Thyroid hormone therapy in patients with concomitant
diabetes mellitus (see PRECAUTIONS: DRUG INTERACTIONS, Ins ulin
or Oral Hypoglycemics regarding interaction and dose adjustment with insulin)
or insipidus or adrenal cortical insufficiency may aggravate the intensity of
their symptoms. Appropriate adjustments of the various therapeutic measures
directed at these concomitant endocrine diseases are required.
The therapy of myxedema coma requires simultaneous
administration of glucocorticoids. (See PRECAUTIONS – Adjunctive
Hypothyroidism decreases and hyperthyroidism increases
the sensitivity to anticoagulants. Prothrombin time should be closely monitored
in thyroid-treated patients on anticoagulants and dosage of the latter agents
adjusted on the basis of frequent prothrombin time determinations.
Oral therapy should be resumed as soon as the clinical
situation has been stabilized and the patient is able to take oral medication.
If L-thyroxine rather than liothyronine sodium is used in initiating oral therapy,
the physician should bear in mind that there is a delay of several days in the
onset of Lthyroxine activity and that intravenous therapy should be
Many investigators recommend that corticosteroids be
administered routinely in the initial emergency treatment of all patients with
myxedema coma. Patients with pituitary myxedema should receive adrenocortical
hormone replacement therapy at or before the start of Triostat therapy.
Similarly, patients with primary myxedema may also require adrenocortical
hormone replacement therapy since a rapid return to normal body metabolism from
a severely hypothyroid state may result in acute adrenocortical insufficiency
In considering the need to elevate blood pressure, it
should be kept in mind that tissue metabolic requirements are markedly reduced
in the hypothyroid patient. Because arrhythmias and circulatory collapse have
infrequently occurred following the concomitant administration of thyroid
hormones and vasopressor therapies, use caution when administering these therapies
concomitantly. (See PRECAUTIONS: DRUG INTERACTIONS, Vasopressors.)
Hyponatremia is frequently present in myxedema coma, but
usually resolves without specific therapy as the metabolic status of the
patient is improved with thyroid hormone treatment. Fluid therapy should be administered
with great care to prevent cardiac decompensation. In addition, some patients
with myxedema have inappropriate secretion of ADH and are susceptible to water
In some patients, respiratory depression has been a
significant factor in the development or persistence of the comatose state.
Decreased oxygen saturation and elevated CO2 levels respond quickly to artificial
Infection is often present in myxedema coma and should be
looked for and treated appropriately.
Concomitant use of Triostat and artificial
rewarming of patients is contraindicated. Although patients in myxedema coma
are often hypothermic, most investigators believe that artificial rewarming is
of little value or may be harmful. The peripheral vasodilation produced by
external heat serves to further decrease circulation to vital internal organs
and to increase shock if present. It has been reported that the administration
of liothyronine sodium will restore a normal body temperature in 24 to 48 hours
if heat loss is prevented by keeping the patient covered with blankets in a
Treatment of patients with thyroid hormones requires the
periodic assessment of thyroid status by means of appropriate laboratory tests besides
the full clinical evaluation. Serum T3 and TSH levels should be monitored to
assess dosage adequacy and biologic effectiveness.
Carcinogenesis, Mutagenesis and Impairment Of Fertility
A reportedly apparent association between prolonged
thyroid therapy and breast cancer has not been confirmed and patients on
thyroid for established indications should not discontinue therapy. No confirmatory
long-term studies in animals have been performed to evaluate carcinogenic
potential, mutagenicity, or impairment of fertility in either males or females.
Pregnancy Category A: Thyroid hormones do not
readily cross the placental barrier. The clinical experience to date does not
indicate any adverse effect on fetuses when thyroid hormones are administered
to pregnant women. On the basis of current knowledge, thyroid replacement
therapy to hypothyroid women should not be discontinued during pregnancy.
Minimal amounts of thyroid hormones are excreted in human
milk. Thyroid hormones are not associated with serious adverse reactions and do
not have a known tumorigenic potential. However, caution should be exercised
when thyroid hormones are administered to a nursing woman.
Clinical studies of liothyronine sodium did not include
sufficient numbers of subjects aged 65 and over to determine whether they
respond differently from younger subjects. Other reported clinical experience
has not identified differences in responses between the elderly and younger
patients. In general, dose selection for an elderly patient should be cautious,
usually starting at the low end of the dosing range, reflecting the greater frequency
of decreased hepatic, renal, or cardiac function, and of concomitant disease or
other drug therapy. This drug is known to be substantially excreted by the kidney,
and the risk of toxic reactions to this drug may be greater in patients with
impaired renal function. Because elderly patients are more likely to have
decreased renal function, care should be taken in dose selection, and it may be
useful to monitor renal function.
There is limited experience with Triostat in the
pediatric population. Safety and effectiveness in pediatric patients have not