eMedicine Specialties > Endocrinology > Thyroid
Hypothyroidism: Treatment & Medication
Updated: Jul 23, 2009
- Overview
- Differential Diagnoses & Workup
- Treatment & Medication
- Follow-up
Treatment
Medical Care
The treatment goals for hypothyroidism are the reversal of clinical progression and the corrections of metabolic derangements as evidenced by normal blood levels of TSH and free T4. Thyroid hormone is administered to supplement or replace endogenous production. In general, hypothyroidism can be adequately treated with a constant daily dose of levothyroxine (LT4).
Clinical benefits begin in 3-5 days and level off after 4-6 weeks. Anticipated full replacement doses may be initiated in individuals who are otherwise young and healthy. In elderly patients or those with known ischemic heart disease, treatment should begin with one fourth to one half the expected dose, and the dose should be adjusted in small increments no sooner than 4-6 weeks.
Achieving a TSH level within the reference range may be slowed because of delay of hypothalamic-pituitary axis readaptation and may take several months. After dose stabilization, patients can be monitored with annual clinical evaluations and TSH monitoring. Patients should be monitored for symptoms and signs of overtreatment, which include tachycardia, palpitations, nervousness, tiredness, headache, increased excitability, sleeplessness, tremors, and possible angina.
A meta-analysis of randomized controlled trials of thyroxine-triiodothyronine combination therapy (T4 + T3) versus thyroxine monotherapy (T4) for treatment of clinical hypothyroidism found no difference in the effectiveness of the combination vs monotherapy in bodily pain, depression, fatigue, body weight, anxiety, quality of life, total cholesterol, LDL-C, HDL-C and triglyceride levels. Hence, T4 monotherapy remains the treatment of choice.9
Pregnancy
Hypothyroidism in pregnancy is associated with preeclampsia, anemia, postpartum hemorrhage, cardiac ventricular dysfunction, spontaneous abortion, low birth weight, impaired cognitive development, and fetal mortality. Even mild disease may be associated with adverse affects for offspring.
Increased dosage requirements should be anticipated during pregnancy, especially in the first and second trimesters. Studies have suggested that patients with hypothyroidism should augment the LT4 dose by 30% at the confirmation of pregnancy, followed by adjustments according to TSH levels. For previously diagnosed women, serum TSH should be measured every 3-4 weeks during the first half of pregnancy and every 6 weeks thereafter. LT4 dose should be adjusted to maintain a serum TSH less than 2.5 mIU/L. TSH and free T4 levels should be measured every 3-4 weeks after every dosage adjustment.10
Autoimmune thyroid disease without overt hypothyroidism has been associated with a higher miscarriage rate. Negro et al showed that euthyroid Caucasian women with positive anti-TPO antibodies treated with levothyroxine during the first trimester had lower miscarriage rates when compared with those who were not treated. They also had lower incidence of premature delivery, comparable to women without thyroid antibodies.11 This will need to be confirmed by other studies, and, if confirmed, there will be an indication to treat euthyroid pregnant women who have thyroid antibodies.12 and an independent expert panel13 found inconclusive evidence to recommend aggressive treatment of patients with TSH levels of 4.5-10 mIU/L. The Endocrine Society recommends thyroxine replacement in pregnant women with subclinical hypothyroidism14 ; the American College of Obstetricians and Gynecologists does not recommend it as a routine measure.15
Ultrasonography may have prognostic value in subclinical hypothyroidism. In an Italian study, progression to overt hypothyroidism occurred more often in patients whose ultrasonographic thyroid scan showed diffuse hypoechogenicity (an indication of chronic thyroiditis).16
Following subclinical hypothyroidism and treating on a case-by-case basis is reasonable. Treatment of subclinical hypothyroidism has been shown to reduce total cholesterol, non-HDL cholesterol, and apolipoprotein B,17 and to decrease arterial stiffness and systolic blood pressure.18 In patients with concomitant subclinical hypothyroidism and iron deficiency anemia, iron supplementation may be ineffective if LT4 is not given.19
The American Association of Clinical Endocrinologists (AACE) guidelines state that treatment is indicated in patients with TSH levels above 10 mIU/mL or in patients with TSH levels between 5 and 10 mIU/mL in conjunction with goiter and/or positive antithyroid peroxidase antibodies, as these patients have the highest rates of progression to overt hypothyroidism. An initial dose of 25-50 mcg/d of LT4 can be used and can be titrated every 6-8 weeks, to achieve a target TSH of between 0.3 and 3 mIU/mL.20
Myxedema coma
An effective approach is to use intravenous LT4 at a dose of 4 mcg/kg of lean body weight, or approximately 200-250 mcg as a bolus in a single or divided dose, depending on the patient's risk of cardiac disease followed by 100 mcg 24 hours later and then 50 mcg daily IV or PO along with stress doses of intravenous glucocorticoids. Adjustment of the dose can then be made based on clinical and laboratory along with stress doses of intravenous glucocorticoids. Use of intravenous triiodothyronine is controversial and based on expert opinion. It has a higher frequency of adverse cardiac events and is generally reserved for patients who are not improving clinically on LT4. LT3 can be given initially as a 10 mcg IV bolus and repeated every 8-12 hours until the patient can take maintenance oral doses of T4. Advanced age, high dose T4 therapy, and cardiac complications had the highest associations with mortality.21
Surgical Care
Surgery is indicated for large goiters that compromise tracheoesophageal function; surgery is rarely needed in patients with hypothyroidism and is more common in the treatment of hyperthyroidism.
