013; 108: 656-676Crossref PubMed Scopus (1163) Google ScholarThree fourths of patients with raised transaminases in coeliac disease do not have a separate disorder and these individuals respond well to gluten withdrawal.21Castillo N.E. Vanga R.R. Theethira T.G. et al.Prevalence of abnormal liver function tests in celiac disease and the effect of a gluten-free diet in the US population.Am J Gastroenterol. 2015; 110: 1216-1222Crossref PubMed Scopus (42) Google Scholar Patients with coeliac disease have higher likelihood of developing autoimmune hepatitis and primary biliary cirrhosis.22Garud S. Leffler D. Dennis M. et al.Interaction between psychiatric and autoimmune disorders in coeliac disease patients in the Northeastern United States.Aliment Pharmacol Ther. 2009; 29: 898-905Crossref PubMed Scopus (45) Google Scholar6.Answer A,C and DDengue is a common arthropod-borne viral fever in South-East Asia. It is a non-hepatotropic virus, however, liver dysfunction is common. Hepatitis is common and can be found in 60–90% of dengue-infected patients.23Anand A.C. Garg H.K. Approach to clinical syndrome of jaundice and encephalopathy in tropics.J Clin Exp Hepatol. 2015; 5: S116-S130Abstract Full Text Full Text PDF PubMed Scopus (20) Google Scholar, 24Tan S. Bujang M.A. The clinical features and outcomes of acute liver failure associated with dengue infection in adults: a case series.Braz J Infect Dis. 2013; 17: 164-169Crossref PubMed Scopus (33) Google Scholar Most of the cases with hepatitis have mild disease. Usually the AST levels are more than ALT levels probably due to skeletal muscle injury.25Nguyen T.L. Nguyen T.H. Tieu N.T. The impact of dengue haemorrhagic fever on liver function.Res Virol. 1997; 148: 273-277Crossref PubMed Scopus (139) Google Scholar Severe dengue can even manifest with acute liver failure. Other gastrointestinal manifestations include acalculous cholecystitis, acute pancreatitis, acute parotitis and diarrhea. 80% of the cases develop hepatomegaly, and jaundice is seen in 60%. Both these symptoms are more common in severe dengue (93% and 94.5% respectively); thus being important predictors of severe dengue.26Roy A. Sarkar D. Chakraborty S. Chaudhuri J. Ghosh P. Chakraborty S. Profile of hepatic involvement by dengue virus in dengue infected children.North Am J Med Sci. 2013; 5: 480-485Crossref PubMed Scopus (36) Google Scholar The presence of dengue virus antigens and nucleic acid has been shown in liver tissue using immunohistochemistry, in situ hybridization and in situ polymerase chain reaction techniques.27Jessie K. Fong M.Y. Devi S. Lam S.K. Wong K.T. Localization of dengue virus in naturally infected human tissues, by immunohistochemistry and in situ hybridization.J Infect Dis. 2004; 189: 1411-1418Crossref PubMed Scopus (462) Google Scholar7.Answer C, D and EJaundice leading to encephalopathy in infants has been called bilirubin encephalopathy or kernicterus. It occurs due to staining of the basal ganglia of infants by unconjugated bilirubin.23Anand A.C. Garg H.K. Approach to clinical syndrome of jaundice and encephalopathy in tropics.J Clin Exp Hepatol. 2015; 5: S116-S130Abstract Full Text Full Text PDF PubMed Scopus (20) Google Scholar, 28Connolly A.M. Volpe J.J. Clinical features of bilirubin encephalopathy.Clin Perinatol. 1990; 17: 371-379PubMed Google Scholar The most common cause is any type of hemolytic anemia, usually due to Rh or ABO incompatibility. Other causes include congenital or acquired disorders of bilirubin metabolism. Low birth weight, hypothermia, anoxia, acidosis, sepsis, hypoalbuminemia, and meningitis are risk factors.29Gould C.F. Lowe J.D. Richardson R.R. Ly J.Q. Campbell S.E. Beall D.P. Bilirubin encephalopathy.Appl Radiol. 2004; 33: 37-40Google Scholar In the first few days, infants were present with somnolence, hypotonia, and loss of the Moro reflex. They later develop irreversible changes leading to hypertonia of the extensor muscle groups. Patients who survive develop choreoathetosis, sensorineural hearing loss, dental dysplasia, gaze abnormalities and mild mental retardation.30Maisels M.J. Baltz R.D. Bhutani V.K. et al.Neonatal jaundice and kernicterus.Pediatrics. 2001; 108: 763-765Crossref PubMed Scopus (141) Google Scholar8.Answers B and DHigh-dose corticosteroids are usually first-line therapy for acute cellular rejection. Methylprednisolone is the most commonly used agent. 