A1,
A2,
B,
C1,
C2,
D,
E,
F,
G-H,
I-K,
L,
M,
N,
O,
P1,
P2,
Q-R,
S,
T,
U-V,
W-Z
Synthroid Side Effects, and Drug Interactions - Levothyroxine
Synthroid Side Effects, and Drug Interactions - Levothyroxine
SIDE EFFECTS
Adverse reactions other than those indicative of thyrotoxicosis
as a result of therapeutic
overdosage, either initially or during the maintenance periods,
are rare (see OVERDOSAGE).
Craniosynostosis has been associated with iatrogenic hyperthyroidism
in infants receiving thyroid
hormone replacement
therapy. Inadequate doses of levothyroxine sodium
may produce or fail to resolve
symptoms of hypothyroidism. Hypersensitivity reactions to the product
excipients, such as rash
and urticaria, may occur. Partial hair
loss may occur during the
initial months of therapy,
but is generally transient. The incidence
of continued hair loss is unknown. Pseudotumor cerebri has been
reported in pediatric
patients receiving thyroid
hormone replacement
therapy.
DRUG INTERACTIONS
The magnitude and
relative importance of the effects noted below are likely to be
patient specific
and may vary by such factors as age, gender, race, intercurrent
illnesses, dose of either
agent, additional concomitant medications, and timing of drug
administration. Any agent
that alters thyroid hormone synthesis, secretion, distribution,
effect on target
tissues, metabolism, or elimination
may alter the optimal therapeutic
dose of levothyroxine sodium.
Levothyroxine Sodium Absorption: The following agents
may bind and decrease absorption
of levothyroxine sodium
from the gastrointestinal tract: aluminum
hydoxide, cholestyramine resin, colestipol hydrochloride, ferrous
sulfate, sodium polystyrene
sulfonate, soybean flour
(e.g., infant formula), sucralfate.
Binding to Serum Proteins: The following agents may
either inhibit levothyroxine sodium
binding to serum proteins
or alter the concentrations of serum
binding proteins: androgens and related anabolic hormones, asparaginase,
clofibrate, estrogens and estrogen-containing compounds, 5-fluorouracil,
furosemide, glucocorticoids, meclofenamic acid, mefenamic acid,
methadone, perphenazine, phenylbutazone, phenytoin, salicylates,
tamoxifen.
Thyroid Physiology: The following agents may alter
thyroid hormone or TSH levels,
generally by effects on thyroid
hormone synthesis, secretion,
distribution, metabolism, hormone
action, or elimination, or altered TSH
secretion: aminoglutethimide, p-aminosalicylic acid, amiodarone,
androgens and related anabolic hormones, complex
anions (thiocyanate, perchlorate, pertechnetate), antithyroid
drugs, b-adrenergic blocking agents,
carbamazepine, chloral
hydrate, diazepam, dopamine and dopamine agonists, ethionamide,
glucocorticoids, heparin, hepatic
enzyme inducers, insulin, iodinated cholestographic agents, iodine-
containing compounds, levodopa, lovastatin, lithium, 6-mercaptopurine,
metoclopramide, mitotane, nitroprusside, phenobarbital, phenytoin,
resorcinol, rifampin, somatostatin analogs, sulfonamides, sulfonylureas,
thiazide diuretics.
Adrenocorticoids: Metabolic clearance
of adrenocorticoids is decreased in hypothyroid
patients and increased in hyperthyroid patients, and may therefore
change with changing thyroid
status.
Amiodarone: Amiodarone therapy alone can cause
hypothyroidism or hyperthyroidism.
Anticoagulants (Oral): The hypoprothrombinemic effect
of anticoagulants may be potentiated, apparently by increased catabloism
of vitamin K-dependent
clotting factors.
Antidiabetic Agents (Insulin, Sulfonylureas): Requirements
for insulin or oral
antidiabetic agents
may be reduced in hypothyroid
patients with diabetes
mellitus and may subsequently increase with the initiation of thyroid
hormone replacement
therapy.
b-Adrenergic Blocking Agents:
Actions of some of beta-blocking agents may be impaired when hypothyroid
patients become euthyroid.
Cytokines (interferon, interleukin): Cytokines have
been reported to induce both hyperthyroidism
and hypothyroidism.
Digitalis Glycosides: Therapeutic effects of digitalis
glycosides may be reduced. Serum digitalis
levels may be decreased in hyperthyroidism or when a hypothyroid
patient becomes euthyroid.
Ketamine: Marked hypertension
and tachycardia
have been reported in association
with concomitant
administration
of levothyroxine sodium and ketamine.
Maprotiline: Risk of cardiac
arrhythmias may increase.
Sodium Iodide (123I and 131I), Sodium
Pertechnetate Tc99m: Uptake of radiolabeled ions may be
decreased.
Somatrem/Somatropin: Excessive concurrent use of
thyroid hormone may accelerate epiphyseal closure. Untreated hypothyroidism
may interfere with the growth
response to somatrem
or somatropin.
Theophylline: Theophylline clearance
may decrease in hypothyroid patients and return toward normal
when a euthyroid state
is achieved.
Tricyclic Antidepressants: Concurrent use may increase
the therapeutic
and toxic effects of both
drugs, possibly due to increased catecholamine sensitivity. Onset
of action of tricyclics
may be accelerated.
Sympathomimetic Agents: Possible increased risk
of coronary insufficiency in patients with coronary artery disease.
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