Initial Visit

Hypothyroidism is a disorder of diverse causes in which the thyroid gland fails to secrete adequate amounts of thyroid hormone. The overwhelming majority of cases are due to primary thyroid gland failure because of chronic autoimmune (Hashimoto's) thyroiditis, radioactive iodine therapy, or surgery. Therefore, the following discussion will emphasize primary hypothyroidism.

Medical History.--A comprehensive medical history can uncover symptoms that will help establish the diagnosis in the patient with previously undiagnosed hypothyroidism. If the diagnosis has already been made, it is important to confirm it by history and to document pretreatment thyroid function abnormalities whenever possible. In the past, patients frequently were treated with thyroid hormone for reasons that would not be acceptable by current standards. In addition, many patients previously treated with thyroid hormone have forgotten the reasons for this therapy, as well as the adequacy of their clinical response. Patients should be asked about symptoms of tiredness, weakness, fatigue, sleepiness, cold intolerance, dry skin, hoarseness, constipation, joint pains, muscle cramps, mental impairment, depression, menstrual disturbances in women and especially menorrhagia, infertility, and weight gain.

Physical Examination.--A comprehensive physical examination should be performed during the initial evaluation. Findings from the physical examination that may indicate hypothyroidism include goiter or a nonpalpable thyroid gland, bradycardia, edema, hoarseness, delayed relaxation of deep tendon reflexes, slow speech, and cool, dry skin.

Laboratory Evaluation.[ref. 1]--To establish the diagnosis of hypothyroidism, a serum TSH measurement and a free T4 estimate (or direct measurement) should be performed. When autoimmune thyroiditis is the suspected underlying cause, it is helpful to confirm antithyroid antibody titers, either antimicrosomal antibody (anti-TPO antibody) or antithyroglobulin antibody. The antimicrosomal antibody test is more sensitive and specific. If the TSH level is low, inappropriately normal, or insufficiently elevated in the presence of low T4 values, central hypothyroidism caused by hypothalamic or pituitary disease should be excluded before starting thyroid replacement therapy. Also, thyroid function tests obtained from ill hospitalized patients must be interpreted with caution, since serum T4 and/or TSH levels may suggest hypothyroidism.

Treatment Plan.[ref. 9]--Levothyroxine sodium is the treatment of choice for the routine management of hypothyroidism. Levothyroxine preparations are manufactured in many different dosages and allow precise titration of an individual patient's requirements. Adults with hypothyroidism require approximately 1.7 microg/kg of body weight per day for full replacement. Children may require higher doses (up to 4 microg/kg of body weight per day). Older patients may need less than 1 microg/kg per day. Therapy is usually initiated in patients under the age of 50 years with full replacement. For those patients who are older than 50 years, or in younger patients with a history of cardiac disease, a lower initial dosage is indicated, starting with 0.025 to 0.05 mg of levothyroxine daily, with clinical and biochemical reevaluations at 6- to 8-week intervals until the serum TSH concentration is normalized. Some individuals older than 50 years, such as those recently treated for hyperthyroidism or those known to have had hypothyroidism for only a short time, such as a few months, may be treated with full replacement doses of levothyroxine. Certain drugs, eg, cholestyramine, ferrous sulfate, sucralfate, and aluminum hydroxide antacids, may interfere with levothyroxine absorption from the gut. Levothyroxine administration should be spaced at least 4 hours apart from these medications. Other drugs, especially the anticonvulsants phenytoin and carbamazepine and the antituberculous agent rifampin, may accelerate levothyroxine metabolism, necessitating higher levothyroxine doses.