Patient's question:
Alias: Acute False Yellow Liver Atrophy of Obstetrics, Idiopathic Fatty Liver of Pregnancy, Fatty Liver Change of Pregnancy in Obstetrics, Acute False Yellow Liver Atrophy of Obstetrics, Idiopathic Fatty Liver of Pregnancy, Fatty Liver Change of Pregnancy in Obstetrics, Acute of PregnancyDoctor's answer:
Non-alcoholic fatty liver disease, also known as obstetric acute pseudos yellowness liver atrophy, is a rare and fatal disease specific to late pregnancy. The disease onset is abrupt, with rapid changes in condition, occurring between weeks 28 and 40 of pregnancy. It is more common in first-time mothers around 35 weeks of gestation, with higher occurrences in cases of pregnancy-induced hypertension, twin pregnancies, and male fetuses.Acute fatty liver of pregnancy (AFLP), also known as obstetric acute pseudos yellowness liver atrophy, is a rare and fatal disease specific to late pregnancy. The disease onset is abrupt, with rapid changes in condition, and its clinical manifestations resemble acute viral hepatitis. Previous literature reports maternal and fetal mortality rates of 75% and 85%, respectively. However, if early diagnosis, early treatment, and timely termination of pregnancy are achieved, maternal mortality can be reduced, and infant mortality can be lowered to 58.3%.
### Pathogenic Factors or Etiology
The etiology of AFLP is unclear. Since AFLP occurs in late pregnancy and only recovery is possible with termination of pregnancy, it is hypothesized that hormonal changes induced by pregnancy disrupt fatty acid metabolism, leading to the accumulation of free fatty acids in hepatocytes and other organs such as the kidneys, pancreas, and brain, causing multi-organ damage. In recent years, there have been reports of multiple recurrent cases and genetic defects in offspring, suggesting that it may be a congenital genetic disorder. Additionally, factors such as viral infection, poisoning, drugs (e.g., tetracycline), malnutrition, and pregnancy-induced hypertension may also contribute to the damage of mitochondrial fatty acid oxidation.