FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2746335859> ?p ?o ?g. }

• W2746335859 endingPage "743" @default.
• W2746335859 startingPage "733" @default.
• W2746335859 abstract "Liver dysfunction and jaundice are traditionally viewed as late features of sepsis and other critical illnesses and are associated with a complicated ICU stay. However, study results suggest that cholestatic alterations occur early in the course of critical illnesses, perceived only as minor abnormalities in routinely used biochemical liver tests. Inflammation-induced alterations in the transport of bile acids (BAs) appear to drive BAs and bilirubin toward the systemic circulation. Ongoing BA synthesis with an, at least partial, loss of feedback inhibition further contributes to elevated circulating BAs and bilirubin. To what extent these changes reflect a biochemical epiphenomenon, true illness-induced liver dysfunction, or a beneficial and adaptive response to illness should be investigated further. Because of the lack of specificity of standard laboratory tests, especially in the context of a complex systemic condition such as critical illness, identifying true cholestatic liver dysfunction remains a great challenge. However, high levels of cholestatic markers that are sustained in patients with prolonged critical illness almost always indicate a complicated illness course and should be monitored closely. Preventing cholestatic liver dysfunction comprises minimizing inflammation and hypoxia in the liver and preventing hyperglycemia, avoiding early use of parenteral nutrition, and reducing the administration of avoidable drugs. Future research on the effects of BAs and on modulating underlying drivers of cholestasis induced by critical illness is warranted as this could open perspectives for a targeted diagnostic approach and ultimately for novel therapies to improve outcome. Liver dysfunction and jaundice are traditionally viewed as late features of sepsis and other critical illnesses and are associated with a complicated ICU stay. However, study results suggest that cholestatic alterations occur early in the course of critical illnesses, perceived only as minor abnormalities in routinely used biochemical liver tests. Inflammation-induced alterations in the transport of bile acids (BAs) appear to drive BAs and bilirubin toward the systemic circulation. Ongoing BA synthesis with an, at least partial, loss of feedback inhibition further contributes to elevated circulating BAs and bilirubin. To what extent these changes reflect a biochemical epiphenomenon, true illness-induced liver dysfunction, or a beneficial and adaptive response to illness should be investigated further. Because of the lack of specificity of standard laboratory tests, especially in the context of a complex systemic condition such as critical illness, identifying true cholestatic liver dysfunction remains a great challenge. However, high levels of cholestatic markers that are sustained in patients with prolonged critical illness almost always indicate a complicated illness course and should be monitored closely. Preventing cholestatic liver dysfunction comprises minimizing inflammation and hypoxia in the liver and preventing hyperglycemia, avoiding early use of parenteral nutrition, and reducing the administration of avoidable drugs. Future research on the effects of BAs and on modulating underlying drivers of cholestasis induced by critical illness is warranted as this could open perspectives for a targeted diagnostic approach and ultimately for novel therapies to improve outcome." @default.
• W2746335859 created "2017-08-31" @default.
• W2746335859 creator A5010676881 @default.
• W2746335859 creator A5035530316 @default.
• W2746335859 creator A5042145557 @default.
• W2746335859 date "2018-03-01" @default.
• W2746335859 modified "2023-10-05" @default.
• W2746335859 title "Cholestatic Alterations in the Critically Ill" @default.
• W2746335859 cites W1551962418 @default.
• W2746335859 cites W1714819896 @default.
• W2746335859 cites W1842949686 @default.
• W2746335859 cites W1898928487 @default.
• W2746335859 cites W1964122395 @default.
• W2746335859 cites W1964571289 @default.
• W2746335859 cites W1965625918 @default.
• W2746335859 cites W1966408369 @default.
• W2746335859 cites W1967056255 @default.
• W2746335859 cites W1969435907 @default.
• W2746335859 cites W1972665722 @default.
• W2746335859 cites W1973459352 @default.
• W2746335859 cites W1980366428 @default.
• W2746335859 cites W1980717583 @default.
• W2746335859 cites W1980944102 @default.
• W2746335859 cites W1984332693 @default.
• W2746335859 cites W1987777210 @default.
• W2746335859 cites W1989404241 @default.
• W2746335859 cites W1991384293 @default.
• W2746335859 cites W1991796759 @default.
• W2746335859 cites W1992075095 @default.
• W2746335859 cites W1998609605 @default.
• W2746335859 cites W2000754297 @default.
• W2746335859 cites W2002121467 @default.
• W2746335859 cites W2007670274 @default.
• W2746335859 cites W2009569201 @default.
• W2746335859 cites W2009648599 @default.
• W2746335859 cites W2019332725 @default.
• W2746335859 cites W2021032925 @default.
• W2746335859 cites W2021238888 @default.
• W2746335859 cites W2024705421 @default.
• W2746335859 cites W2025300958 @default.
• W2746335859 cites W2029253842 @default.
• W2746335859 cites W2033987199 @default.
• W2746335859 cites W2034930488 @default.
• W2746335859 cites W2039104165 @default.
• W2746335859 cites W2043666615 @default.
• W2746335859 cites W2045499771 @default.
• W2746335859 cites W2047747888 @default.
• W2746335859 cites W2058419808 @default.
• W2746335859 cites W2066590648 @default.
• W2746335859 cites W2069243984 @default.
• W2746335859 cites W2071108985 @default.
• W2746335859 cites W2071896216 @default.
• W2746335859 cites W2076706503 @default.
• W2746335859 cites W2081028309 @default.
• W2746335859 cites W2081710964 @default.
• W2746335859 cites W2082313692 @default.
• W2746335859 cites W2083523566 @default.
• W2746335859 cites W2087577664 @default.
• W2746335859 cites W2090175582 @default.
• W2746335859 cites W2091438598 @default.
• W2746335859 cites W2095002839 @default.
• W2746335859 cites W2095128491 @default.
• W2746335859 cites W2100018795 @default.
• W2746335859 cites W2106515170 @default.
• W2746335859 cites W2110258828 @default.
• W2746335859 cites W2111157610 @default.
• W2746335859 cites W2115285670 @default.
• W2746335859 cites W2118073002 @default.
• W2746335859 cites W2121901734 @default.
• W2746335859 cites W2130420663 @default.
• W2746335859 cites W2131940641 @default.
• W2746335859 cites W2132423441 @default.
• W2746335859 cites W2139518083 @default.
• W2746335859 cites W2140962831 @default.
• W2746335859 cites W2142945080 @default.
• W2746335859 cites W2142991094 @default.
• W2746335859 cites W2145050940 @default.
• W2746335859 cites W2146074518 @default.
• W2746335859 cites W2146939418 @default.
• W2746335859 cites W2150055309 @default.
• W2746335859 cites W2150902017 @default.
• W2746335859 cites W2155270860 @default.
• W2746335859 cites W2160553550 @default.
• W2746335859 cites W2162310928 @default.
• W2746335859 cites W2166972699 @default.
• W2746335859 cites W2167088056 @default.
• W2746335859 cites W2172129947 @default.
• W2746335859 cites W2182818190 @default.
• W2746335859 cites W2268800856 @default.
• W2746335859 cites W2307805172 @default.
• W2746335859 cites W2401719360 @default.
• W2746335859 cites W2442246762 @default.
• W2746335859 cites W2611140688 @default.
• W2746335859 cites W408608 @default.
• W2746335859 cites W4253558349 @default.
• W2746335859 cites W4293201222 @default.
• W2746335859 doi "https://doi.org/10.1016/j.chest.2017.08.018" @default.
• W2746335859 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/28847548" @default.

• next