Treatment of hyperthyroidism has many objectives, including
* (1) Inhibiting the synthesis and secretion of thyroid
hormone by the thyroid gland
* (2) Blocking beta adrenergic receptors to limit the clinical
manifestations (symptoms) of hyperthyroidism
* (3) 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 propylthiouracil (PTU).
Methimazole inhibits organification of iodide (to iodine) to decrease
the thyroid gland's synthesis of T4 and T3 (the active thyroid
hormone). 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 very rarely granulocytopenia (a decrease in the total
number of a type of white blood cell called granulocytes in the
blood).
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 <1%) and include
rash, itch, GI upset. Very rarely, there may be a life threatening
problem with reduction in blood cells (agranulocytosis) or platelet
cells (thrombocytopenia).
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 (pounding of the heart), 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 should be treated, usually with PTU,
to maintain thyroid hormone concentrations in the upper level
normal to mild level hyperthyroidism region (to minimize fetal
effects of PTU since some does cross the placenta).
Many women with hyperthyroidism have an elevation in TSH like
autoantibodies. If these maternal TSH like autoantibodies cross
the placenta during pregnancy they may precipitate fetal thyrotoxicosis
which 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.
|
