propylthiouracil and Hyperthyroxinemia

Pregnancy is characterised by a physiological increase in bound thyroxine but normal values of free hormone. Human chorionic gonadotrophin (hCG may stimulate the thyroid to produce hyperemesis gravidarum (with mild to moderate hyperthyroidism) or result in high thyroid hormone levels associated with gestational trophoblastic disease. Hyperthyroidism occurring during pregnancy is usually due to Graves' disease and must be treated to prevent congenital anomalies, low birth weight and premature labour. Thionamide drugs should be used with a preference for propylthiouracil (PTU) and continued in low doses up to labour. Breast feeding is possible in patients on low dose PTU. In the management of hypothyroidism during pregnancy thyroxine dose may require to be increased but excess dosage should be avoided because of its unwanted effects on foetal cerebral maturation. Neonatal hyperthyroidism due to transplacental passage of thyroid stimulating antibodies (TsAb) should be checked for in pregnant patients with autoimmune thyroid disease. As antithyroid drugs cross the placenta they may be used as therapy in this condition. Prevention of neonatal goitre is vital. Postpartum development of hyperthyroidism may be due to an exacerbation of pre-existing Graves' disease, development of new Graves' hyperthyroidism or postpartum thyroiditis with transient hyperthyroidism. Differentiation by measurement of TsAb and thyroidal iodine uptake is important because of therapeutic considerations.

Topics: Antithyroid Agents; Embryonic and Fetal Development; Female; Graves Disease; Humans; Hyperthyroxinemia; Immunoglobulins, Thyroid-Stimulating; Infant, Newborn; Iodine; Pregnancy; Pregnancy Complications; Propylthiouracil; Thyroid Gland; Thyroiditis, Autoimmune

Numerous clinical observations have provided evidence for a tight connection between impairments in the functions of the hypothalamo-hypophyseal-thyroid system and nervous and mental disorders. The aim of the present work was to compare the effects of experimental decreases and increases in blood thyroxine levels on the extents of two types of pathological freezing reaction in male Wistar rats--spontaneous catalepsy and catalepsy evoked by pinches at the nape of the neck (pinch-induced catalepsy). Chronic administration of the thyroxine synthesis inhibitor propylthiouracil (5 mg/kg/day for 28 days) significantly decreased the blood hormone level and sharply increased the proportion of animals showing spontaneous catalepsy and the immobility time, but had no effect on the extent of pinch-induced catalepsy. At the same time, chronic administration of thyroxine (0.1 mg/kg/day for 28 days), which produced significant increases in blood hormone levels, had no effect on the extent of spontaneous catalepsy but significantly increased the proportion of animals showing pinch-induced catalepsy and the duration of this type of catalepsy. It is concluded that both insufficiency and excess of thyroid hormones have cataleptogenic actions, but enhance different types of catalepsy.

Topics: Animals; Antithyroid Agents; Behavior, Animal; Drug Administration Schedule; Freezing Reaction, Cataleptic; Hyperthyroxinemia; Male; Methimazole; Propylthiouracil; Rats; Rats, Wistar; Thyroid Hormones; Thyroxine; Time Factors