Neonatal jaundice and liver disease

2013 ◽  
pp. 259-272
Author(s):  
Janet M Rennie ◽  
Giles S Kendall
Author(s):  
G. D. Maiti ◽  
Arup Ratan Pal ◽  
Tony Jose ◽  
Monica Saraswat

Background: Intrahepatic cholestasis of pregnancy (IHCP) is the most common cholestatic liver disease, which may impact the foeto-maternal health. The present study is conducted to determine various factors including maternal and neonatal outcome in IHCP comparing with the controls.Methods: In this prospective case control study, pregnancy with IHCP is compared with asymptomatic non-IHCP controls. Classical pruritus, icterus, elevated liver enzymes were considered in diagnostic criteria of IHCP. Dermatological lesion, acute or chronic liver disease, and other causes of pruritus were excluded from study.Results: Out of 100 patients, 50 cases and 50 controls were included in this study. Incidence of IHCP was seen 3.914% of which 66% were primi presented maximum at 31-33 weeks. 86% of IHCP responded to medication. Mean value of ALT, AST and ALP was found significantly raised (p value-<0.001) in IHCP patients. 66% in IHCP and 64% in non-IHCP group had normal delivery and remaining 34% and 36 % had caesarean delivery respectively. There was no significant increase in foetal distress or low Apgar (<7 at 5 min) at birth or adverse neonatal or maternal outcome in IHCP group. However, there was a statistically high meconium stained liquor (MSL), neonatal jaundice, IUGR and NICU admission were noted in the IHCP group in comparison to non-IHCP group.Conclusions: There is a significant incidence of IHCP in the obstetrical population. The biochemical changes, meconium stained liquor, neonatal jaundice, IUGR and NICU admission were significantly high in IHCP in pregnancy.


2017 ◽  
Vol 103 (4) ◽  
pp. 170-176
Author(s):  
Jake P Mann ◽  
Kathy Gallagher ◽  
Emer Fitzpatrick ◽  
Anil Dhawan

Liver disease in children can present in many ways from the frequently encountered prolonged neonatal jaundice to the comparatively rare acute liver failure. In this article, we will discuss ‘red flags’ of liver disease, the initial investigations required and when to refer to a specialist liver centre. Across all presentations, the degree of elevation of alanine aminotransferase or aspartate aminotransferase provides only little diagnostic information. Measurement of clotting is vital, and coagulopathy should be followed by a trial of intravenous vitamin K before being repeated.


Author(s):  
Michael Kaplan ◽  
Ronald J. Wong ◽  
Eric Sibley ◽  
David K. Stevenson

Author(s):  
Odell T. Minick ◽  
Hidejiro Yokoo

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.


2020 ◽  
Vol 134 (16) ◽  
pp. 2189-2201
Author(s):  
Jessica P.E. Davis ◽  
Stephen H. Caldwell

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.


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

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