Your hormones | The Pituitary Foundation
Normally TSH is the more sensitive test due to the relationship between TSH and fT4 being log/linear. ACTH would be the last pituitary hormone to be lost. ACTH is also known as corticotrophin. TSH, Thyroid, Stimulates the thyroid gland to secrete its own hormone, which is called thyroxine. TSH is also known as. Thyroid-stimulating hormone is a pituitary hormone that stimulates the thyroid gland to produce thyroxine (T4), and then triiodothyronine (T3) which stimulates.
A normal increase in prolactin is seen after TRH stimulation in isolated TSH deficiency and can be used to differentiate TSH deficiency hypothyroidism from hypopituitary or hypothalamic hypothyroidism Table I.
Intraindividual variation in free T4 is quite small. In patients with a failure of the pituitary or hypothalamus, this negative feedback is not seen. Since TSH cannot demonstrate the normal negative feedback, used alone, TSH is not diagnostic of central hypothyroidism. A combined TSH and fT4 are a better approach. Patients with central hypothyroidism often lack a nocturnal TSH surge.
It is believed that bio-inactive TSH accounts for this phenomenon. The anterior pituitary produces several hormones that, in turn stimulate other glands i.
It was previously thought that the anterior pituitary hormones drop off in a predictable manner, growth hormone being the first to decline, followed by luteinizing hormone and follicle stimulating hormone. Those decreases would be followed by TSH. ACTH would be the last pituitary hormone to be lost. However, there is no one analyte to test for pituitary function, and selective deficiencies of pituitary hormone are possible.
Prolactin is often used as an indicator of pituitary function, since some pituitary tumors secret prolactin. When pituitary failure is suspected, each of the functions of the anterior pituitary should be evaluated.
Test Results Indicative of the Central Secondary or Tertiary Hypothyroidism It has been suggested that the best confirmation of hypothyroidism from any cause is an evaluation of response to a trial dose of thyroxine supplement.
For a change in analytical value to have clinical significance, the difference should take into account analytical and biological variations. In particular, does your patient take any medications - OTC drugs or Herbals - that might affect the lab results?
TSH or free T4 levels may be diagnostically misleading in cases of abnormalities in hypothalamus or pituitary function, in which the usual negative feedback is not seen and TSH may remain within normal limits. Misinterpretation due to the inclusion of biologically inactive TSH isoforms in TSH assays can lead to a missed diagnosis of central hypothyroidism.
TSH assays include biologically inactive TSH isoforms, which are secreted when the pituitary is damaged or when hypothalamic TRH stimulation is deficient. Most thyroid testing is performed by either immunoassay, in which labeled and unlabeled ligands compete for a limited number of antibody sites, or immunometric assays, in which an antibody is bound to a solid surface rather than an antibody.
Cross reactivity of auto-antibodies or heterophilic antibodies can affect diagnostic accuracy of competitive binding-based tests. The term heterophilic antibodies is often loosely applied to relatively weak antibodies with multiple activity sites, known as auto-antibodies, seen in auto immune disorders; broadly reactive antibodies induced by infections or exposure to therapy containing monoclonal mouse antibodies HAMA ; or human anti-animal immunoglobulins produced against well defined, specific antigens following exposure to therapeutic agents containing animal antigen or by coincidental immunization through exposure to animal antigens.
Auto-antibodies and heterophilic antibody interferences can sometimes be detected by simply using a different manufacturer's method that employs a slightly different antibody. Tests in which dilutions are acceptable, such as total T4, total T3, or TSH, but not free T4 or free T3, may be checked for linearity of response to help identify heterophilic antibody interference.
Most circulating thyroid hormones are bound to protein. Only that hormone that is free is biologically active. Variations in binding protein will cause variations in concentrations of total hormones. T3 and T4 circulate in the body bound to thyroid binding globulin TBG ; transthyretin, formally known as thyroxine binding prealbumin; and serum albumin.
Physiological shifts toward greater total hormone binding will decrease available free hormone. Theoretically, free T3 and free T4 are not affected analytically by binding, but in reality, all of the free methods are binding dependent to varying degrees. Phenytoin, carbamazepine, aspirin, and furosemide compete with thyroid hormone for protein binding sites and, thus, acutely increase free hormones and reduce total hormones. Eventually, a normal equilibrium is reestablished where free levels normalize at the expense of total levels.
