Thyroid function tests in normal pregnancies (third trimester) and in women with intrahepatic cholestasis of pregnancy or with acute hepatitis in pregnancy

Background: Intrahepatic cholestasis of pregnancy (ICP) is a disease of unk nown 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 environment factor (s) modulate the expressivity of a genetic predi sposing 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. Materials and methods: From 1983 to 1986, 13 normal pre gnancies (3rd trimester), 26 ICP patients (with 30 pregnancies) and 4 patie nts 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 pa tients, measurements were repeated in puerperium. Urinary 24 h iodine excre tion 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 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 rT 3 (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 bad clinical signs of hypo o r hyperthyroidism. A "euthyroid sick syndrome" was detected in 2 ICP patien ts and in 2 acute hepatitis in pregnancy. In puertertum of ICP patients, T3 and rT3 returned to levels in non-pregnant women. Conclusions: In ICP pati ents, TFT show similar trends than in more severe hepatic and non-hepatic d iseases. Although thyroid binding-globulin was not measured in our patients , the pattern of TFT suggests that an impaired peripheral (hepatic?) deiodi nation of T4 is responsible for these changes. The influence of a dietary i odine deficiency can be ruled out.