The role of placental iodine storage in the neonatal thyroid stimulating hormone surge: iodine as a driving force to adapt the terrestrial life

Author(s):  
M. Karaoglan ◽  
E. İşbilen
1978 ◽  
Vol 61 (2) ◽  
pp. 441-448 ◽  
Author(s):  
Arthur R. C. Harris ◽  
Dana Christianson ◽  
M. Susan Smith ◽  
Shih-Lieh Fang ◽  
Lewis E. Braverman ◽  
...  

PEDIATRICS ◽  
1977 ◽  
Vol 59 (6) ◽  
pp. 948-950
Author(s):  
David R. Brown ◽  
J. Michael McMillin

We have previously reported a case of anterior pituitary insufficiency in a 14-year-old girl following closed head trauma.1 Endocrine evaluation one year after her accident revealed hypopituitarism manifested by cachexia, hypothyroidism, hypogonadism, and hypoadrenocorticism. Laboratory studies demonstrated deficiencies of adrenocorticotropic hormone, thyroid-stimulating hormone (TSH), growth hormone, and gonadotropic hormones (follicle-stimulating hormone and luteinizing hormone). We postulated that her hypopituitarism was due to anterior pituitary gland destruction rather than stalk section or hypothalamic damage. We have recently measured her serum prolactin concentrations following provocative stimulation with thyrotropin-releasing hormone (TRH), and these results strengthen the evidence for direct anterior pituitary gland destruction and provide a more complete delineation of her endocrinologic function.


1994 ◽  
Vol 266 (1) ◽  
pp. E57-E61 ◽  
Author(s):  
A. Giustina ◽  
M. Licini ◽  
M. Schettino ◽  
M. Doga ◽  
G. Pizzocolo ◽  
...  

The aim of our study was to elucidate the physiological role of the neuropeptide galanin in the regulation of anterior pituitary function in human subjects. Six healthy men (age range 26-35 yr, body mass index range 20-24 kg/m2) underwent in random order 1) an intravenous bolus injection of growth hormone-releasing hormone (GHRH)-(1-29)-NH2 (100 micrograms) + thyrotropin-releasing hormone (TRH, 200 micrograms) + luteinizing hormone-releasing hormone (LHRH, 100 micrograms) + corticotropin-releasing hormone (CRH, 100 micrograms), and 2) intravenous saline (100 ml) at time 0 plus either human galanin (500 micrograms) in saline (100 ml) or saline (100 ml) from -15 to +30 min. Human galanin determined a significant increase in serum GH (GH peak: 11.3 +/- 2.2 micrograms/l) from both baseline and placebo levels. No significant differences were observed between GH values after galanin and those after GHRH alone (24.3 +/- 5.2 micrograms/l). Human galanin significantly enhanced the GH response to GHRH (peak 49.5 +/- 10 micrograms/l) with respect to either GHRH or galanin alone. Human galanin caused a slight decrease in baseline serum adrenocorticotropic hormone (ACTH; 16.3 +/- 2.4 pg/ml) and cortisol levels (8 +/- 1.5 micrograms/dl). Galanin also determined a slight reduction in both the ACTH (peak 27 +/- 8 pg/ml) and cortisol (peak 13.8 +/- 1.3 micrograms/dl) responses to CRH. Baseline and releasing hormone-stimulated secretions of prolactin, thyroid-stimulating hormone, LH, and follicle-stimulating hormone were not altered by galanin. Our data suggest a physiological role for the neuropeptide galanin in the regulation of GH secretion in humans.(ABSTRACT TRUNCATED AT 250 WORDS)


2020 ◽  
Vol 26 (11) ◽  
pp. 1304-1311
Author(s):  
Anat Tsur ◽  
Elchanan Dreyfuss ◽  
Rosane Ness-Abramof ◽  
Rena Pollack ◽  
Avivit Cahn

