Abstract：
:Hyperemesis gravidarum (HG) is the most severe form of illness within the spectrum of nausea and vomiting of pregnancy. Liver disease, usually consisting of mild serum transaminase elevation, occurs in almost 50% of patients with HG. While multiple risk factors have been proposed, the etiology and underlying mechanism of maternal liver disease associated with HG remains unclear. In this report, we hypothesize that impairment of mitochondrial fatty acid oxidation (FAO) plays a role in the pathogenesis of maternal liver disease associated with HG. We hypothesize that women heterozygous for FAO defects develop HG associated with liver disease while carrying fetuses with FAO defects due to accumulation of fatty acids in placenta and subsequent generation of reactive oxygen species. Alternatively, it is possible that starvation leading to peripheral lipolysis and increased load of fatty acids in maternal-fetal circulation, combined with reduced capacity of the mitochondria to oxidize fatty acids in mothers heterozygous for FAO defects, can also cause HG and liver injury while carrying non-affected fetuses. The rationale for this hypothesis is discussed.
journal_name
Med Hypothesesjournal_title
Medical hypothesesauthors
Outlaw WM,Ibdah JAdoi
10.1016/j.mehy.2005.05.035keywords:
subject
Has Abstractpub_date
2005-01-01 00:00:00pages
1150-3issue
6eissn
0306-9877issn
1532-2777pii
S0306-9877(05)00282-3journal_volume
65pub_type
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