Figure 2.

Hypothesis illustrating the possible role of fetal and maternal mitochondrial trifunctional protein mutations in developing AFLP. (A) Carrying an LCHAD‐deficient fetus 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. (B) Environmental stress may lead to the further accumulation of toxic metabolites in the genetically susceptible mother, causing maternal liver disease. Reproduced with permission from Hammoud.13