Consultations
Patients with a nodular thyroid, suspicious thyroid nodules, or compressive symptoms such as dysphagia; pregnant women; patients with underlying cardiac disorders or other endocrine disorders; persons younger than 18 years; and those unresponsive to treatment should be referred to an endocrinologist.
Some patients with thyroiditis can develop hyperthyroidism (or symptoms consistent with hyperthyroidism) before developing hypothyroidism and may benefit from consultation with an endocrinologist.
Suspected myxedema coma is a medical emergency with a high risk of mortality that requires initiation of parenteral (intravenous) LT4 and glucocorticoids prior to laboratory confirmation. An urgent endocrinology consultation should be obtained.
Rarely an increase in size of a goiter in a patient with autoimmune thyroid disease could be a lymphoma and should be evaluated by an endocrinologist.
Diet
No specific diets are required for hypothyroidism.
Subclinical hypothyroidism has been seen in increased frequency in patients with greater iodine intake. The World Health Organization recommends a daily dietary iodine intake of 150 mcg for adults, 200 mcg for pregnant and lactating women, and 50-120 mcg for children.
Activity
Patients who have hypothyroidism have generalized hypotonia and may be at risk for ligamental injury, particularly from excessive force across joints. Thus, patients should exercise caution with certain activities, such as contact sports or heavy physical labor.
Patients with uncontrolled hypothyroidism may have difficulty maintaining concentration in low-stimulus activities and may have slowed reaction times. Patients should use caution if an activity has a risk of injury (eg, operating presses or heavy equipment, driving).
Medication
The goals of pharmacotherapy are to reduce morbidity and to prevent complications.
Thyroid hormone replacement
Levothyroxine is generally considered to be the treatment of choice for patients with hypothyroidism.
Levothyroxine (Synthroid, Levoxyl, Levothroid, Unithroid)
In active form, influences growth and maturation of tissues. Involved in normal growth, metabolism, and development. Produces stable levels of T3 and T4. Administered as a single dose in the morning on an empty stomach. May be administered PO/IV/IM. Has long half-life (7-10 d), and parenteral dosing is rarely needed (except when PO is unavailable, patient is on continuous enteral feeds, or in emergency, such as myxedema coma). Initial subtherapeutic doses are recommended to avoid the stress of rapid metabolic change in elderly patients and in those with coronary artery disease or severe COPD.
