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Lipid Droplet Isolation for Quantitative Mass Spectrometry Analysis
Published on: April 17, 2017
Lipid profile in children with acute viral hepatitis A
Mukadder Ayse Selimoglu1, Ibrahim Caner, Leyla Yildiz
1Department of Pediatric Gastroenterology, Hepatology and Nutrition, Faculty of Medicine, Atatürk University, Erzurum, Turkey. ayseselimoglu@hotmail.com
Background:
Most of the knowledge about lipid parameters in acute hepatitis is originated from adult studies. In this study, the authors investigated lipid profile of children with acute hepatitis A (AVH) at diagnosis and recovery in order to observe the behavior of lipid parameters in such children.
Methods:
A total of 28 children (mean age, 8.2 +/- 2.7 years) with AVH and 20 gender and age-matched healthy children were included. In addition to the routine tests, triglyceride, cholesterol, low-density lipoprotein (LDL), high-density lipoprotein (HDL), plasma apo A-I and apo B were studied at diagnosis and recovery.
Results:
Serum triglyceride and apo B level was higher, and apo A-I level was lower in patients compared to healthy children (P < 0.01, <0.05 and <0.01, respectively). On admission, three children had fulminant hepatic failure (FHF). Serum lipid parameters were evaluated in respect with the presence of icterus and FHF, and found that apo A-I level was lower in icteric children and LDL and apo A-I were lower in FHF compared to others (P < 0.05, P < 0.01 and P < 0.05, respectively). At recovery, while triglyceride, cholesterol, LDL, and apo B decreased (P < 0.01), HDL and apo A-I increased (P < 0.01). Serum apo A-I level was inversely correlated with serum ammonia level but was positively correlated with serum albumin (P < 0.05).
Conclusions:
It was shown that serum triglyceride and apo B level increased, but apo A-I level decreased in patients with AVH. While cholestasis lowers apo A-I level, severe hepatic damage lowers both apo A-I and LDL. These parameters return to normal levels within 30 days. An interesting relationship between ammonia and apo A-I deserves further investigations, speculatively focused on hepatocyte nuclear factor 4 alpha.
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