Acute fatty liver of pregnancy

The cause of acute fatty liver of pregnancy (AFLP) is not fully understood. Genetics may play a role. Recent studies indicate that AFLP may be the result of a mitochondrial dysfunction in the oxidation of fatty acids in the liver. More specifically, there may be a deficiency of long-chain 3-hydroxyacyl-CoA dehydrogenase, an enzyme used to break down long chain fatty acids. Babies with this deficiency can develop life-threatening liver, heart and neuromuscular problems unless they are started on a special low-fat formula. For this reason, it has been suggested that babies born to women with AFLP be tested for fatty acid oxidation disorders. Although the risk of AFLP in subsequent pregnancies is unknown, it can occur in future pregnancies, even if testing for long- chain 3-hydroxyacyl-CoA dehydrogenase (LCHAD) deficiency is negative.

The diagnosis of acute fatty liver disease of pregnancy (AFLP) is usually made based on clinical findings, includng setting, presentation, and laboratory and imaging results. Laboratory tests that may be helpful include serum aminotransferases, serum bilirubin, coagulation studies, electrolytes, serum glucose, uric acid levels, creatinine and white blood count. Imaging tests are used primarily to exclude other diagnoses. Liver biopsy is diagnostic, but not always possible during pregnancy.

Treatment of acute fatty liver of pregnancy (AFLP) involves stabilizing the mother and delivery of the baby. Detailed information about management of both mother and baby is available through Medscape Reference.