Study Title:

Multi-Systemic Effects of Thyroid Hormone

Study Abstract

Thyroid hormones (T4 = 3,5,3’,5’tetraiodo- L -thyronine and T3 = 3,5,3’ tri-iodo-Lthyronine)
are iodine amino acids produced and secreted by the thyroid gland. TSH
(thyroid stimulating hormone) secretion from the pituitary is stimulated by TRH
(thyrotropin-releasing hormone) secretion from the hypothalamus. Thyroid hormones
control all body systems. Thyroid hormones are required for maintenance of heart
functions and rhythm, obtaining adequate bone mass, linear growth, initiation of puberty,
and ensuring fertility. They also play a role in strengthening the immune response. Overt
hypothyroidism causes bleeding while there is a thrombotic tendency in hyperthyroidism.
Both hyperthyroidism and hypothyroidism cause insulin resistance. The weight of
adrenal glands and the amount of corticosterone produced decrease in hypothyroidism.
Hypothyroidism creates a negative inotropic and chronotropic picture in heart.
Renin-angiotensin-aldosterone system (RAS) RAS activation is seen in hyperthyroidism,
the renin levels are decreased in hypothyroidism. Angiotensin converting enzyme (ACE)
inhibition and angiotensin receptor blockage may be beneficial in the treatment of
myocardial hypertrophy secondary to hyperthyroidism. Thyroid hormone is needed to
achieve growth and peak bone mass. Thyroid hormone (T3) plays a role in both bone
development and destruction. It stimulates IGF-1 (insulin like growth factor-1), IGF-1R
(IGF-1 receptor), osteocalcin, type 1 collagen, alkaline phosphatase, metalloproteinases 9
and 13 and FGF-R1 (fibroblast growth factor receptor 1) expression in osteoblasts. The
IL-6 (interleukin 6), PGE2 (prostaglandin E2), RANKL (receptor activator of nuclear
factor kappa-B ligand) expression increases in osteoclasts with the effect of T3. T3 also
has a synergistic effect with parathormone (PTH) and vitamin D in osteoclasts. Thyroid
hormone also has an important effect on muscle. Myo D (myosin D) and myogenin,
active in myoblast differentiation and skeletal muscle repair, are induced by T3.
Myopathic changes such as muscle weakness, myasthenic syndrome and rhabdomyolysis
have been reported in most hypothyroid patients. Hyperthyroidism results in an increase
in gluconeogenesis. Thyrotoxicosis is characterized by an increase in the glucose cycle
(turnover). There is deterioration in insulin activity, increase in free fat acids, decreased
insulin secretion, and increase in lipolysis. A clinical picture of insulin resistance
therefore develops. Hypothyroidism is associated with dysfunction of the adrenals and
gonads. ACTH (adrenocorticotropic hormone) secretion increases and LH (luteinizing
hormone) secretion decreases in hypothyroid rats. PRL (prolactin) increases due to both
the TRH increase and the possible paracrine/autocrine effect of high VIP (vasoactive
intestinal peptide) in hypothyroidism. This causes menstrual irregularities.
In conclusion, both the deficiency and excess of thyroid hormones cause adverse
results in all systems. Recognition of both conditions in time and initiation of appropriate
treatment is important in terms of avoiding the complications that may occur, especially
in the neonatal period.

Study Information

(pp. 61-68)

Full Study