Heparin stimulates lipoprotein lipase, liberating free fatty acids, which inhibit total T4 protein binding and elevate free T4. Free fatty acids are known to affect some methods.
Estrogens increase TBG, increasing total thyroid hormones. Liver disease, androgens, and nephrotic syndrome decrease TBG, decreasing total thyroid hormones. Indole acetic acid, which accumulates in uremia, may interfere with thyroid binding. Pregnancy is associated with lower albumin levels.
Thyroid hormone action on ACTH secretion.
Therefore, albumin-dependent methods are not suitable for accessing thyroid status during pregnancy. In adulthood, TSH increased in the elderly. Age related reference ranges, or at least ratio adjusted reference ranges should be used.
Glucocorticosteroids can lower T3 and inhibit TSH production. This interaction is of particular concern in sick, hospitalized patients in whom the elevated TSH in primary hypothyroidism may be obscured.
Propanolol has an inhibitory effect on T4 to T3 conversion.
In addition, changes in TSH are 10 times more sensitive in reflecting an abnormality in thyroid hormone homeostasis compared to FT3 or FT4 [ 4 ]. Similar to our finding, other studies of subclinical hypothyroidism typically report a relationship between the biomarker of interest e.
Our results and those of Iranmanesh et al. It is of interest to consider these observations together with the well-established opposite effects, i. Thus when cortisol levels are manipulated through pathologic as well as physiologic ranges, a negative relationship is found between cortisol and TSH. Both exogenous and endogenous i.
These studies all taken together suggest a physiologic feedback loop where lower thyroid function increases cortisol, but cortisol feeds back to reduce TSH; this hypothesis is consistent with the observations that in the case of primary hypothyroidism elevated TSH cortisol is elevated, but in the setting of primarily elevated cortisol TSH is suppressed.
Clearly further clinical studies, for instance studies that incrementally administer TSH and evaluate cortisol levels, are needed in order to better understand the mechanisms involved in the TSH-cortisol relationship.
In summary these initial data, that add to what is already known about frank hypothyroidism and cortisol, demonstrate a potentially important relationship between TSH and cortisol in apparently healthy young individuals. The finding that this relationship appears to hold in the controversial TSH range of 2. Thyroid stimulating hormone; T4: Competing interests The authors have no competing interests to declare. JU and LMD provided crucial clinical and scientific endocrine and thyroid functioning expertise.
JU and LCK assisted with data analytic strategies. All authors made intellectual revisions to the entire manuscript, edited all sections of the manuscript and approved this version of the submitted manuscript. We thank Michele M.
Thyroid hormone action on ACTH secretion.
Stine, our research assistants in the Biobehavioral Health Studies Lab, and the GCRC nursing staff for assistance with data collection, and Rick Ball for guidance on the biological assays.
Thyroid hormone in health and disease. The Colorado thyroid disease prevalence study. Laboratory Medicine Practice Guidelines: National Academy of Clinical Biochemistry; An Update for Primary Care Physicians.
National health and nutrition examination survey III thyroid-stimulating hormone TSH -thyroperoxidase antibody relationships demonstrate that TSH upper reference limits may be skewed by occult thyroid dysfunction. J Clin Endocrinol Metabol.
The thyrotropin reference range should remain unchanged. The evidence for a narrower thyrotropin reference range is compelling.
Subclinical thyroid disease - Scientific review and guidelines for diagnosis and management. J Am Med Assoc. Dynamics of hour endogenous cortisol secretion and clearance in primary hypothyroidism assessed before and after partial thyroid hormone replacement. Impact of gender, menstrual cycle phase, and oral contraceptives on the activity of the hypothalamus-pituitary-adrenal axis.
Revista Brasileira De Psiquiatria. Glucocorticoid effects on memory function over the human life span. Why stress is bad for your brain.
Well-being, health-related quality of life and cardiovascular disease risk profile in women with subclinical thyroid disease - a community-based study.