AFLP causes nausea and vomiting, abdominal pain especially in the upper abdomen (epigastrium), jaundice (yellowing), frequent thirst (polydipsia) and increased urination (polyuria), fatigue, headache, and altered mental state.
Laboratory features of AFLP include profoundly low blood sugar (hypoglycemia), elevated liver enzymes (e.g., serum transaminase activity) and low levels of platelets (cell fragments in blood needed for clotting). The liver is infiltrated with fat.
AFLP is treated by delivering the baby as soon as possible. Early diagnosis of AFLP and prompt delivery dramatically improve the outcome and the once-bleak outlook.
Women with AFLP generally improve soon after delivery, unless the liver damage is severe. As a general rule, AFLP does not usually recur during a subsequent pregnancy.
However, AFLP has been found associated in some cases with an abnormality of fatty-acid metabolism. This abnormality is a deficiency of the enzyme long-chain-3-hydroxyacyl-CoA dehydrogenease (LCHAD). The mother (and father) have 50% of normal LCHAD activity and the fetus has no LCHAD activity. The metabolic disease in the baby's liver apparently causes the fatty liver disease in the mother. In cases of AFLP due to LCHAD deficiency, there is a 25% (or greater) risk of AFLP in each pregnancy.