Thyroid disease is defined as a condition of malfunction of thyroid.
Hyperthyroidism is a condition in which the thyroid gland is over active
and produces too much thyroid hormones. Hypothyroidism is a condition
in which the thyroid gland is under active and produces very little
thyroid hormones. Thyroid cancer is defined as condition in which the
cells in the thyroid gland have become cancerous.
Thyroid hormone resistance syndrome
Thyroid hormone resistance syndrome is defined as a condition of which
affected individuals have elevated serum thyroid hormone levels and
inappropriately normal or elevated thyroid-stimulating hormone (TSH) but
are usually clinically euthyroid and require no treatment. Selective
pituitary resistance to thyroid hormone (PRTH) is characterized by
resistance in the pituitary gland but not in peripheral tissues(a).
E. Treatments
1. The table
Table. Suggested therapeutic approaches for resistance to thyroid hormone (RTH) patients.
___________________________________________________________________
Drugs Untoward effects and limitations
___________________________________________________________________
TRIAC Effective in almost all patients
D-T4 Effective in almost all patients
T3 Production of daily peaks of very high T3 concentrations, which
contribute to maintain clinical hyperthyroidism
Bromocriptine Transient effect owing to TSH escape from inhibition
Sms analog Transient effect owing to TSH escape from inhibition
Corticosteroid Cause of severe inhibition of hypothalamic-pituitary-adrenal axis function and cushingoid features
Antithyroid drugs Cause of further increase in TSH circulating level
with consequent increase of goiter size and to hyperplasia at pituitary
thyrotroph level
b-blockers Effects limited to b-adrenergic blockade. Propranolol
inhibits peripheral conversion of T4 to T3, causing a worsening of
tissue hypometabolic state. Cardiac selective compounds, such as
atenolol devoid of effect on peripheral T4 conversion, appear to be more
useful(31).
2. Limitation
According to the study by the Fitzsimons Army Medical Center, the
thyroid hormone resistance syndromes are disorders in which the body’s
tissues are resistant to the effects of thyroid hormone. Generalized
resistance to thyroid hormone (GRTH) is characterized by resistance in
the pituitary gland and in most or all of the peripheral tissues.
Affected individuals have elevated serum thyroid hormone levels and
inappropriately normal or elevated thyroid-stimulating hormone (TSH) but
are usually clinically euthyroid and require no treatment. Selective
pituitary resistance to thyroid hormone (PRTH) is characterized by
resistance in the pituitary gland but not in peripheral tissues.
Patients have elevated serum thyroid hormone levels and normal or
elevated TSH levels and are clinically thyrotoxic. Therapy is usually
necessary, but current choices are not completely satisfactory.
Selective peripheral resistance to thyroid hormone (PerRTH) is
characterized by resistance in peripheral tissues but not in the
pituitary. The only patient thus far described had normal serum thyroid
hormone and TSH levels but was clinically hypothyroid and improved with
thyroid hormone administration. All of these disorders are probably more
common than is generally recognized and are often misdiagnosed and
inappropriately treated. GRTH, in most cases studied, results from a
mutation in the thyroid hormone receptor beta gene causing an amino acid
substitution in or a partial or complete deletion of the thyroid
hormone-binding domain of the receptor. The causes of PRTH and PerRTH
remain to be determined(32). Other studies indicated that in this age of
rapidly advancing knowledge, it is reasonable to expect that the not
too distant future will bring specific treatments for RTH. This will
probably not be in the form of gene therapy as the dominant expression
would require excision of the defective gene. The most simple genetic
approach, one within the realm of current technology, is the selection
of an oocyte from the affected mother that does not harbor the abnormal
allele for in vitro fertilization followed by implantation into the
donor. This insures a fetus without RTH but does not guarantee a normal
pregnancy and fetal development. The development of TH agonists and
antagonists that are TR-isoform specific would allow the stimulation or
blockade of specific tissue effects that are perturbed in a given
individual with RTH(33).
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Sources
(31) http://www.hotthyroidology.com/editorial_79.html
(32) http://www.ncbi.nlm.nih.gov/pubmed/8475937
(33) http://jcem.endojournals.org/content/84/2/401.ful
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