Korean J Obstet Gynecol.  2012 Sep;55(9):649-654. 10.5468/KJOG.2012.55.9.649.

Acute fatty liver of pregnancy with fetal microvesicular hepatic steatosis

• Han WS
• Seo YS
• Im SY

• KMID: 2274137
• DOI: http://doi.org/10.5468/KJOG.2012.55.9.649

Abstract

Acute fatty liver of pregnancy (AFLP) is a serious maternal disease occurring in the third trimester of pregnancy with significant perinatal and maternal mortality. Until recently the pathogenesis of AFLP was unknown and still has not been fully elucidated. However, recent molecular advances suggest that AFLP may result from mitochondrial dysfunction. Several reports have documented a strong association between AFLP and a deficiency of the enzyme long-chain 3-hydroxyacyl-CoA dehydrogenase in the fetus, a disorder of mitochondrial fatty acid beta-oxidation. Therefore in this case, through findings of liver biopsy from dead fetus, we report possible causal relationship between fetal liver disease and maternal AFLP with literature reviews.

Keyword

Acute fatty liver of pregnancy; Fatty liver; Long-chain 3-hydroxyacyl-CoA dehydrogenase

MeSH Terms

Biopsy
Fatty Liver
Female
Fetus
Humans
Liver
Liver Diseases
Maternal Mortality
Oxidoreductases
Pregnancy
Pregnancy Complications
Pregnancy Trimester, Third
Fatty Liver
Oxidoreductases
Pregnancy Complications

Figure

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  Fig. 1 Microscopic findings of liver biopsy of dead fetus (Gram stain). (A) Low-power view (×100). (B) High-power view (×200). There are diffuse parenchymal hemorrhage with focal hemorrhagic infarction and microvesicular fatty metamorphosis (steatosis).

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  Fig. 2 Hypothesis illustrating the possible role of fetal and maternal MTP mutations in developing AFLP. Carrying an LCHAD deficient fetus (A) is the major determining factor in the development of maternal illness. Hepatotoxic metabolites produced by the fetus and/or placenta may cause liver disease in the obligate heterozygous mother when combined with the metabolic stress of the third trimester. Environmental stress (B) may lead to the further accumulation of toxic metabolites in the genetically susceptible mother causing maternal liver disease. LCHAD, long-chain 3-hydroxyacyl-CoA dehydrogenase; AFLP,acute fatty liver of pregnancy; MTP, mitochondrial trifunctional protein. (From Ibdah. World J Gastroenterol 2006;12:7397-404 [15]).

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