Isolated maternal hypothyroxinemia has no adverse effects on perinatal outcome. Moreover, unlike subclinical hypothyroidism, there was a low prevalence of thyroid peroxidase antibodies and no correlation between TSH and free T(4) levels in women with hypothyroxinemia, leading us to question its biological significance.

Coassolo and colleagues are to be congratulated for building a very large database on women with prior cesarean. 1 This important work and its related findings should help in the difficult task of counseling a patient between a trial of labor and elective repeat cesarean. In their latest publication, 1 they concluded that the risk of uterine rupture was not increased at or beyond 41 weeks of gestation. The rate of uterine rupture in 1,643 women who delivered at or beyond 41 weeks (1.46%) was almost significantly greater than at less than 41 weeks (0.97%) (relative risk 1.51, 95% confidence interval [CI] 0.97-2.36). However, the difference was reduced after adjustment for confounding factors (odds ratio 1.25, 95% CI 0.78 -1.98).These findings are slightly different from ours. 2 We recorded a higher rate of uterine rupture (odds ratio 2.85, 95% CI 1.27-6.42) in women delivering at or beyond 41 weeks of gestation. Due to the smaller size of our study and the rarity of uterine rupture, the CI was very large. It is possible that the real relative risk for uterine rupture at or beyond 41 weeks is closer to 1.5 than 2.9. However, to find such a difference, the calculation of gestational age must be accurate, because inaccuracies will most likely mix the 2 groups (before and after 41 weeks) and reduce the difference between them. In our study, the large majority, if not all, of patients had a first-or second-trimester ultrasound examination for the purpose of dating before 20 weeks of gestation. Although Coassolo et al 1 wrote that women with an unknown or inaccurate gestational age estimate at delivery were excluded; they did not define their method of obtaining an accurate gestational age estimate. We believe that such a study should only include women who underwent antenatal ultrasound before 20 weeks to obtain accu-rate estimated dates of delivery and accurate results.

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Acute fatty liver of pregnancy (AFLP) is a rare and dreaded complication of pregnancy, almost exclusively seen in the third trimester. The histopathologic features of AFLP closely resemble those seen in metabolic disorders characterized by deficiency of fatty acid oxidative enzymes. Several reports have established a strong association between AFLP in the mother and fetal deficiency of the enzyme long-chain L-3-hydroxyacyl-CoA dehydrogenase (LCHAD). However, these studies have an inevitable selection bias resulting from ascertainment through an affected infant, rather than an unselected population of patients with AFLP. We retrospectively examined a series of 10 women with pregnancies complicated by AFLP to determine the prevalence of the common LCHAD mutation (G1528C) in this population. The existing LCHAD primers, which produce a 640-bp amplicon (IJlst L, Ruiter JP, Hoovers JM, Jakobs ME, Wanders RJ: J Clin Invest 98: 1028 -1033, 1996), were modified to make them amenable to analysis of fragmented DNA obtained from microdissected formalin-fixed material. None of the patients were found to harbor the common G1528C mutation. It is likely that AFLP arising in the context of fetal LCHAD deficiency represents only one of the possible etiologies for this uncommon disorder, and the metabolic basis of AFLP is more heterogeneous than previously believed. A spectrum of maternal liver disorders can occur during pregnancy. Many, such as hepatitis or drug-induced hepatotoxicity, can also be seen in nonpregnant individuals, whereas others, including preeclampsia and intrahepatic cholestasis of pregnancy, are unique to the gravid state (1). AFLP is an uncommon but clinically severe form of hepatopathy that is seen almost exclusively in the third trimester of pregnancy. AFLP manifests with jaundice, which can rapidly progress to severe coagulopathy, fulminant hepatic failure, and death of both mother and fetus. Approximately 50% of affected patients have preeclampsia with high blood pressure, proteinuria, and peripheral edema, and up to 20% may have AFLP coexisting with the HELLP syndrome (1). AFLP derives its name from the presence of marked microvesicular steatosis in the liver, often with involvement of the heart, kidneys, and pancreas. Recent studies have reported a maternal mortality rate of 10 -20% with AFLP, underscoring the need for early diagnosis and intervention. The cornerstone of therapy is delivery of the fetus, and the clinical condition dramatically ameliorates in the postpartum period.In recent years, investigators have speculated that AFLP/ HELLP syndrome and certain inherited fatty acid oxidation disorders, specifically LCHAD deficiency, may share a common pathogenic mechanism, based on striking similarities in hepatic pathology. This empirical association was strengthened by reports of AFLP or HELLP syndrome occurring during the third trimester in mothers bearing children with LCHAD deficiency. For example, Wilcken et al. (2) were the first to report the occurrence of AFLP and HELLP syndrome in six of six...

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