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Background and Objectives: Clinical fetal thyrotoxicosis is a rare disorder occurring in 1–5% of pregnancies with Graves’ disease. Although transplacental passage of maternal TSH receptor stimulating autoantibodies (TRAb) to the fetus occurs early in gestation, their concentration in the fetus is reduced until the late second trimester, and reaches maternal levels in the last period of pregnancy. The mortality of fetal thyrotoxicosis is 12–20%, mainly due to heart failure. Case report: We present a case of fetal and neonatal thyrotoxicosis with favorable evolution under proper treatment in a 37-year-old woman. From her surgical history, we noted a thyroidectomy performed 12 years ago for Graves’ disease with orbitopathy and ophthalmopathy; the patient was hormonally balanced under substitution treatment for post-surgical hypothyroidism and hypoparathyroidism. From her obstetrical history, we remarked a untreated pregnancy complicated with fetal anasarca, premature birth, and neonatal death. The current pregnancy began with maternal euthyroid status and persistently increased TRAb, the value of which reached 101 IU/L at 20 weeks gestational age and decreased rapidly within 1 month to 7.5 IU/L, probably due to the placental passage, and occurred simultaneously with the development of fetal tachycardia, without any other fetal thyrotoxicosis signs. In order to treat fetal thyrotoxicosis, the patient was administered methimazole, in addition to her routine substitution of 137.5 ug L-Thyroxine daily, with good control of thyroid function in both mother and fetus. Conclusions: Monitoring for fetal thyrotoxicosis signs and maternal TRAb concentration may successfully guide the course of a pregnancy associated with Graves’ disease. An experienced team should be involved in the management.

Background and Objectives: Anabolic androgenic steroids (AAS), used as a therapy in various diseases and abused in sports, are atherogenic in supraphysiological administration, altering the plasma lipid profile. Taurine, a conditionally-essential amino acid often used in dietary supplements, was acknowledged to delay the onset and progression of atherogenesis, and to mitigate hyperlipidemia. The aim of the present study was to verify if taurine could prevent the alterations induced by concomitant chronic administration of high doses of AAS nandrolone decanoate (DECA) in rats. Materials and Methods: Thirty-two male Wistar rats, assigned to 4 equal groups, were treated for 12 weeks either with DECA (A group), taurine (T group), both DECA and taurine (AT group) or vehicle (C group). Plasma triglycerides (TG), total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), hepatic triglycerides (TGh) and liver non-esterified fatty acids (NEFA) were then determined. Results: DECA elevated TG level in A group vs. control (p = 0.01), an increase prevented by taurine association in AT group (p = 0.04). DECA decreased HDL-C in A group vs. control (p = 0.02), while taurine tended to increase it in AT group. DECA decreased TGh (p = 0.02) in A group vs. control. Taurine decreased TGh in T (p = 0.004) and AT (p < 0.001) groups vs. control and tended to lower NEFA (p = 0.08) in AT group vs. A group. Neither DECA, nor taurine influenced TC and LDL-C levels. Conclusions: Taurine partially prevented the occurrence of DECA negative effects on lipid profile, suggesting a therapeutic potential in several conditions associated with chronic high levels of plasma androgens, such as endocrine disorders or AAS-abuse.