Objective: While guidelines propose a single elevated prolactin measurement drawn without excess venipuncture stress as sufficient for diagnosing hyperprolactinemia, this may lead to unnecessary evaluation in the setting of stress-induced hyperprolactinemia. In this study, we aimed to define the role of the cannulated prolactin test in confirming hyperprolactinemia. Methods: We conducted a retrospective review of 757 patients with unexplained hyperprolactinemia who performed a cannulated prolactin test in a community-based referral endocrine clinic between 2000–2015. The prolactin test consisted of “test-baseline” levels taken at rest (T0), and cannulated measurements at 60 and 90 minutes (T60 and T90) without repeated venipuncture. The most recent prolactin level performed prior to the test (referral-prolactin) was collected. Results: Referral-prolactin was available for 621 (82%) patients, of whom 324 (52.2%) normalized at T0. The probability of normoprolactinemia at T0 was 50% if referral-prolactin was 2.0-fold the upper-limit-of-normal (ULN), yet only 5% if referral-prolactin was 5.0-fold the ULN. Of the 359 patients with hyperprolactinemia at T0, prolactin normalized at T60 and/or T90 in 99 (27.6%) patients. The probability of normoprolactinemia was low (<5%) in those with T0 prolactin levels >2.4-fold ULN. Overall, of 757 prolactin tests performed, only 260 (34.3%) patients had persistent hyperprolactinemia. Conclusion: Patients with referral-prolactin levels >5.0-fold the ULN, or a rested-prolactin (T0) >2.4-fold the ULN are unlikely to normalize during the cannulated test and consideration should be made to proceed directly with pituitary imaging. In patients with prolactin levels below these thresholds, the cannulated prolactin test may considerably reduce unnecessary investigations, treatment, and cost. Abbreviations: CHS = Clalit Health Services; IV = intravenous; T0 = at baseline; T60 = at 60 minutes; T90 = at 90 minutes; TSH = thyroid-stimulating hormone; ULN = upper limit of normal


2018 ◽  
Vol 14 (2) ◽  
pp. 72-80
Author(s):  
Svetlana V. Charinzeva ◽  
Elizaveta S. Taskina

Background. Endocrine ophthalmopathy (EOP) is an autoimmune orbit disease characterized by soft retrobulbar tissues damage. The level of antibodies to the thyroid-stimulating hormone receptor (TSHRAbs) is considered as a laboratory marker of EOP activity. Interleukins 17 (IL-17) and 23 (IL-23) play an important role in the pathogenesis of some autoimmune diseases and directly correlate with clinical activity. At present, there is an open question about the role of these cytokines in EOP and their relationship with TSHRAbs. Aims. To assess pathogenetic role of IL-17, IL-23 and TSHRAbs in patients with EOP. Materials and methods. The study included 50 people (100 eyes) at the age of 43 [35; 50] years. Three study groups were formed: 32 patients with moderate severity of EOP (clinical group), 18 patients with thyroid pathology without EOP (comparison group) and 15 healthy subjects (control group). All groups were comparable in age and sex. The diagnosis was verified clinically, laboratory and instrumentally. A comprehensive ophthalmologic examination and blood sampling were performed to determine the concentrations of IL-17, IL-23 and TSHRAbs. Statistical processing of the data was carried out in the program “Statistica 10.0”, StatSoft, Inc. Results. An increase in the level of TSHRAbs was observed in all phases of EOP activity in comparison with both comparison group and control (p < 0.05). But in the active phase TSHRAbs level reached the maximum values in 100% of patients. An increase in the IL-17 concentration in 5,3 times was found in the active EOP in comparison with the control group (p < 0.05). Concentration of TSHRAbs and IL-17 in blood serum directly correlates with EOP activity (p < 0.001). After carrying out pulse therapy with glucocorticosteroids, the consentration of IL-17 decreased almost to zero. There were no significant differences in the level of IL-23 in the groups (p = 0.56). Conclusions. Determination of TSHRAbs and IL-17 levels in serum can be used as a laboratory diagnostic marker of EOP activity.  


1961 ◽  
Vol 201 (6) ◽  
pp. 1049-1052 ◽  
Author(s):  
M. Jay Goodkind ◽  
David H. Fram ◽  
Michael Roberts

Normal and thyroidectomized guinea pigs were subjected to treatment with either triiodothyronine or thyroid-stimulating hormone. Determinations of myocardial catecholamine content and serum protein-bound iodine revealed a significant increase in myocardial norepinephrine content in the markedly thyrotoxic animal, and a significant decrease in norepinephrine content of the myocardium of hypothyroid animals. The significance of these findings in defining the role of catecholamines in various states of thyroid function is discussed.


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