STUDIES ON THE THYROID GLAND. V. THE THYROID STIMULATING HORMONE FROM THE ANTERIOR PITUITARY. SOME CHEMICAL PROPERTIES1

2010 ◽  
Vol 10 (1-2) ◽  
pp. 126-130 ◽  
Author(s):  
Marie Krogh ◽  
Harald Okkels
2008 ◽  
Vol 109 (1) ◽  
pp. 17-22 ◽  
Author(s):  
Michelle J. Clarke ◽  
Dana Erickson ◽  
M. Regina Castro ◽  
John L. D. Atkinson

Object Thyroid-stimulating hormone (TSH)–secreting pituitary adenomas are rare, representing < 2% of all pituitary adenomas. Methods The authors conducted a retrospective analysis of patients with TSH-secreting or clinically silent TSH-immunostaining pituitary tumors among all pituitary adenomas followed at their institution between 1987 and 2003. Patient records, including clinical, imaging, and pathological and surgical characteristics were reviewed. Twenty-one patients (6 women and 15 men; mean age 46 years, range 26–73 years) were identified. Of these, 10 patients had a history of clinical hyperthyroidism, of whom 7 had undergone ablative thyroid procedures (thyroid surgery/131I ablation) prior to the diagnosis of pituitary adenoma. Ten patients had elevated TSH preoperatively. Seven patients presented with headache, and 8 presented with visual field defects. All patients underwent imaging, of which 19 were available for imaging review. Sixteen patients had macroadenomas. Results Of the 21 patients, 18 underwent transsphenoidal surgery at the authors' institution, 2 patients underwent transsphenoidal surgery at another facility, and 1 was treated medically. Patients with TSH-secreting tumors were defined as in remission after surgery if they had no residual adenoma on imaging and had biochemical evidence of hypo-or euthyroidism. Patients with TSH-immunostaining tumors were considered in remission if they had no residual tumor. Of these 18 patients, 9 (50%) were in remission following surgery. Seven patients had residual tumor; 2 of these patients underwent further transsphenoidal resection, 1 underwent a craniotomy, and 4 underwent postoperative radiation therapy (2 conventional radiation therapy, 1 Gamma Knife surgery, and 1 had both types of radiation treatment). Two patients had persistently elevated TSH levels despite the lack of evidence of residual tumor. On pathological analysis and immunostaining of the surgical specimen, 17 patients had samples that stained positively for TSH, 8 for α-subunit, 10 for growth hormone, 7 for prolactin, 2 for adrenocorticotrophic hormone, and 1 for follicle-stimulating hormone/luteinizing hormone. Eleven patients (61%) ultimately required thyroid hormone replacement therapy, and 5 (24%) required additional pituitary hormone replacement. Of these, 2 patients required treatment for new anterior pituitary dysfunction as a complication of surgery, and 2 patients with preoperative partial anterior pituitary dysfunction developed complete panhypopituitarism. One patient had transient diabetes insipidus. The remainder had no change in pituitary function from their preoperative state. Conclusions Thyroid-stimulating hormone–secreting pituitary lesions are often delayed in diagnosis, are frequently macroadenomas and plurihormonal in terms of their pathological characteristics, have a heterogeneous clinical picture, and are difficult to treat. An experienced team approach will optimize results in the management of these uncommon lesions.


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)


1960 ◽  
Vol 199 (3) ◽  
pp. 437-444 ◽  
Author(s):  
Melvin J. Fregly

The effects of cortisone acetate and thyroxine, administered separately or in combination, on colonic cooling rate (CCR) have been studied in restrained, adrenalectomized rats subjected to air at 5°C. Thyroxine alone at 5.0 µg/day reduced the rapid CCR of adrenalectomized rats but failed to return it to that of sham-operated rats. Cortisone acetate alone at 1.0 mg/day reduced CCR but also failed to restore it to normal. A higher dose (2.0 mg/day) was even less effective. Administration of 5.0 µg/day thyroxine simultaneously with 2.0–2.5 mg cortisone acetate returned CCR to that of sham-operated rats. Simultaneous administration of cortisone acetate with graded doses of thyroid stimulating hormone (TSH) to adrenalectomized rats resulted in greater reduction of CCR than with either treatment alone. Cortisone acetate did not appear to interfere either with tissue utilization of thyroxine or with thyroid gland response to TSH administration. The cooling test has also proved a useful tool for comparing potencies of a synthetic (dexamethasone) and a naturally occurring steroid (progesterone) with that of cortisone acetate. Dexamethasone is estimated to have a potency 700 times that of cortisone acetate, while progesterone is only one-third as potent.


1971 ◽  
Vol 49 (4) ◽  
pp. 559-567 ◽  
Author(s):  
A. ŚLEBODZIŃSKI ◽  
Z. MACH ◽  
W. MALINOWSKA

SUMMARY Nine-day chick embryos received grafts of hypothalamus, adenohypophysis, thyroid, and fat (controls) from 0-, 7-, 14- and 21-day-old rabbits to the chorio-allantois. In addition, aqueous rabbit adenohypophysial and hypothalamic extracts were given to 1-day-old chicks. Animals injected with thyrotrophin and saline served as controls. On the 5th day of incubation of treated embryos, or 24 h after the administration of the extracts, the chicks were killed and their thyroids studied histologically. The hypothalamic grafts or extracts activated the chick thyroid gland and a similar trend was found in adenohypophysial or thyroid-stimulating hormone-treated chicks. The degree of activation of the embryo chick thyroid gland was related to the age of the donor rabbit. In general, thyroidstimulating hormone-releasing factor activity in hypothalamic heterografts or extracts appeared first in 14-day-old rabbits and was correlated with increasing thyrotrophic potency of the rabbit adenohypophysis.


1968 ◽  
Vol 46 (3) ◽  
pp. 449-452 ◽  
Author(s):  
A. E. Zimmerman ◽  
C. C. Yip

The effects of increasing or decreasing the endogenous secretion of thyroid-stimulating hormone on the iodinating activity of the rat thyroid gland were investigated. The thyroid iodinating activity of rats on 0.01% propylthiouracil in the drinking water increased linearly for 3 days and reached a maximum of 230 to 240% of the control on or about the fourth day of treatment. The daily injection of thyroxine (10 μg/100 g intraperitoneally) or hypophysectomy resulted in a rapid decrease in the iodinating activity between the first and second day, approaching a basal level by the third day. When the iodinating activity was suppressed for 4 days by daily injections of thyroxine, the activity began to rise on the fifth day after termination of thyroxine treatment.


1996 ◽  
Vol 17 (1) ◽  
pp. 39-45 ◽  
Author(s):  
Anna Capaldo ◽  
Vincenza Laforgia ◽  
Rosaria Sciarrillo ◽  
Antimo Cavagnuolo

AbstractInsulin was administered to Podarcis sicula in winter, when the thyroid gland is inhibited. The activity of the thyroid increased, plasma concentrations of thyroid hormones and hepatic 5'-monodeiodinase activity (MDA) increased, and thyroid stimulating hormone (TSH) concentrations fell to undetectable values. This result confirms the influence of insulin on the activity of the thyroid gland in the lizard species studied. The mechanisms are still unclear, although there is evidence which leads us to believe that insulin is directly responsible for thyroid activation.


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