Hypothyroidism is treated by replacing the deficient thyroid hormone.
Synthroid (a synthetic thyroxine compound) is the most common and usually the best treatment.
It allows a woman to convert circulating T4 (thyroxine) to the more active metabolite thyronine (T3)
within the cells of the body.
Desiccated thyroid extract differs from thyroxine compounds since it also contains thyronine (T3).
The amount of T3 in the extract is greater than that normally secreted by the thyroid gland so these medications
can be counterproductive in terms of treatment for ovulatory dysfunction.
Synthroid is typically started at a low dose (25-50 mcg per day). The dose of medication is adjusted as needed
according to bloodwork obtained 4-8 weeks after a change in dose. The final dose required is dependent on the
initial degree of hypothyroidism.
Once stabilized (euthyroid) on medication a sensitive TSH assay should be checked regularly (at least once a year)
for all infertility patients. Testing is more often if the woman has had recent onset thyroiditis since her own
thyroid function may continue to deteriorate with the progression of thyroiditis.
Overtreating a patient with hypothyroidism or providing thyroid hormone replacement empirically for a euthyroid patient
is potentially harmful. Hyperthyroidism (even if through overtreatment with medication) is associated with osteoporosis
(decreased bone mineral content). Thyroid hormone stimulates bone resorption to decrease overall bone mineral content.
The mechanism for the increased bone resorption appears to involve direct effects of thyroid hormone on the bone as
well as effects involving vitamin D, calcitonin and parathyroid hormone.
Hypothyroidism in pregnancy should be treated with medication. Careful monitoring with monthly TSH concentrations for
the first trimester and every few months thereafter is recommended (often increased medication is required due to
increased circulating blood volume in pregnancy). Hypothyroidism in pregnancy has been associated with preeclampsia,
intrauterine growth retardation and possibly spontaneous abortions (miscarriages).
Treatment of hyperthyroidism has many objectives, including
- Inhibiting the synthesis and secretion of thyroid hormone by the thyroid gland
- Blocking beta adrenergic receptors to limit the clinical manifestations (symptoms) of hyperthyroidism
- Treating associated medical problems that can either exacerbate hyperthyroidism or can be exacerbated by hyperthyroidism
The initial objective of treatment is to inhibit thyroid hormone synthesis and secretion while controlling beta adrenergic
stimulation (if excessive). The two primary medications used to limit thyroid hormone production are methimazole and
Methimazole inhibits organification of iodide (to iodine) to decrease the thyroid glandís synthesis of T4 and T3.
This medication is taken by mouth and you initially see an effect in 2-4 weeks. T4 has a long half life in the circulation
(about 1 week) and there is a large store of T4 within the thyroid gland so decreasing the circulating T4 concentration
takes a relatively long time. Repeat blood studies are usually performed 4-8 weeks after changing a dose to allow maximal
effect of the medication. The major side effects of methimazole are rash, gastrointestinal upset and granulocytopenia.
PTU inhibits the incorporation of iodine into thyroid hormone and also inhibits the peripheral conversion of T4 to the
more active form T3 (methimazole does not have this ability). Therefore, PTU is usually used when rapid reduction of
thyroid function is desired. Side effects are uncommon (reported in less than 1%) and include rash, itch, and GI upset.
Rarely, there may be a life threatening problem with reduction in blood cells (agranulocytosis) or platelet cells
Medication to control the beta adrenergic stimulation associated with hyperthyroidism includes a family of "beta blockers",
including propanolol. The beta blocking agents rapidly control the beta adrenergic manifestations, which include tachycardia
(fast heart rate), palpitations, high blood pressure, cardiac arrhythmias (such as atrial fibrillation), constriction of the
lung (especially during asthma attacks), migraine headaches (exact mechanism is unclear) and tremor.
Propanolol competitively blocks the beta adrenergic receptors in the heart muscle (myocardium), the lung
(bronchial smooth muscle) and blood vessels (vascular smooth muscle). Propanolol is given orally (or IV if necessary),
and the dosage depends on the exact reason for administration.
Once the patient has returned to the euthyroid (normal) state a decision is made about long term treatment.
If pregnancy is immediately desired, then continuing on PTU is usually advised because it is as effective as methimazole
and does not cross the placenta as readily. If pregnancy is not immediately desired, then many women will decide to
undergo "definitive therapy" involving radioactive iodine. The radioactive iodine is selectively taken up by the
thyroid gland and is designed to destroy the bulk of the thyroid gland. Most of these patients eventually become
hypothyroid and require lifelong thyroid hormone replacement. It must be determined with certainty that the patient
is not pregnant prior to administering the radioactive dose since the medication will cross the placenta and can be
taken up by the fetal thyroid. Pregnancy is usually delayed for at least 6 months after radioactive iodine treatment.
Hyperthyroidism in pregnancy also should be treated, usually with PTU, to maintain thyroid hormone concentrations in
the upper level normal to mild hyperthyroidism range (to minimize fetal effects of PTU since some does cross the placenta).
If maternal TSH like autoantibodies cross the placenta they may precipitate fetal thyrotoxicosis and may result in a stillborn.
PTU given to the pregnant woman also helps treat fetal thyrotoxicosis. Untreated hyperthyroidism in pregnancy is
associated with preeclampsia, intrauterine growth retardation, and fetal heart failure. Monitoring of thyroid function
should continue throughout pregnancy, similar to the recommended regimen for hypothyroidism.