Adult
1.6 mcg/kg/d PO; higher doses may be required in pregnancy; in elderly and those with coronary disease or severe COPD, start at 25-50 mcg/d PO, increase by 25-50 mcg/d q4-8wk until desired response achieved
Maintenance: 50-200 mcg PO qam
Subclinical hypothyroidism: If treated an initial dose of LT4 25-50 mcg/d can be used and titrated q6-8wk to achieve a target TSH between 0.3 and 3 mIU/mL
Myxedema coma: 200-250 mcg IV bolus, followed by 100 mcg the next day and then 50 mcg/d PO or IV along with T3; use smaller doses in patients with cardiovascular disease; patients should first receive stress dose steroids in case they have concomitant primary or secondary adrenal insufficiency (see above)
Pediatric
Neonate to 6 months: 25-50 mcg/d PO
6-12 months: 50-75 mcg/d PO
1-6 years: 75-100 mcg/d PO
6-12 years: 100-150 mcg/d PO
>12 years: 150 mcg/d PO
Hepatic enzyme inducers (phenytoin) may increase degradation of, antidiabetic agents, theophylline, adrenocorticoids, digoxin, and anticoagulants, which may need dose adjustments; IV phenytoin may release thyroid hormone from thyroglobulin; effects of TCAs and sympathomimetics may be increased; cholestyramine, sucralfate, iron may decrease absorption; estrogens may decrease response to thyroid hormone therapy in patients with nonfunctioning thyroid glands; activity of some beta-blockers may decrease when patient with hypothyroidism is converted to a euthyroid state; beta-blockers may decrease conversion of T3 to T4
Documented hypersensitivity, uncorrected adrenal insufficiency; acute MI uncomplicated by hypothyroidism; untreated thyrotoxicosis
Pregnancy
A - Fetal risk not revealed in controlled studies in humans
Precautions
Caution in elderly patients and patients with renal insufficiency, hypertension, ischemia, angina, and other cardiovascular diseases; periodically monitor thyroid status; because of the risk of adrenal crisis, T4 should not be administered without corticosteroids in any patient with suspected adrenal insufficiency, either primary or secondary
Liothyronine (Cytomel, Triostat)
Synthetic form of the natural thyroid hormone T3 converted from T4. Used when a rapid effect is desired perioperatively or for nuclear medicine studies. Not intended as sole maintenance therapy. Can be used in combination with levothyroxine in small doses (5-15 mcg/d). Duration of activity is short (half-life is 12-24 h) and allows for quick dosage adjustments in event of overdosage. May be preferred when GI absorption is impaired (95% absorbed compared to 50-80% of T4) or if peripheral conversion is impaired.
Dosage recommendations are for short-term use in special circumstances (see above) with the guidance of an endocrinologist.
Adult
Initial: 25 mcg/d PO in divided bid; increase by 12.5-25 mcg/d PO q1-2wk until desired response achieved
Maintenance: 50-100 mcg/d PO
Myxedema coma: 10 mcg IV and repeated q8 -12h until patient can take PO maintenance oral dose of T4 (see above)
Elderly patients or patients with suspected or known coronary disease: Avoid because of high risk of cardiovascular manifestations
Pediatric
5 mcg/d PO; increase by 5 mcg q3d until desired response achieved
Hepatic enzyme inducers (phenytoin) may increase degradation; of antidiabetic agents, theophylline, adrenocorticoids, digoxin, and anticoagulants, these may need dose adjustments; IV phenytoin may release thyroid hormone from thyroglobulin; effects of TCAs and sympathomimetics may be increased; cholestyramine may decrease absorption; estrogens may decrease response to thyroid hormone therapy in patients with nonfunctioning thyroid glands; activity of some beta-blockers may decrease when hypothyroid patient converted to euthyroid state; beta-blockers may decrease conversion of T3 to T4
Documented hypersensitivity; uncorrected adrenal insufficiency; acute MI uncomplicated by hypothyroidism; untreated thyrotoxicosis; cardiac arrhythmias; suspected or known coronary disease
Pregnancy
A - Fetal risk not revealed in controlled studies in humans
Precautions
Caution in elderly patients and patients with renal insufficiency, hypertension, ischemia, angina, and other cardiovascular diseases; periodically monitor thyroid status; because of risk of adrenal crisis, liothyronine should not be administered without corticosteroids in any patient with suspected adrenal insufficiency, either primary or secondary
Desiccated thyroid (Armour Thyroid)
Derived from extract of bovine or porcine thyroid glands. Some manufacturers standardize based on bioassays; others use iodine content. Desiccated thyroid is referred to as natural thyroid and generally contains T3 and T4 in a 1:4 ratio. It is made in the following strengths 1/8, 1/4, 1/2, 1, 2, and 3 grain as well as 4 and 5 grain tabs. One grain (60 mg) contains about 38 mcg of T4 and 9 mcg of T3. Because these preparations contain variable quantities of T3, they should not be prescribed for patients with known or suspected cardiac disease (see above).
