Thyroid Hormone Binding Inhibition in Critically ill Patients – Who is the Inhibitor?

Schifferdecker, E.; Hering, S.; Böhm, Bernhard; Förster, H; Althoff, P.-H.; Schulz, F.; Schöffling, Κ.

doi:10.1055/s-0029-1210963

Cited by 8 publications

(6 citation statements)

References 7 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…In case of rapid onset of stress situations, e.g., severe illness, the time frame of the described control mechanisms would be too long to be effective, if plasma protein binding of thyroid hormones remained unchanged. However, in critical illness the extent of plasma protein binding is reduced owing to decreased concentrations of binding proteins and the existence of certain binding inhibitors (57, 58, 159). This effect is putatively mediated via cytokines (160).…”

Section: Mechanisms Of Thyroid Allostasismentioning

confidence: 99%

“…About 30% of hospitalized patients (54) and more than 60% of patients affected by critical illness (55, 56) experience transient changes in serum concentrations of TSH and thyroid hormones. Characteristic patterns are low levels of free and total 3,3′,5-triiodothyronine (T3) (39, 40, 56), impaired plasma protein binding of thyroid hormones (57, 58) and, in more severe cases, thyrotropic adaptation with a downward shift of the set point characterized by paradoxically low TSH levels in the presence of normal or even low concentrations of FT4 (59, 60). Conversely, serum concentrations of 3,5,5′-triiodothyronine (rT3) and 3,5-diiodothyronine (3,5-T2) are typically increased (39, 40, 61–63).…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Thyroid Allostasis–Adaptive Responses of Thyrotropic Feedback Control to Conditions of Strain, Stress, and Developmental Programming

Hoermann²,

et al. 2017

View full text Add to dashboard Cite

The hypothalamus–pituitary–thyroid feedback control is a dynamic, adaptive system. In situations of illness and deprivation of energy representing type 1 allostasis, the stress response operates to alter both its set point and peripheral transfer parameters. In contrast, type 2 allostatic load, typically effective in psychosocial stress, pregnancy, metabolic syndrome, and adaptation to cold, produces a nearly opposite phenotype of predictive plasticity. The non-thyroidal illness syndrome (NTIS) or thyroid allostasis in critical illness, tumors, uremia, and starvation (TACITUS), commonly observed in hospitalized patients, displays a historically well-studied pattern of allostatic thyroid response. This is characterized by decreased total and free thyroid hormone concentrations and varying levels of thyroid-stimulating hormone (TSH) ranging from decreased (in severe cases) to normal or even elevated (mainly in the recovery phase) TSH concentrations. An acute versus chronic stage (wasting syndrome) of TACITUS can be discerned. The two types differ in molecular mechanisms and prognosis. The acute adaptation of thyroid hormone metabolism to critical illness may prove beneficial to the organism, whereas the far more complex molecular alterations associated with chronic illness frequently lead to allostatic overload. The latter is associated with poor outcome, independently of the underlying disease. Adaptive responses of thyroid homeostasis extend to alterations in thyroid hormone concentrations during fetal life, periods of weight gain or loss, thermoregulation, physical exercise, and psychiatric diseases. The various forms of thyroid allostasis pose serious problems in differential diagnosis of thyroid disease. This review article provides an overview of physiological mechanisms as well as major diagnostic and therapeutic implications of thyroid allostasis under a variety of developmental and straining conditions.

show abstract

Section: Mechanisms Of Thyroid Allostasismentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Thyroid Allostasis–Adaptive Responses of Thyrotropic Feedback Control to Conditions of Strain, Stress, and Developmental Programming

Hoermann²,

et al. 2017

View full text Add to dashboard Cite

show abstract

“…This complex constellation, referred to as euthyroid sick syndrome or nonthyroidal illness syndrome (NTIS), is characterised by three components that may occur singly or in combination: low TSH and normal or low FT4 levels phenomenologically similar to central hypothyroidism (transient thyrotropic adaptation, occasionally leading to low-T4 syndrome) [201], impaired protein binding of thyroid hormones [202, 203], and reduced formation of T3 with simultaneously increased conversion to rT3 (low-T3 syndrome) [22–24]. Few observations report that the iodothyroacetic acids TRIAC and TETRAC are increased in NTIS and starvation [204–206].…”

