Amount of Thyroid-stimulating Hormone in Anterior Pituitary of the Thyroidectomized Rabbit

1934 ◽  
Vol 32 (3) ◽  
pp. 484-485 ◽  
Author(s):  
G. Ch'En ◽  
H. B. Van Dyke
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)


2021 ◽  
Vol 12 ◽  
Author(s):  
Yi Fang ◽  
He Wang ◽  
Ming Feng ◽  
Wentai Zhang ◽  
Lei Cao ◽  
...  

ObjectiveNo accurate predictive models were identified for hormonal prognosis in non-functioning pituitary adenoma (NFPA). This study aimed to develop machine learning (ML) models to facilitate the prognostic assessment of pituitary hormonal outcomes after surgery.MethodsA total of 215 male patients with NFPA, who underwent surgery in four medical centers from 2015 to 2021, were retrospectively reviewed. The data were pooled after heterogeneity assessment, and they were randomly divided into training and testing sets (172:43). Six ML models and logistic regression models were developed using six anterior pituitary hormones.ResultsOnly thyroid-stimulating hormone (p &lt; 0.001), follicle-stimulating hormone (p &lt; 0.001), and prolactin (PRL; p &lt; 0.001) decreased significantly following surgery, whereas growth hormone (GH) (p &lt; 0.001) increased significantly. The postoperative GH (p = 0.07) levels were slightly higher in patients with gross total resection, but the PRL (p = 0.03) level was significantly lower than that in patients with subtotal resection. The optimal model achieved area-under-the-receiver-operating-characteristic-curve values of 0.82, 0.74, and 0.85 in predicting hormonal hypofunction, new deficiency, and hormonal recovery following surgery, respectively. According to feature importance analyses, the preoperative levels of the same type and other hormones were all important in predicting postoperative individual hormonal hypofunction.ConclusionFluctuation in anterior pituitary hormones varies with increases and decreases because of transsphenoidal surgery. The ML models could accurately predict postoperative pituitary outcomes based on preoperative anterior pituitary hormones in NFPA.


1976 ◽  
Vol 44 (4) ◽  
pp. 504-505 ◽  
Author(s):  
William W. Winternitz ◽  
James A. Dzur

✓ A patient presented with hypopituitarism, 2 years after severe head trauma. Deficits of growth hormone, follicle-stimulating hormone, luteinizing hormone, and borderline thyroid-stimulating hormone (TSH) were demonstrated. Normal TSH-releasing hormone (TRH) response and elevated prolactin indicated viable anterior pituitary tissue with inadequate hypothalamic control. Precautions are suggested for recognition and treatment of this syndrome.


Author(s):  
Gary Butler ◽  
Jeremy Kirk

• The pituitary is formed of two anatomically and embryologically distinct lobes: ◦ anterior pituitary: which secretes growth hormone (GH), gonadotropins (luteinizing hormone (LH) and follicle-stimulating hormone (FSH)), adrenocorticotropic hormone (ACTH), thyroid-stimulating hormone (TSH), and prolactin ◦ posterior pituitary: which secretes vasopressin and oxytocin. • Hypopituitarism is deficiency of one or more pituitary hormones. Some hormones, e.g. GH (LH/FSH), are more likely to present with isolated deficiencies, while others, e.g. TSH, ACTH, are more often found as part of multiple pituitary hormone deficiency (MPHD). • Deficiencies may be congenital (including genetic) or acquired; secondary to tumour, trauma, infiltration, infection, or irradiation. • GH deficiency: ◦ diagnosed using a combination of clinical, radiological, and biochemical assessment (including GH stimulation testing) ◦ treatment is with GH (including if necessary into adulthood). • LH/FSH deficiency: ◦ If acquired, often one of the first anterior pituitary hormones to be lost. ◦ Congenital forms: ■ present with cryptorchidism and/or micropenis in males ■ may occur in isolation, or in association with anosmia (Kallmann and CHARGE syndromes). ◦ Treatment: sex steroid therapy to induce secondary sexual characteristics, and recombinant FSH/LH to induce fertility potential. • ACTH deficiency: ◦ Unlike primary adrenal problems, hyperpigmentation does not occur. ◦ Although mineralocorticoid production is preserved, hyponatraemia may still occur. ◦ Treatment is with hydrocortisone. • TSH deficiency: ◦ TSH may be low, normal, or raised (but inappropriate for free thyroxine level). ◦ Treatment is with thyroxine. • Vasopressin deficiency: ◦ produces cranial diabetes insipidus ◦ treatment is with DDAVP (orally or nasally). • Prolactin and oxytocin deficiency rarely produce clinical problems.


1974 ◽  
Vol 61 (1) ◽  
pp. 15-19 ◽  
Author(s):  
MELVIN CHING

SUMMARY The tadpole, in metamorphic stasis, has been used as a bioassay recipient for thyroid-stimulating hormone (TSH). The validity of its use for this purpose, however, has not been tested critically, particularly with respect to the effect of other hormones, most notably, growth hormone (GH) and luteinizing hormone (LH). Growth hormone has been shown to influence thyroid function and LH is a common contaminant of pituitary TSH preparations. Tadpoles of Rana pipiens, arrested at a particular metamorphic stage, received various concentrations of LH alone, a combination of doses of GH and TSH, or GH and rat anterior pituitary extract. Growth hormone was ineffective in re-inducing metamorphosis in 78% of cases, whereas LH stimulated metamorphosis in the tadpoles.


1980 ◽  
Vol 86 (2) ◽  
pp. 357-362 ◽  
Author(s):  
TAKAMURA MURAKI ◽  
TERUO NAKADATE ◽  
YUKIKO TOKUNAGA ◽  
RYUICHI KATO

Morphine reduced the release of thyroid-stimulating hormone (TSH) which was stimulated by exposure to cold and by thyroidectomy as well as reducing the basal level of TSH in the serum of male rats. The inhibitory effect of morphine was antagonized by naloxone which did not enhance the basal or cold-induced TSH release. Pretreatment with morphine did not reduce the release of TSH induced by exogenous thyrotrophin-releasing hormone (TRH) but enhanced it. This effect of morphine was also antagonized by naloxone. The above results suggested that the effect of morphine in reducing levels of serum TSH was not mediated by blocking the effect of TRH on the anterior pituitary gland, but that it was probably mediated by the inhibition of the release of TRH.


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