Pruebas de función tiroidea en embarazadas normales (tercer trimestre) y en embarazadas con colestasis gravídica o con hepatitis aguda
Background: Intrahepatic cholestasis of pregnancy (ICP) is a disease of unknown cause characterized by pruritus and biochemical cholestasis in the 3rd trimester of pregnancy. Its pathogenesis may be due to the interaction of abnormalities in the metabolism of estrogens and progesterone, while still unknown environmental factor (s) modulate the expressivity of a genetic predisposing trait. Aims: To verify if thyroid function tests (TFT) are altered in ICP as in other hepatic diseases and whether a dietary iodine deficiency could be involved. Material and methods: From 1983 to 1986, 13 normal pregnancies (3rd trimester), 26 ICP patients (with 30 pregnancies) and 4 patients with acute non-A non-B hepatitis in pregnancy, were studied. Serum T3, rT3, T4, fT4 and TSH (before and after TRH) were measured by RIA; in ICP patients, measurements were repeated in puerperium. Urinary 24 h iodine excretion was measured in normal pregnancies and in 6 ICP patients. Results: In normal pregnancies, T3 (3.00±0.22 nmol/L) and rT3 (0.40±0.03 nmol/L) were higher than the values detected in non-pregnant women; other TFT were unchanged. Urinary iodine excretion was normal in all individuals tested. Patients with acute hepatitis in pregnancy or with ICP had lower T3 than normal pregnancies (1.82±0.19 nmol/L in hepatitis; 2.24±0.12 nmol/L in ICP; p<0.01) and higher rT3 (0.80±0.25 nmol/L in hepatitis; 0.54±0.05 nmol/L in ICP; p<0.05), while other TFT were unchanged. None of them had clinical signs of hypo or hyperthyroidism. A "euthyroid sick syndrome" was detected in 2 ICP patients and in 2 acute hepatitis in pregnancy. In puerperium of ICP patients, T3 and rT3 returned to levels in non-pregnant women. Conclusions: In ICP patients, TFT show similar trends than in more severe hepatic and non-hepatic diseases. Although thyroid binding-globulin was not measured in our patients, the pattern of TFT suggests that an impaired peripheral (hepatic?) deiodination of T4 is responsible for these changes. The influence of a dietary iodine deficiency can be ruled out. (Rev Méd Chile 2000; 128: 35-43).