scholarly journals Thyroid-stimulating hormone binding to beef thyroid membranes. Role of N-acetylneuraminic acid.

1976 ◽  
Vol 251 (14) ◽  
pp. 4247-4253 ◽  
Author(s):  
W V Moore ◽  
L Feldman
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


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