Extracorporeal Support in Liver Disease: Plasma Exchange/Plasmapheresis

2018 ◽  
pp. 71-73
Author(s):  
Deepti Sachan
Keyword(s):  
Liver Disease ◽  
Plasma Exchange ◽  
Extracorporeal Support

Plasma Exchange in Liver Disease

2015 ◽  
pp. 115-123
Author(s):  
G. Brunner ◽  
H. L�sgen
Keyword(s):  
Liver Disease ◽  
Plasma Exchange

scholarly journals Plasma exchange as treatment for acute fatty liver disease of pregnancy

2021 ◽  
Author(s):  
Mohammed Aabdi ◽  
Yassine Mellagui ◽  
Jamal Ouachaou ◽  
Essad Ounci ◽  
Houssam Bkiyar ◽  
...  
Keyword(s):  
Liver Disease ◽  
Fatty Liver ◽  
Plasma Exchange ◽  
Fatty Liver Disease ◽  
Acute Fatty Liver

Crystalloid Inclusions in Hepatocyte Mitochondria and Their Similarity to Cytoplasmic Crystalloids

1974 ◽  
Vol 32 ◽  
pp. 198-199
Author(s):  
Odell T. Minick ◽  
Hidejiro Yokoo
Keyword(s):  
Liver Disease ◽  
Alcoholic Liver Disease ◽  
Special Interest ◽  
Structural Variations ◽  
Mitochondrial Alterations ◽  
The Matrix ◽  
Crystalloid Inclusions ◽  
Liver Biopsies

Mitochondrial alterations were studied in 25 liver biopsies from patients with alcoholic liver disease. Of special interest were the morphologic resemblance of certain fine structural variations in mitochondria and crystalloid inclusions. Four types of alterations within mitochondria were found that seemed to relate to cytoplasmic crystalloids.Type 1 alteration consisted of localized groups of cristae, usually oriented in the long direction of the organelle (Fig. 1A). In this plane they appeared serrated at the periphery with blind endings in the matrix. Other sections revealed a system of equally-spaced diagonal lines lengthwise in the mitochondrion with cristae protruding from both ends (Fig. 1B). Profiles of this inclusion were not unlike tangential cuts of a crystalloid structure frequently seen in enlarged mitochondria described below.

Healing gone wrong: convergence of hemostatic pathways and liver fibrosis?

2020 ◽  
Vol 134 (16) ◽  
pp. 2189-2201
Author(s):  
Jessica P.E. Davis ◽  
Stephen H. Caldwell
Keyword(s):  
Wound Healing ◽  
Liver Disease ◽  
Hepatic Fibrosis ◽  
Cell Activation ◽  
Stellate Cell ◽  
Factor Xa ◽  
Clinical Trial Data ◽  
Chronic Liver ◽  
Healing Response ◽  
Wound Healing Response

Abstract Fibrosis results from a disordered wound healing response within the liver with activated hepatic stellate cells laying down dense, collagen-rich extracellular matrix that eventually restricts liver hepatic synthetic function and causes increased sinusoidal resistance. The end result of progressive fibrosis, cirrhosis, is associated with significant morbidity and mortality as well as tremendous economic burden. Fibrosis can be conceptualized as an aberrant wound healing response analogous to a chronic ankle sprain that is driven by chronic liver injury commonly over decades. Two unique aspects of hepatic fibrosis – the chronic nature of insult required and the liver’s unique ability to regenerate – give an opportunity for pharmacologic intervention to stop or slow the pace of fibrosis in patients early in the course of their liver disease. Two potential biologic mechanisms link together hemostasis and fibrosis: focal parenchymal extinction and direct stellate cell activation by thrombin and Factor Xa. Available translational research further supports the role of thrombosis in fibrosis. In this review, we will summarize what is known about the convergence of hemostatic changes and hepatic fibrosis in chronic liver disease and present current preclinical and clinical data exploring the relationship between the two. We will also present clinical trial data that underscores the potential use of anticoagulant therapy as an antifibrotic factor in liver disease.

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