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Pituitary emergencies:
Published in Nadia Barghouthi, Jessica Perini, Endocrine Diseases in Pregnancy and the Postpartum Period, 2021
Jessica Perini, Nadia Barghouthi, Gayatri Jaiswal
Necrosis of the thyrotrophs of the pituitary will impair secretion of TSH, which stimulates the production of thyroid hormone by the thyroid gland.Symptoms of hypothyroidism will not be apparent in the immediate postpartum period due to the long half-life of thyroid hormone (7 days).Symptoms of hypothyroidism include fatigue, weight gain, trouble concentrating, cold intolerance, and constipation. Severe symptoms include bradycardia, hypothermia, and altered mental status.
Regulation of the Pituitary Gland by Dopamine
Published in Nira Ben-Jonathan, Dopamine, 2020
Thyrotrophs comprise about 5% of the adult anterior pituitary cell population. Most thyrotrophs are large stellate cells, filled with secretory granules, 100–150 nm in diameter, that are localized at the cell margins [76]. The cells are characterized by a dense arrangement of parallel arrays of rough endoplasmic reticulum. Clustered or isolated elongated TSH cells are also observed. Some cells with secretory granules 150–250 nm in diameter appear sporadically in the gland, and ultrastructurally resemble gonadotrophs. Rat thyrotrophs constitute an heterogeneous cell population in terms of morphology and ultrastructure. Hyperplastic pituitaries resulting from hypothyroidism, contain cells that stain for both TSH and PRL or TSH and GH derived from transdifferentiated somatotrophs or lactotrophs into thyrotrophs.
Neuroendocrine Morphology
Published in Paul V. Malven, Mammalian Neuroendocrinology, 2019
Thyrotroph cells that secrete TSH comprise about 3 % of pars anterior cells in rats, and their secretory vesicles are very small (i.e., diameters of about 50 nm). Thyrotrophs appear to be strictly monohormonal (i.e., secrete a single hormone). In contrast, gonadotrophs may be either monohormonal or bihormonal, secreting LH and/or follicle-stimulating hormone (FSH), and there are species differences as regards the relative proportions of these monohormonal and bihormonal gonadotrophs. Moreover, the proportions of LH only, FSH only, and LH + FSH gonadotrophs may also depend on physiological status. Secretory vesicles present in gonadotrophs have diameters of intermediate size, and it is unclear whether LH and FSH always exist in separate secretory vesicles within individual gonado-troph cells.
Pituitary hyperplasia mimicking thyrotropin-producing pituitary adenoma in the patient with resistance to thyroid hormone: a case report
Published in International Journal of Neuroscience, 2021
Onnicha Suntornlohanakul, Chutintorn Sriphrapradang
There were previous reports that described the presence of pituitary hyperplasia in RTH-β patients who had p.R438H mutations [14,15]. To date, this is the first case report of pituitary hyperplasia in RTH-β patient with p.R383H mutation. In previous report, the patient presented with goiter and sinus tachycardia as our patient [15]. Initial TFTs showed high FT4, but TSH was not measured. The initial diagnosis of primary hyperthyroidism was established and treated with radioiodine ablation. During follow-up, there was persistently high FT4 with non-suppressible TSH. Hence, the tests to differentiate between TSHoma and RTH-β were undertaken. Pituitary enlargement was demonstrated from imaging, but the RTH-β was diagnosed due to preserved TSH response and normal α-GSU. After administrating supraphysiological dose of thyroxine, the pituitary size was reduced [15]. However, pituitary hyperplasia did not appear in all RTH-β patients with persistently high TSH levels [14,16]. The possible mechanism of pituitary hyperplasia is compensatory hyperplasia in resistant thyrotrophs because they perceive as insufficient thyroid hormone state. In this case, we decided to do not treat with thyroxine to restore TSH secretion to normal levels because thyroxine may precipitate palpitation. Some experts have suggested that RTH-β may predispose to the development of pituitary adenoma [17]. Even though there is no recommendation for the follow-up of the pituitary imaging in RTH-β patients, there may be a rationale to follow-up MRI in such of this case.
The possible ameliorative role of Lycopene on Tributyltin induced thyroid damage in adult male albino rats (histological, immunohistochemical and biochemical study)
Published in Ultrastructural Pathology, 2023
Ghada A Elsammak, Aliaa Talaat, Samar Reda
Some follicles showed hyperplasia. Chiamolera and Wondisford (2009) explained that reduced thyroid hormone levels stimulate the pituitary, causing the thyrotrophs to generate more TSH, which causes hyperplasia of follicular cells and colloid area shrinkage.36 Congested blood vessels were explained by Shady and Noor El-den (2010), who stated that lipid peroxidation and oxidative stress cause congestion and dilatation of blood vessels by promoting their wall lesion. Also, hyperemia is a mechanism for removal of the toxin.37
Thyroid stimulating hormone (TSH) autoregulation reduces variation in the TSH response to thyroid hormones
Published in Temperature, 2018
Stephen Paul Fitzgerald, Nigel Geoffrey Bean
TSH autoregulation gives individual thyrotrophs the ability to communicate with each other, by sensing the total TSH output of the pituitary gland. The individual thyrotrophs respond to this signal adjusting their individual TSH curves to serve homeostasis. By this mechanism the thyrotrophs are able to function to some extent as an integrated organ rather than as just a collection of individual cells responding individually to the ambient thyroid hormone levels.