374. Using acylcarnitine screening for identification of newborn fatty acid oxidation disorders (FAOD) from pregnancies complicated by acute fatty liver

2018 ◽  
Vol 13 ◽  
pp. S46
Author(s):  
Sheba Jarvis ◽  
Michael Champion ◽  
Yusof Rahman ◽  
Charles Turner ◽  
Neil Dalton ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Fatty Liver ◽  
Fatty Acid Oxidation ◽  
Acid Oxidation ◽  
Fatty Acid Oxidation Disorders ◽  
Acute Fatty Liver

scholarly journals Acute fatty liver of pregnancy: an update on mechanisms

2011 ◽  
Vol 4 (3) ◽  
pp. 99-103 ◽  
Author(s):  
Sathish Kumar Natarajan ◽  
Kavitha R Thangaraj ◽  
Ashish Goel ◽  
C E Eapen ◽  
K A Balasubramanian ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Fatty Acid ◽  
Fatty Liver ◽  
Fatty Acid Oxidation ◽  
Acid Oxidation ◽  
Maternal Circulation ◽  
Subcellular Organelles ◽  
Microvesicular Steatosis ◽  
Acute Fatty Liver ◽  
And Oxidative Stress

Acute fatty liver of pregnancy (AFLP), characterized by hepatic microvesicular steatosis, is a sudden catastrophic illness occurring almost exclusively in the third trimester of pregnancy. Defective fatty acid oxidation in the fetus has been shown to be associated with this disease. Since the placenta has the same genetic makeup as the fetus and as AFLP patients generally recover following delivery, we hypothesized that the placenta might be involved in pathogenesis of this disease. In an animal model of hepatic microvesicular steatosis (using sodium valproate), we found that microvesicular steatosis results in mitochondrial structural alterations and oxidative stress in subcellular organelles of the liver. In placentas from patients with AFLP, we observed placental mitochondrial dysfunction and oxidative stress in subcellular organelles. In addition, defective placental fatty acid oxidation results in accumulation of toxic mediators such as arachidonic acid. Escape of these mediators into the maternal circulation might affect the maternal liver resulting in microvesicular steatosis.

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