scholarly journals Abstract No. 456 Comparing the incidence of radioembolization-induced liver disease between patients with and without hepatic surgery prior to radioembolization

2021 ◽  
Vol 32 (5) ◽  
pp. S113
Author(s):  
M. Rupasinghe ◽  
V. Ramachandran ◽  
F. Al-Khouja ◽  
D. Fernando ◽  
F. Dayyani ◽  
...  
Keyword(s):  
Liver Disease ◽  
Hepatic Surgery

Non-Hepatic Surgery in Chronic Liver Disease Patients: What are the Risks?

2015 ◽  
Vol 5 ◽  
pp. S29
Author(s):  
Rajesh Panwar ◽  
Srinivasan Ramachandran ◽  
Arif Ali Khan ◽  
Sujoy Pal ◽  
Nihar Dash ◽  
...  
Keyword(s):  
Liver Disease ◽  
Chronic Liver Disease ◽  
Chronic Liver ◽  
Hepatic Surgery

The Patient with Liver Disease for Non-hepatic Surgery

2012 ◽  
pp. 333-351
Author(s):  
Katherine Palmieri ◽  
Robert N. Sladen
Keyword(s):  
Liver Disease ◽  
Hepatic Surgery

The Patient with Liver Disease Undergoing Non-hepatic Surgery

2018 ◽  
pp. 389-411
Author(s):  
Katherine Palmieri ◽  
Robert N. Sladen
Keyword(s):  
Liver Disease ◽  
Hepatic Surgery

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.

Keratin 8 mutations in patient with cryptogenic liver disease

2001 ◽  
Vol 120 (5) ◽  
pp. A45-A45
Author(s):  
N KU ◽  
R GISH ◽  
T WRIGHT ◽  
M OMARY
Keyword(s):  
Liver Disease ◽  
Keratin 8

Does the Mayo Clinic end-stage liver disease model (MELD) accurately allocate organs to 2A patients?

2001 ◽  
Vol 120 (5) ◽  
pp. A77-A77
Author(s):  
C SPONSELLER ◽  
S RAMRAKHIANI ◽  
A BEFELER
Keyword(s):  
Liver Disease ◽  
Mayo Clinic ◽  
Disease Model ◽  
End Stage Liver Disease ◽  
End Stage
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