Lack of Nocturnal Serum Thyrotropin Surge after Surgery*

Bartalena, Luigi; Martino, Enio; Brandi, Ls; Falcone, M; Pacchiarotti, Alessandro; Ricci, C; Bogazzi, Fausto; Grasso, Lucia; Mammoli, Claudia; Pinchera, Aldo

doi:10.1210/jcem-70-1-293

Cited by 47 publications

(26 citation statements)

References 26 publications

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“…Subsequently, circulating TSH and T4 levels often return to`normal' whereas T3 levels remain low. Although mean serum TSH concentrations are indistinguishable from normal values at that time point, the normal nocturnal TSH surge has been shown to be absent (31,32). The magnitude of the T3 drop within 24 h has been found to re¯ect the severity of the illness (33,34).…”

Section: Changes In the Acute Phase Of Critical Illnessmentioning

confidence: 99%

Novel insights into the neuroendocrinology of critical illness

Berghe

2000

European Journal of Endocrinology

226

104

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An unexplained hallmark of prolonged critical illness is the fact that food does not prevent or reverse protein wasting, while fat is paradoxically accrued. This`wasting syndrome' often persists after the underlying disease has been resolved and thus perpetuates intensive care dependency. Although the crucial role of an intact hypothalamus±pituitary axis for homeostasis during stress is well recognized, the differences between the neuroendocrine changes observed in acute and prolonged critical illness were only recently described. Novel insights in this area are reviewed here.The initial endocrine stress response consists primarily of a peripheral inactivation of anabolic pathways while pituitary activity is essentially ampli®ed or maintained. These responses presumably provide the metabolic substrates and host defense required for survival and to delay anabolism, and thus should be considered as adaptive and bene®cial. Persistence of this acute stress response throughout the course of critical illness was hitherto assumed. This assumption has now been invalidated, since a uniformly reduced pulsatile secretion of ACTH, TSH, LH, prolactin (PRL) and GH has been observed in protracted critical illness, causing diminished stimulation of several target organs. Impaired pulsatile secretion of anterior pituitary hormones in the chronic phase of critical illness seems to have a hypothalamic rather than a pituitary origin, as administration of relevant releasing factors evoked immediate and pronounced pituitary hormone release. A reduced availability of TRH, one of the endogenous ligands of the GH-releasing peptide (GHRP) receptor (such as the recently discovered ghrelin) and, in very long-stay critically ill men, also of GHRH, appear to be involved. This hypothesis was further explored by investigating the effects of continuous i.v. infusion of GHRH, GHRP, TRH and their combinations for several days. Pulsatile secretion of GH, TSH and PRL was re-ampli®ed by relevant combinations of releasing factors which also substantially increased circulating levels of IGF-I, GH-dependent binding proteins, thyroxine and tri-iodothyronine (T3) while avoiding a rise in reverse T3. Active feedback-inhibition loops prevented overstimulation of target organs and metabolic improvement was noted with the combined infusion of GHRP and TRH. Whether this novel endocrine strategy will also enhance clinical recovery from critical illness remains to be explored.

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Section: Changes In the Acute Phase Of Critical Illnessmentioning

confidence: 99%

Novel insights into the neuroendocrinology of critical illness

Berghe

2000

European Journal of Endocrinology

226

104

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“…Patients with CH have a blunted nocturnal surge (84,85) in TSH circadian secretion (86)(87)(88). However, this may be found in NTI (89), in post-operative patients (90,91), during starvation (92), and in severe primary hypothyroidism (93). The TRH stimulation test is used in the diagnosis of CH (94,95), but its value has been questioned (96,97).…”

Section: Central Hypothyroidismmentioning

confidence: 99%

GH replacement in adults: interactions with other pituitary hormone deficiencies and replacement therapies

Filipsson

Johannsson

2009

European Journal of Endocrinology

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Severe GH deficiency (GHD) in adults has been described as a clinical entity. However, some of the features associated with GHD could be due to unphysiological and inadequate replacement of other pituitary hormone deficiencies. This may be true for glucocorticoid replacement that lacks a biomarker making dose titration and monitoring difficult. Moreover, oral estrogen replacement therapy decreases IGF1 levels compared with the transdermal route, which attenuates the responsiveness to GH replacement therapy in women. In addition, in untreated female hypogonadism, oral estrogen may augment the features associated with GHD in adult women. Important interactions between the hormones used for replacing pituitary hormone deficiency occur. Introducing GH replacement may unmask both an incipient adrenal insufficiency and central hypothyroidism. Therefore, awareness and proper monitoring of these hormonal interactions are important in order to reach an optimal replacement therapy. This review will focus on the complex hormonal interactions between GH and other pituitary hormones in GHD and in GH replacement. European Journal of Endocrinology 161 S85-S95

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“…Serum thyrotropin (TSH) concentration is usually normal, although suppressed values may be found in a minority of patients (1). In addition, a decrease in the nocturnal surge of TSH has been consistently reported in patients with NTI (8)(9)(10)(11)(12). Abnormalities of TSH glycosylation causing its decreased biological activity were also described (13).…”

Section: Introductionmentioning

confidence: 99%