Some portions of the hormone remain, unbound to the
carrier protein. These are called free hormones:
Hormone Bound % Free % Carrier protein
Free T3 and Free T4 are the “Physiologically active
Measurement of these hormones is more relevant in
clinical conditions where the levels of total hormones does
Thyroid hormones have a negative feedback on the pituitary.
Whenever, the concentrations of T3 and T4 are high, the
release of TSH is inhibited from the pituitary. When the
thyroid hormones levels are low, it is stimulated. But this
need not be true always (Fig. 24.4).
Newborn infants normally have circulating levels of T4 that
are considerably higher than normal adults; but within
the first week of life, the values would have decreased
markedly. Failure or extreme deficiency of T4 production
occurs at a frequency of approximately 1 in 4000 live births.
If this deficiency is left untreated, growth deficit, neurologic
impairment and mental retardation (cretinism) result.
Such infants are characterized by low circulating levels of
T4 and, in thyroid gland failure (primary hypothyroidism),
by very high levels of TSH. The disorders are markedly
affected by the stage of development during which the
defect arises. Later-phase development results in transient
abnormalities, especially in premature infants, whereas
permanent disorders result from early-stage defects.
Since early diagnosis on clinical grounds is difficult
and since initiation of treatment before three months of
age appears to be necessary to prevent neurologic defects,
neonatal screening for hypothyroidism has become a key
test in neonatal patient management.
Anti-TPO (Thyroid Peroxidase Antibodies)
The anti-TPOs are autoantibodies directed against the
enzyme peroxidase. Because the antibodies bind to the
microsomal part of the thyroid cells, they are known as
thyroid microsomal antibodies.
¾ TPO antibody tests are used to distinguish between
¾ It is positive in Hashimoto’s disease whereas in nontoxic
goiter, it is normally negative.
¾ Twenty percent of patient’s thyrotoxic patients have
high titers of anti-TPO antibodies.
¾ The presence of anti-TPO antibodies and elevated TSH
is a predictor of future hypothyroidism.
Anti-Tg (Anti-Thyroglobulin Antibodies)
Antibodies are produced against thyroglobulin. These
autoantibodies gradually destroy the thyroid tissue and
prevent the production of thyroid hormones, causing
hypothyroidism. Presence of Tg-antibodies indicates
Hashimoto’s disease. However, they are less often present
and less pathogenic than anti-TPO antibodies.
FIG. 24.4: Thyroid hormones—feedback mechanism
In 1956, Adams and Purces demonstrated in the sera of
TSH. The name applied to this factor was long-acting
thyroid stimulator (LATS). It does not appear to have
its origin in the pituitary and has been classified as a 7S
γ-globulin. The LATS is now considered to be a thyroid
autoantibody. Since, it may persist for years following
total thyroidectomy, the nature of the antigen is unknown.
It is considered one of a group of thyroid-stimulating
immunoglobulins. These antibodies are stimulators and
do not destroy thyroid tissue as do the anti-thyroglobulin
and antimicrosomal antibodies. The presence of certain
HLA antigens (HLA-B8 and HLA-DR3) indicated an
approximate fourfold increase in risk for Graves’ disease.
The frequent finding of LATS in the sera of patients with
malignant exophthalmos and Graves’ disease makes its
detection an important part of thyrodiagnostic evaluations.
The LATS has been overwhelmingly associated with a
complex of symptoms known as Graves’ disease. Studies
showed that positive LATS findings in patients without
Graves’ disease are “low positive”. In patients with active
Graves’ disease or patients who are presently in remission,
“low” as well as unequivocally “high” results are found.
Infants born of mothers with Graves’ disease may also
suffer from this illness because of the transplacental
passage of LATS from the maternal to fetal circulation.
Fortunately, prenatal testing can warn the physician of this
potential threat; under alert management such infants will
recover since the LATS will undergo metabolic destruction.
Low levels of thyroid hormones.
Primary Hypothyroidism—Where the low levels of
thyroid hormones are due to failure of the thyroid gland.
Secondary Hypothyroidism—Where the low levels
of thyroid hormones are caused by failure of the
hypothalamic-pituitary system to produce TRH or TSH or
Subclinical Hypothyroidism—Elevated TSH levels in the
absence of any clinical symptoms.
High levels of thyroid hormones.
Autoimmune disease—Graves’ disease.
Thyroiditis—Inflammation of the thyroid gland.
Tumors in the Thyroid—T3 toxicosis, T4 toxicosis.
¾ Due to a high dose of T4 therapy.
¾ Induced in patients with goiters if iodine is administered.
Abnormal thyroid hormones due to other disorders. Severe
illness or injury can induce changes in thyroid hormone
levels. In seriously ill patients TSH, T3 and T4 levels may
decrease, and a severe decrease often signifies that the
Overactivity (Hypothyroidism) Underactivity (Hyperthyroidism)
Decreased energy, physical and
3. Warm moist skin Dry rough skin
Tests for Thyroid Function Generally Recommended in
¾ Abnormal weight loss or gain.
¾ Typical symptoms of hypothyroidism—tiredness,
lethargy, intolerance to cold.
¾ Constipation, bradycardia, increased menstruation.
¾ In children—if they fail to grow normally. If ability to
comprehend is less and mental growth is found to be
insufficient. If puberty is delayed.
¾ Symptoms of hyperthyroidism—tiredness, hot,
tachycardia, short of breath, increased appetite but
lose weight, muscular atrophy, characteristic features
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