Adult
Initial: 30 mg/d PO; increase by 15-30 mg/d PO q4wk until desired response achieved
Maintenance: 60-180 mg/d PO
Pediatric
Neonate to 6 months: 15-30 mg/d PO
6-12 months: 30-45 mg/d PO
1-6 years: 45-60 mg/d PO
6-12 years: 60-90 mg/d PO
>12 years: 60-180 mg/d PO
Hepatic enzyme inducers (phenytoin) may increase degradation of antidiabetic agents, theophylline, adrenocorticoids, digoxin, and anticoagulants, which may need dose adjustments; IV phenytoin may release thyroid hormone from thyroglobulin; effects of TCAs and sympathomimetics may be increased; cholestyramine, sucralfate, iron may decrease absorption; estrogens may decrease response to thyroid hormone therapy in patients with nonfunctioning thyroid glands; activity of some beta-blockers may decrease when hypothyroid patient is converted to a euthyroid state; beta-blockers may decrease the conversion of T3 to T4
Documented hypersensitivity; uncorrected adrenal insufficiency; acute MI uncomplicated by hypothyroidism; untreated thyrotoxicosis; known or suspected cardiac disease
Pregnancy
A - Fetal risk not revealed in controlled studies in humans
Precautions
Caution in elderly patients and patients with renal insufficiency, hypertension, ischemia, angina, and other cardiovascular diseases; monitor thyroid status periodically; because of the risk of adrenal crisis, thyroid hormone replacement should not be administered without corticosteroids in any patient with suspected adrenal insufficiency, either primary or secondary
More on Hypothyroidism |
| Overview: Hypothyroidism |
| Differential Diagnoses & Workup: Hypothyroidism |
 Treatment & Medication: Hypothyroidism |
| Follow-up: Hypothyroidism |
| References |
| Further Reading |
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Further Reading
Related eMedicine topics:
Autoimmune Thyroid Disease and Pregnancy
Congenital Hypothyroidism
Embryology of the Thyroid and Parathyroids
Hyperthyroidism [Endocrinology]
Hyperthyroidism [Pediatrics: General Medicine]
Hypothyroidism [Pediatrics: General Medicine]
Hypothyroidism and Myxedema Coma
Hypothyroid Myopathy
Thyroid Anatomy
Thyroid Disease
Thyroid Nodules
Clinical guidelines:
Management of thyroid dysfunction during pregnancy and postpartum: an Endocrine Society clinical practice guideline. The Endocrine Society - Disease Specific Society. 2007. 79 pages. NGC:005884
Screening for congenital hypothyroidism: U.S. Preventive Services Task Force reaffirmation recommendation statement. United States Preventive Services Task Force - Independent Expert Panel. 1996 (revised 2008 Mar). 6 pages. NGC:006354
Screening for thyroid disease: recommendation statement. United States Preventive Services Task Force - Independent Expert Panel. 1996 (revised 2004 Jan 20). 7 pages. NGC:003266
Subclinical thyroid disease: scientific review and guidelines for diagnosis and management. Consensus Conference Panel on Subclinical Thyroid Disease - Independent Expert Panel. 2004 Jan 14. 11 pages. NGC:003902
Update of newborn screening and therapy for congenital hypothyroidism. American Academy of Pediatrics - Medical Specialty Society
American Thyroid Association - Professional Association. 2006 Jun. 14 pages. NGC:005029
Clinical trials:
Evaluation of Patients With Thyroid Disorders
Generic vs. Name-Brand Levothyroxine
Growth Hormone and GnRH Agonist in Adolescents With Acquired Hypothyroidism
Maternal Hypothyroidism in Pregnancy
Neurocognitive and Metabolic Effects of Mild Hypothyroidism
Keywords
hypothyroidism, thyroid, thyroiditis, thyroid hormone, thyroid function, thyroid nodule, thyroid treatment, thyroid goiter, thyroid medication, thyroid medicine, thyroid problem, myxedema coma, cretinism, hypothyrosis, hypothyroidea, thyrotropin, TSH, tertiary hypothyroidism, thyrotropin releasing-hormone, TRH, thyroxine, T4, triiodothyronine, T3, Hashimoto disease, Hashimoto thyroiditis, primary hypothyroidism, secondary hypothyroidism, congenital hypothyroidism, cold intolerance, weight gain, menstrual disturbances, periorbital puffiness, goiter, autoimmune thyroiditis, iodine deficiency, de Quervain thyroiditis, subacute thyroiditis, postpartum autoimmune thyroid disease, amiodarone, interferon alpha, thalidomide, stavudine, central hypothyroidism, subclinical hypothyroidism
