Thyroid disease is common in younger women and may be a factor in reproductive dysfunction. Once adequately treated this disorder is associated with successful pregnancy outcome. The key is to recognize and to treat thyroid disorders in the reproductive-age woman before conception. Pregnancy is a euthyroid state that is normally maintained by complex changes in thyroid physiology. The fetal hypothalamic-pituitary-thyroid system develops independently and the process is generally complete by the 12 ^th week of intrauterine life. Early pregnancy is characterized by an increase in maternal T4 secretion stimulated by hCG and an increase in TBG, resulting in elevated total serum T4 in pregnancy. Maternal T4 is important in fetal brain development. There is evidence in human subjects that substantial maternal T4 can cross the placenta during pregnancy, and this is particularly important when there is fetal thyroid agenesis. Maternal and fetal/ neonatal outcomes in pregnancy are adversely affected if severe hypothyroidism is undiagnosed or inadequately treated. Thyroid function tests should be obtained during gestation in women taking thyroxine and appropriate dose adjustments should be made for Free T4 and TSH levels outside the normal range. TSH-receptor blocking antibodies from the mother are a recognized cause of congenital hypothyroidism in the fetus and neonate that can be permanent or transient. Pathophysiologic conditions of hCG secretion such as gestational trophoblastic disease and hyperemesis gravidarum may present as thyrotoxicosis in the first trimester of pregnancy. However the main cause of hyperthyroidism in pregnancy is Graves ' disease. The mainstay of treatment is antithyroid drugs and either propylthiouracil or methimazole may be used safely. Subtotal thyroidectomy, after medical control, is the alternative treatment, but radioiodine ablation is contraindicated. Postpartum thyroiditis can present with transient hyperthyroidism which subsequently evolves into hypothyroidism.

The role of thyroid scintigraphy in ruling out thyroiditis in patients with thyrotoxicosis is well known. However its role in prognostic decision-making with regards to lifelong thyroxin replacement has not been critically evaluated. We undertook a retrospective analysis in this regard. Totally 62 patients of thyroiditis were retrospectively evaluated with respect to clinical findings, thyroid hormonal profile, thyroid scan findings and long term follow-up to 5 yrs. The thyroid scan was performed with ^99m TcO ~. The scan appearances varied from low uptake to very high intense uptake. Those with low uptake were classified as acute thyroiditis while those with high intense uptake were classified as resolving phase of thyroiditis. 46 of 62 patients had thyrotoxic hormonal profile and scan showed low uptake pattern. While in remaining 16 patients the scan showed high tracer uptake with raised TSH value suggesting resolving phase of thyroiditis. In this group, 4 patients (25%) with high uptake on thyroid scan and high TSH values did not undergo thyroxin replacement therapy during 1 to 3 years of follow up. This is an intriguing finding and raises critical question about life long thyroxin replacement in these patients based only on TSH values. Our study suggests that patients with high TSH values and high uptake on thyroid scan would need clinical observation without the thyroxin replacement therapy on the routine basis.

Thyroid dysfunction is known with lithium intake. Commonly encountered problems with lithium are goitre, hypothyroidism and thyroiditis. Literature regarding association with thyrotoxicosis is conflicting. It has been used in the treatment of thyrotoxicosis and also known to rarely produce thyrotoxicosis. We report a case of lithium induced thyrotoxicosis which subsided following discontinuation of treatment

An adolescent female experienced 9 episodes of brief cyclic illness during a period of 15 months, with most attacks being during menstrual period. Each episode used to last 4 to 8 days presenting with symptoms of acute psychosis. After 2-3 days patient would experience a generalised seizure. Following these acute episodes violent psychotic behaviour would subside; patient would remain alone, aloof and muttered to self. All symptoms would subside by 4 to 8 days and the patient would return to a state of partial normalcy. CT, MRI, EEG, revealed no abnormality. Initial thyroid function tests report was suggestive of thyrotoxicosis. Antithyroid medications for a short period lead to complete state of normalcy. After nine months of follow-up patient is doing well with no further psychosis or seizure attack.