80% episodes of acute cellular rejection resolve. In most of those who do not respond, a repeat course is effective. Improvement in biochemical parameters and histology occurs within 3–5 days of successful therapy. Cytomegalovirus and pneumocystis prophylaxis for three to six months is indicated in these patients.31Adams D.H. Neuberger J.M. Patterns of graft rejection following liver transplantation.J Hepatol. 1990; 10: 113Abstract Full Text PDF PubMed Scopus (81) Google Scholar, 32Adams D.H. Neuberger J.M. Treatment of acute rejection.Semin Liver Dis. 1992; 12: 80Crossref PubMed Scopus (41) Google Scholar Anti-interleukin antibodies like basiliximab and daclizumab are effective and may lead to resolution of steroid-resistant rejection in up to 75% cases.33Fernandes M.L. Lee Y.M. Sutedja D. et al.Treatment of steroid-resistant acute liver transplant rejection with basiliximab.Transplant Proc. 2005; 37: 2179Abstract Full Text Full Text PDF PubMed Scopus (15) Google Scholar9.Answers A, B and CThe main pathway for ethanol metabolism is by oxidation to acetaldehyde. Alcohol dehydrogenase plays the most important role. Other pathways include microsomal oxidation, mainly via cytochrome P 2E1(CYP2E1) (∼10%) and catalase pathway. CYP2E1 is mainly concentrated in the perivenular zone 3 hepatocytes.34Cederbaum A.I. Alcohol metabolism.Clin Liver Dis. 2012; 16: 67-685Abstract Full Text Full Text PDF Scopus (647) Google Scholar, 35Lu Y. Cederbaum A.I. CYP2E1 and oxidative liver injury by alcohol.Free Radic Biol Med. 2008; 44: 723-738Crossref PubMed Scopus (580) Google Scholar Less than 10% of ethanol is excreted unchanged.36Norberg A. Jones A.W. Hahn R.G. Gabrielsson J.L. Role of variability in explaining ethanol pharmacokinetics: research and forensic applications.Clin Pharmacokinet. 2003; 42: 1-31Crossref PubMed Scopus (200) Google Scholar Reduced glutathione and hemeoxygenase-1 protect the liver against oxidative damage.37Louvet A. Mathurin P. Nat Rev Gastroenterol Hepatol. 2015; 12: 231-242Crossref PubMed Scopus (539) Google Scholar10.Answers A, B and CHCC is commonly associated with portal vein thrombosis (PVT). It is associated with worse survival and indicates advanced disease. PVT is more commonly seen in patients with low serum albumin and high AFP levels.38Connolly G.C. Chen R. Hyrien O. et al.Incidence, risk factors and consequences of portal vein and systemic thromboses in hepatocellular carcinoma.Thromb Res. 2008; 122: 299-306Abstract Full Text Full Text PDF PubMed Scopus (80) Google Scholar HCC patients with PVT have a higher frequency of MTHFR and prothrombin gene G20210A mutations.39Chawla Y.K. Bodh V. Portal vein thrombosis.J Clin Exp Hepatol. 2015; 5: 22-40Abstract Full Text Full Text PDF PubMed Scopus (96) Google Scholar, 40D’Amico M. Pasta L. Sammarco P. MTHFR C677TT, PAI1 4G-4G, V Leiden Q506, and prothrombin G20210A in hepatocellular carcinoma with and without portal vein thrombosis.J Thromb Thrombolysis. 2009; 28: 70-73Crossref PubMed Scopus (28) Google Scholar Contrast enhanced ultrasound can detect tumor invasion in 100% and correctly characterize it in 98% of patients, thus making it superior for detection than color Doppler sonography and computed tomography.41Rossi S. Rosa L. Ravetta V. et al.Contrast-enhanced versus conventional and color Doppler sonography for the detection of thrombosis of the portal and hepatic venous systems.Am J Roentgenol. 2006; 186: 763-773Crossref PubMed Scopus (107) Google Scholar Both radio frequency ablation and transarterial radioembolization with yttrium-90 glass microspheres appear to be safe and well tolerated in patients with portal vein obstruction without cavernous transformation.42Salem R. Lewandowski R. Roberts C. et al.Use of yttrium-90 glass microspheres (TheraSphere) for the treatment of unresectable hepatocellular carcinoma in patients with portal vein thrombosis.J Vasc Interv Radiol. 2004; 15: 335-345Abstract Full Text Full Text PDF PubMed Scopus (169) Google ScholarRadiation therapy is considered to be treatment of choice for selected patients with HCC and PV invasion especially for those with a favorable performance status.43Sotiropoulos G.C. Radtke A. Schmitz K.J. et al.Liver transplantation in the setting of hepatocellular carcinoma and portal vein thrombosis: a challenging dilemma?.Dig Dis Sci. 2008; 53: 1994-1999Crossref PubMed Scopus (26) Google Scholar The authors have none to declare. 5Fisher L. Fisher A. Vitamin D and parathyroid hormone in outpatients with noncholestatic chronic liver disease.Clin Gastroenterol Hepatol. 2007; 5: 513-520Abstract Full Text Full Text PDF PubMed Scopus (162) Google Scholar." @default.
• W2917559947 created "2019-03-02" @default.