Section: Allostatic and Pathological Conditionsmentioning

confidence: 99%

“…Additionally, if certain input parameters, for example, TBG and binding constants for calculation of G T and G D , are not biochemically determined but, as usual, replaced by standard values, some bias may ensue. Therefore, G T and G D will be overestimated in NTIS, where plasma protein levels are reduced [202, 203]. Although this will usually not pose problems in differential diagnosis, as the impairment of protein binding affects all investigated groups, the person calculating structure parameters and interpreting their results should at least be aware of these difficulties.…”

Section: Allostatic and Pathological Conditionsmentioning

confidence: 99%

TSH and Thyrotropic Agonists: Key Actors in Thyroid Homeostasis

Dietrich

Landgrafe

Fotiadou

2012

Journal of Thyroid Research

115

183

View full text Add to dashboard Cite

This paper provides the reader with an overview of our current knowledge of hypothalamic-pituitary-thyroid feedback from a cybernetic standpoint. Over the past decades we have gained a plethora of information from biochemical, clinical, and epidemiological investigation, especially on the role of TSH and other thyrotropic agonists as critical components of this complex relationship. Integrating these data into a systems perspective delivers new insights into static and dynamic behaviour of thyroid homeostasis. Explicit usage of this information with mathematical methods promises to deliver a better understanding of thyrotropic feedback control and new options for personalised diagnosis of thyroid dysfunction and targeted therapy, also by permitting a new perspective on the conundrum of the TSH reference range.

show abstract

“…Schwankungen der Jodidzufuhr ausgleichen kann. [33,40,43,46] die Bindung. Auch angeborene TBG-Varianten füh-ren zu einer verminderten Bindungskapazität [23].…”

Section: Transport 5 Plasmatransportunclassified

Resorption, Transport und Bioverfügbarkeit von Schilddrüsenhormonen

Dietrich¹,

Brisseau²,

Boehm³

2008

Dtsch med Wochenschr

View full text Add to dashboard Cite

The frequently prescribed classical thyroid hormones (iodothyronines) are critical dose drugs with a narrow therapeutic index. Nowadays the mechanisms of their absorption, which takes place predominantly in the jejunum and ileum, have only partly been elucidated. Bioavailability of iodothyronines whose kinetics is subject to enterohepatic circulation, is about 70 %. Several factors influence their absorption including nutrients, drugs and concomitant diseases. After being absorbed only a small fraction of thyroid hormones circulates freely in plasma, whereas the greater portion is bound to plasma proteins. This binding, too, may be influenced by numerous factors; alterations by certain diseases and physiological conditions may lead to ambiguities in differential diagnosis. Intracellular accumulation of iodothyronines is accomplished by at least ten different active and energy-dependent transporters with variable tissue distribution. Particularly in critical illness (non-thyroidal illness syndrome) alterations of protein binding and membrane transport are common. In therapy of hypothyroid patients different brand-name products lack bioequivalence and thus requiring subsequent monitoring of thyroid status after treatment has been changed among different brand-name versions.

show abstract

Thyroid Hormone Binding Inhibition in Critically ill Patients – Who is the Inhibitor?

Cited by 8 publications

References 7 publications

Thyroid Allostasis–Adaptive Responses of Thyrotropic Feedback Control to Conditions of Strain, Stress, and Developmental Programming

Thyroid Allostasis–Adaptive Responses of Thyrotropic Feedback Control to Conditions of Strain, Stress, and Developmental Programming

TSH and Thyrotropic Agonists: Key Actors in Thyroid Homeostasis

Resorption, Transport und Bioverfügbarkeit von Schilddrüsenhormonen

Contact Info

Product

Resources

About