Results 321 to 330 of about 113,305 (364)
Mechanisms of Cholestasis [PDF]
This article gives an overview of the molecular and cellular mechanisms of cholestasis. Topics reviewed include the pathomechanisms of hereditary cholestasis syndromes, such as progressive familial intrahepatic cholestasis, and hepatocellular transporter defects encountered in various acquired cholestatic disorders, such as intrahepatic cholestasis of ...
Michael Trauner, Gernot Zollner
openaire +2 more sources
Sepsis-associated cholestasis should always be considered as part of the differential diagnosis of jaundice in the hospitalized or critically ill patient. The development of a disproportionate elevation of serum bilirubin in comparison with serum alkaline phosphatase and serum aminotransferases should be considered an early warning sign of an ...
openaire +3 more sources
Some of the next articles are maybe not open access.
Related searches:
Related searches:
Clinics in Liver Disease, 2000
From the multiple mechanisms of cholestasis presented in this article, a unifying hypothesis may be deduced by parsimony. The disturbance of the flow of bile must inevitably lead to the intracellular retention of biliary constituents. Alternatively, the lack of specific components of bile unmasks the toxic potential of other components, as in the case ...
Kullak-Ublick, G. A., Meier, P. J.
openaire +3 more sources
From the multiple mechanisms of cholestasis presented in this article, a unifying hypothesis may be deduced by parsimony. The disturbance of the flow of bile must inevitably lead to the intracellular retention of biliary constituents. Alternatively, the lack of specific components of bile unmasks the toxic potential of other components, as in the case ...
Kullak-Ublick, G. A., Meier, P. J.
openaire +3 more sources
Natural products for the prevention and treatment of cholestasis: A review
Phytotherapy Research, 2020Cholestasis is a common manifestation of decreased bile flow in various liver diseases. It results in fibrosis and even cirrhosis without proper treatment.
Xiao Ma +9 more
semanticscholar +1 more source
Clinics in Liver Disease, 2008
Cholestasis is a common complication of bacterial infections and sepsis. This article gives a comprehensive overview of the underlying molecular mechanisms of sepsis-associated cholestasis and jaundice, their clinical presentation, and diagnostic and therapeutic management.
Michael Fuchs, Arun J. Sanyal
openaire +3 more sources
Cholestasis is a common complication of bacterial infections and sepsis. This article gives a comprehensive overview of the underlying molecular mechanisms of sepsis-associated cholestasis and jaundice, their clinical presentation, and diagnostic and therapeutic management.
Michael Fuchs, Arun J. Sanyal
openaire +3 more sources
Liver international (Print), 2020
In about 20% of children with cholestasis and normal or low serum gamma‐glutamyltransferase (GGT) activity, no aetiology is identified. We sought new genes implicated in paediatric hepatobiliary disease.
Jing Zhang +11 more
semanticscholar +1 more source
In about 20% of children with cholestasis and normal or low serum gamma‐glutamyltransferase (GGT) activity, no aetiology is identified. We sought new genes implicated in paediatric hepatobiliary disease.
Jing Zhang +11 more
semanticscholar +1 more source
Best Practice & Research Clinical Gastroenterology, 2010
Progressive familial intrahepatic cholestasis (PFIC) type 1, 2 and 3 are due to mutations in ATP8B1, ABCB11 and ABCB4, respectively. Each of these genes encodes a hepatocanalicular transporter, which is essential for the proper formation of bile. Mutations in ABCB4 can result in progressive cholestatic disease, while mutations in ATP8B1 and ABCB11 can ...
Wendy L. van der Woerd +5 more
openaire +3 more sources
Progressive familial intrahepatic cholestasis (PFIC) type 1, 2 and 3 are due to mutations in ATP8B1, ABCB11 and ABCB4, respectively. Each of these genes encodes a hepatocanalicular transporter, which is essential for the proper formation of bile. Mutations in ABCB4 can result in progressive cholestatic disease, while mutations in ATP8B1 and ABCB11 can ...
Wendy L. van der Woerd +5 more
openaire +3 more sources
Seminars in Dermatology, 1995
The pruritus of cholestasis is a difficult clinical problem to manage. The pathogenesis of this symptom is unknown. All conventional therapies have been unsuccessful in isolating a particular group of substances that could be implicated as direct or indirect causative agents.
openaire +5 more sources
The pruritus of cholestasis is a difficult clinical problem to manage. The pathogenesis of this symptom is unknown. All conventional therapies have been unsuccessful in isolating a particular group of substances that could be implicated as direct or indirect causative agents.
openaire +5 more sources
Pediatric Annals, 2016
Jaundice is a key manifestation of hepatobiliary disease in all age groups. Jaundice is a common finding in the first 2 weeks after birth, occurring in 2.4% to 15% of newborns. The neonatal liver is at increased susceptibility to cholestasis, with an incidence ranging from 1 in 2,500 to 1 in 5,000 live births. Etiologies vary, but the most
Melissa G Andrianov, Ruba Azzam
openaire +2 more sources
Jaundice is a key manifestation of hepatobiliary disease in all age groups. Jaundice is a common finding in the first 2 weeks after birth, occurring in 2.4% to 15% of newborns. The neonatal liver is at increased susceptibility to cholestasis, with an incidence ranging from 1 in 2,500 to 1 in 5,000 live births. Etiologies vary, but the most
Melissa G Andrianov, Ruba Azzam
openaire +2 more sources
Pathophysiology of cholestasis
Human Pathology, 1970Abstract Cholestasis is postulated to be a disturbance of the secretion of micelles of bile salts mixed with other solids. This disturbance results in alteration of bile canalicular microvilli, canalicular dilatation, whidening of the pericanalicular ectoplasm, enlargement of the Golgi zone, and increase in smooth endoplasmic reticulum. Cholestasis is
Hans Popper, Fenton Schaffner
openaire +3 more sources

