Sunday, August 21, 2016

Most Common Diseases of 50 Plus: Thyroid Disease : Thyroid hormone resistance syndrome – Treatments In conventional medicine perspective

Kyle J. Norton(Scholar and Master of Nutrients, all right reserved)
Health article writer and researcher; Over 10.000 articles and research papers have been written and published on line, including world wide health, ezine articles, article base, healthblogs, selfgrowth, best before it's news, the karate GB daily, etc.,.
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                         Thyroid disease


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.


             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).

                              The Treatments

in Conventional Medicine                                               
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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