• W2917559947 creator A5048552465 @default.
• W2917559947 creator A5072941129 @default.
• W2917559947 date "2015-09-01" @default.
• W2917559947 modified "2023-09-30" @default.
• W2917559947 title "Hepatobiliary Quiz (Answers)—15 (2015)" @default.
• W2917559947 cites W1607692077 @default.
• W2917559947 cites W1832039973 @default.
• W2917559947 cites W1921758419 @default.
• W2917559947 cites W1976173209 @default.
• W2917559947 cites W1976823670 @default.
• W2917559947 cites W1999580373 @default.
• W2917559947 cites W2007873773 @default.
• W2917559947 cites W2010060324 @default.
• W2917559947 cites W2020626093 @default.
• W2917559947 cites W2026586494 @default.
• W2917559947 cites W2028538822 @default.
• W2917559947 cites W2032762248 @default.
• W2917559947 cites W2039115358 @default.
• W2917559947 cites W2052141603 @default.
• W2917559947 cites W2056253552 @default.
• W2917559947 cites W2057870607 @default.
• W2917559947 cites W2059714773 @default.
• W2917559947 cites W2062366543 @default.
• W2917559947 cites W2069897516 @default.
• W2917559947 cites W2071776803 @default.
• W2917559947 cites W2072051307 @default.
• W2917559947 cites W2079105341 @default.
• W2917559947 cites W2080453532 @default.
• W2917559947 cites W2080960152 @default.
• W2917559947 cites W2082580350 @default.
• W2917559947 cites W2083924402 @default.
• W2917559947 cites W2087470352 @default.
• W2917559947 cites W2098784455 @default.
• W2917559947 cites W2108639407 @default.
• W2917559947 cites W2108757385 @default.
• W2917559947 cites W2111187697 @default.
• W2917559947 cites W2114375543 @default.
• W2917559947 cites W2132670336 @default.
• W2917559947 cites W2134717733 @default.
• W2917559947 cites W2134730949 @default.
• W2917559947 cites W2142618423 @default.
• W2917559947 cites W2148082224 @default.
• W2917559947 cites W2156760391 @default.
• W2917559947 cites W2170866619 @default.
• W2917559947 cites W2422465683 @default.
• W2917559947 cites W4230119926 @default.
• W2917559947 doi "https://doi.org/10.1016/j.jceh.2015.08.008" @default.
• W2917559947 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4632104" @default.
• W2917559947 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/26628847" @default.
• W2917559947 hasPublicationYear "2015" @default.
• W2917559947 type Work @default.
• W2917559947 sameAs 2917559947 @default.
• W2917559947 citedByCount "0" @default.
• W2917559947 crossrefType "journal-article" @default.
• W2917559947 hasAuthorship W2917559947A5048552465 @default.
• W2917559947 hasAuthorship W2917559947A5072941129 @default.
• W2917559947 hasBestOaLocation W29175599472 @default.
• W2917559947 hasConcept C136764020 @default.
• W2917559947 hasConcept C23123220 @default.
• W2917559947 hasConcept C41008148 @default.
• W2917559947 hasConcept C61434518 @default.
• W2917559947 hasConcept C71924100 @default.
• W2917559947 hasConcept C90924648 @default.
• W2917559947 hasConceptScore W2917559947C136764020 @default.
• W2917559947 hasConceptScore W2917559947C23123220 @default.
• W2917559947 hasConceptScore W2917559947C41008148 @default.
• W2917559947 hasConceptScore W2917559947C61434518 @default.
• W2917559947 hasConceptScore W2917559947C71924100 @default.
• W2917559947 hasConceptScore W2917559947C90924648 @default.
• W2917559947 hasIssue "3" @default.
• W2917559947 hasLocation W29175599471 @default.
• W2917559947 hasLocation W29175599472 @default.
• W2917559947 hasLocation W29175599473 @default.
• W2917559947 hasLocation W29175599474 @default.
• W2917559947 hasLocation W29175599475 @default.
• W2917559947 hasOpenAccess W2917559947 @default.
• W2917559947 hasPrimaryLocation W29175599471 @default.
• W2917559947 hasRelatedWork W2071494235 @default.
• W2917559947 hasRelatedWork W2370073206 @default.
• W2917559947 hasRelatedWork W2440682190 @default.
• W2917559947 hasRelatedWork W2748952813 @default.
• W2917559947 hasRelatedWork W2766770000 @default.
• W2917559947 hasRelatedWork W2967287585 @default.
• W2917559947 hasRelatedWork W3091391334 @default.
• W2917559947 hasRelatedWork W4253573160 @default.
• W2917559947 hasRelatedWork W4313346385 @default.
• W2917559947 hasRelatedWork W4317816533 @default.
• W2917559947 hasVolume "5" @default.
• W2917559947 isParatext "false" @default.
• W2917559947 isRetracted "false" @default.
• W2917559947 magId "2917559947" @default.
• W2917559947 workType "article" @default.