Patient description: A 16-year-old girl came to the clinic complaining of weight gain and abnormal menstrual cycles. Her BMI was 24, but she has gained 5 kg in the past few weeks. She gets tired more frequently and does not have energy to go dancing with her friends. Her lab results were remarkable for high TSH levels (15 mU/L) and low free T4 levels (0.18 ng/dl). Her anti-TPO levels were extremely high (136 IU/ml). She was diagnosed with Hashimoto disease. She does not smoke and she is not sexually active.

Clinical trial eligibility criteria: eligible ages (years): 0.5-999.0,  Hyperthyroidism Hypothyroidism Iodine Deficiency The categories of subjects eligible to participate in this study 1. Patients with known or suspected thyroid abnormalities (e.g. hypothyroidism, hyperthyroidism, extreme iodine deficiency, and inherited forms of hypothyroidism resulting from abnormalities in the expression of genes coding for the TSH beta subunit, Pax-8, TTF-2, Pit-I, Tg, PDS, and NIS. 2. Patients with thyroid function test (TFT) abnormalities due to Non-thyroidal illness Abnormalities of serum TH binding proteins leading to euthyroid hyperthyroxinemia or hypotriiodothyronemia Genetic deficiency of thyroxine-binding globulin (TBG) Antibodies to mouse immunoglobulins leading to an artifactual elevation in the TSH ultrasensitive ("3rd generation") assay which may mimic "inappropriate" secretion of TSH. and  for each group of subjects are given below. Patients with known or suspected thyroid abnormalities will be eligible to p rticipate if the individual meets all of the following 1. Stated willingness to comply with all study procedures and availability for the duration of the study. 2. Male or female, aged 6 months+. Hyperthyroid states but are not restricted to: 1. Graves' disease (GD) thought to result from thyroid-stimulating immunoglobulins (TSIg's), a subclass of which also stimulate eye muscle and fatty tissue producing exophthalmos (Graves' ophthalmopathy), as well as the skin in the pretibial area causing pretibial myxedema (Graves' dermopathy); 2. Subacute thyroiditis (SAT), a painful inflammation thought to result from viral infection with Coxsackie, as well as other viruses; 3. Silent thyroiditis, a painless inflammation thought to result from autoimmune attack of thyrocytes by antimicrosomal antibodies directed against thyroid peroxidase (TPO), as well as antithyroglobulin(anti-Tg) antibodies; 4. Single or multiple hyperfunctioning thyroid nodules of unknown etiology, probably resulting from the activation of certain thyroid oncogenes and/or growth factors, such as the thyrotropin (TSH) receptor (TSHR) and the a-subunit of the G protein (Ga); 5. Iodide-induced hyperthyroidism of unknown etiology; 6. Surreptitious administration of thyroid hormone (TH), usually present in patients with underlying psychiatric disease or occasionally related to patients with obesity and other eating disorders 7. Trophoblastic neoplasms, thought to result from high levels of hCG secretion, which, because of its structural similarity to TSH, causes "spillover" of action at the TSHR level; 8. "Inappropriate" secretion of TSH, which may be present either in patients with TSH- producing pituitary tumors (TSHomas) or from a non-neoplastic cause, i.e. pituitary resistance to the action of thyroid hormone (3,4). Hypothyroid states but are not restricted to: 1. Primary (or thyroidal) hypothyroidism, usually resulting from auto-antibodies to thyroid proteins, such as antimicrosomal antibodies to TPO usually associated with lymphocytic (Hashimoto's) thyroiditis (HT) or atrophic thyroiditis, or blocking antibodies to the TSHR, usually in the context of non-goitrous hypothyroidism; 2. Secondary (or pituitary) hypothyroidism, usually resulting from tumors of the pituitary of non-thyrotropic origin such, as growth hormone (GH)-secreting tumors or prolactinomas; 3. Tertiary (or hypothalamic) hypothyroidism, usually resulting from a deficiency in the hypothalamic hormone thyrotropin-releasing hormone (TRH), either of unknown etiology or secondary to a pituitary tumor; 4. Bio-inactive TSH, either relating to an endogenous abnormality of hypothalamic hormones or secondary to pituitary tumors (and usually related to abnormal glycosylation patterns of the TSH molecule); 5. Generalized resistance to thyroid hormone (RTH), a disease which has been shown to be due to abnormalities in the TH receptor, c-erbA-beta (or TR beta). The above are the principal disorders under study, but we may also investigate other abnormalities, such as extreme iodine deficiency, and inherited forms of hypothyroidism resulting from abnormalities in the expression of genes coding for the TSH beta subunit, Pax-8, TTF-2, Pit-I, Tg, PDS, and NIS (among others) There are no for subjects with known or suspected thyroid abnormalities