Uncertainties in endocrine substitution therapy for central endocrine insufficiencies

Persani, Luca; Bonomi, Marco

doi:10.1016/b978-0-444-59602-4.00027-7

Cited by 6 publications

(6 citation statements)

References 87 publications

(135 reference statements)

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“…The production and secretion of TSH by the pituitary gland are positively stimulated by TRH, while TRH also modulates the glycosylation of TSH, which affects TSH bioactivity (Magner 1990). Part of the explanation for unaltered plasma TSH in the presence of decreased pituitary Tshb mRNA as observed in this study may be a discrepancy between the biological activity and the immunological detectability of TSH (Persani & Bonomi 2014).…”

Section: Discussioncontrasting

confidence: 43%

A model for chronic, intrahypothalamic thyroid hormone administration in rats

Zhi

Bisschop

Foppen

et al. 2016

Journal of Endocrinology

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In addition to the direct effects of thyroid hormone (TH) on peripheral organs, recent work showed metabolic effects of TH on the liver and brown adipose tissue via neural pathways originating in the hypothalamic paraventricular and ventromedial nucleus (PVN and VMH). So far, these experiments focused on short-term administration of TH. The aim of this study is to develop a technique for chronic and nucleus-specific intrahypothalamic administration of the biologically active TH tri-iodothyronine (T 3 ). We used beeswax pellets loaded with an amount of T 3 based on in vitro experiments showing stable T 3 release (~5 nmol l −1 ) for 32 days. Upon stereotactic bilateral implantation, T 3 concentrations were increased 90-fold in the PVN region and 50-fold in the VMH region after placing T 3 -containing pellets in the rat PVN or VMH for 28 days respectively. Increased local T 3 concentrations were reflected by selectively increased mRNA expression of the T 3 -responsive genes Dio3 and Hr in the PVN or in the VMH. After placement of T 3 -containing pellets in the PVN, Tshb mRNA was significantly decreased in the pituitary, without altered Trh mRNA in the PVN region. Plasma T 3 and T 4 concentrations decreased without altered plasma TSH. We observed no changes in pituitary Tshb mRNA, plasma TSH, or plasma TH in rats after placement of T 3 -containing pellets in the VMH. We developed a method to selectively and chronically deliver T 3 to specific hypothalamic nuclei. This will enable future studies on the chronic effects of intrahypothalamic T 3 on energy metabolism via the PVN or VMH.

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Section: Discussioncontrasting

confidence: 43%

A model for chronic, intrahypothalamic thyroid hormone administration in rats

Zhi

Bisschop

Foppen

et al. 2016

Journal of Endocrinology

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“…Due to the subnormal cortisol response to stimulation, administration of additional steroid hormone was advised during periods of stress. At a thyroxine dose of 0.05 mg/day, the FT4 concentration remains in the normal range and TSH is no longer used for titration because of the possibility of panhypopituitarism (9). The patient refused further neurosurgical consultation and remains clinically well on her current dosage of thyroid hormone nearly 1 year after her initial diagnosis.…”

Section: Discussionmentioning

confidence: 99%

Concurrent Panhypopituitarism and Hyperprolactinemia Due to a Giant Internal Carotid Aneurysm Revealed by Thyroid Hormone Withdrawal During Follow-Up Management of Thyroid Cancer

Goldman

Gruber

Herman

2016

AACE Clinical Case Reports

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Objective: This article reports a case of secondary hypothyroidism occurring during the withdrawal of thyroid hormone replacement in a patient with thyroid cancer that led to the discovery of simultaneous panhypopituitarism and hyperprolactinemia that were caused by an internal carotid artery aneurysm. The discovery of the secondary hypothyroidism necessitated further pituitary hormone analysis and medical imaging to identify the precise pathologic etiology. Methods: The methods used included the evaluation of selected thyroid and pituitary hormone concentrations and subsequent pituitary magnetic resonance imaging. Results: An 86-year-old African-American female with a history of thyroid cancer exhibited a suppressed serum thyroid-stimulating hormone concentration that failed to increase during progressive lowering of her thyroxine dosage despite it causing a simultaneous subnormal free thyroxine concentration. Laboratory findings indicated secondary hypothyroidism and subsequently panhypopituitarism and hyperprolactinemia. Pituitary magnetic resonance imaging revealed the presence of a large carotid aneurysm that had invaded the sella turcica. Additional hormone analyses revealed elevated prolactin, low gonad

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“…Over the same 12-month period, the ratio of primary to secondary hypothyroidism detected by the above test strategy was 20:1 [11]. Such 20:1 ratio of primary to secondary hypothyroidism [11] might appear grossly overestimated in view of the aforementioned widely held opinion on the rarity of CH [9]. However, the 20:1 ratio is consistent with what can easily be calculated based on a recent meta-analysis [13]: the incidence of hypothyroidism in Europe is 226 per 100,000 per year, which divided by 5.5/100,000 (incidence of CH according to Wardle et al [11]) equals 41: 1.…”

Section: Introductionmentioning

confidence: 92%

“…Both textbooks and papers provide information that CH is (very) rare, ranging from 1:16,000 to 1:120,000 [1], [6], [7], [8], [9], [10]. CH has also been described to occur in fewer than 1% of hypothyroid patients or being about 1000-fold rarer than primary hypothyroidism [2], [6], [7], [8], [9], [10]. However, an important English paper challenged this widely held opinion about the rarity of CH [11].…”

Section: Introductionmentioning

confidence: 99%

Less known aspects of central hypothyroidism: Part 1 – Acquired etiologies

Benvenga

Klose

Vita

et al. 2018

Journal of Clinical & Translational Endocrinology

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Central hypothyroidism (CH) is a rare cause of hypothyroidism. CH is frequently overlooked, as its clinical picture is subtle and includes non-specific symptoms; furthermore, if measurement of TSH alone is used to screen for thyroid function, TSH concentrations can be normal or even above the upper normal reference limit. Indeed, certain patients are at risk of developing CH, such as those with a pituitary adenoma or hypophysitis, those who have been treated for a childhood malignancy, have suffered a head trauma, sub-arachnoid hemorrhage or meningitis, and those who are on drugs capable to reduce TSH secretion.

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Uncertainties in endocrine substitution therapy for central endocrine insufficiencies

Cited by 6 publications

References 87 publications

A model for chronic, intrahypothalamic thyroid hormone administration in rats

A model for chronic, intrahypothalamic thyroid hormone administration in rats

Concurrent Panhypopituitarism and Hyperprolactinemia Due to a Giant Internal Carotid Aneurysm Revealed by Thyroid Hormone Withdrawal During Follow-Up Management of Thyroid Cancer

Less known aspects of central hypothyroidism: Part 1 – Acquired etiologies

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