trophic hormone
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Author(s):  
T.M. Myshunina ◽  
B.B. Guda ◽  
M.Yu. Bolgov ◽  
O.V. Kalinichenko

The aimwas to analyze the literature data on the TSH content in the blood serum of patients with differentiated thyroid carcinomas and to study the hormone content depending on the aggressiveness of the tumors, and also in the presence of some pathological changes in the extra-tumoral tissue that may affect the biological behavior of papillary carcinomas. Material and methods. A retrospective study of the cohort of patients who who had surgery for thyroid tumor. Results. The level of TSH in the serum of patients with papillary or follicular carcinomas is higher (but within the "normal" level) such in patients with nodular goiter. The highest level of hormone is recorded in the blood of women in the case of a combination of metastases in the lymph nodes with intra- and extrathyroid invasion, as well as in women over 45 with stage III/IV disease. In male patients, elevated TSH levels do not undergo significant modulations, depending on the metastatic and/or invasive properties of papillary carcinoma. The level of the hormone in the blood of women in the case of diagnosis in the extra-tumoral tissue of the gland expressed hyperplastic process or chronic thyroiditis is higher compared with patients who have not revealed pathomorphological changes in the gland tissue. Men also have an elevated level of TSH in the presence of chronic thyroiditis in the extra-tumoral tissue. When association of a tumor with adenoma or hyperplasia of the thyroid parenchyma, the content of tropic hormone does not differ from that of men from the comparison group; it is less when a single benign node or diffuse colloid goiter is present in the extra-tumoral tissue. Conclusions. In the blood of patients with thyroid carcinomas, especially in women with invasive papillary carcinomas, there is a higher level of TSH in the blood compared to that in patients with nodular goiter. The modulation of the content of trophic hormone can be affected by pathological changes in the extra-tumoral tissue that accompany the papillary carcinoma.  


Author(s):  
Sunita M C De Sousa ◽  
Peter Earls ◽  
Ann I McCormack

Summary Pituitary hyperplasia (PH) occurs in heterogeneous settings and remains under-recognised. Increased awareness of this condition and its natural history should circumvent unnecessary trans-sphenoidal surgery. We performed an observational case series of patients referred to a single endocrinologist over a 3-year period. Four young women were identified with PH manifesting as diffuse, symmetrical pituitary enlargement near or touching the optic apparatus on MRI. The first woman presented with primary hypothyroidism and likely had thyrotroph hyperplasia given prompt resolution with thyroxine. The second and third women were diagnosed with pathological gonadotroph hyperplasia due to primary gonadal insufficiency, with histopathological confirmation including gonadal-deficiency cells in the third case where surgery could have been avoided. The fourth woman likely had idiopathic PH, though she had concomitant polycystic ovary syndrome which is a debated cause of PH. Patients suspected of PH should undergo comprehensive hormonal, radiological and sometimes ophthalmological evaluation. This is best conducted by a specialised multidisciplinary team with preference for treatment of underlying conditions and close monitoring over surgical intervention. Learning points Normal pituitary dimensions are influenced by age and gender with the greatest pituitary heights seen in young adults and perimenopausal women. Pituitary enlargement may be seen in the settings of pregnancy, end-organ insufficiency with loss of negative feedback, and excess trophic hormone from the hypothalamus or neuroendocrine tumours. PH may be caused or exacerbated by medications including oestrogen, GNRH analogues and antipsychotics. Management involves identification of cases of idiopathic PH suitable for simple surveillance and reversal of pathological or iatrogenic causes where they exist. Surgery should be avoided in PH as it rarely progresses.


Author(s):  
Sumitha S. Hathiramani ◽  
Hans K. Ghayee

This chapter describes the various methods used for quantifying concentrations of circulating hormones and thus assessing endocrine function. The paradigm of feedback regulation (for example, of the hypothalamic-pituitary-target gland axis) is central to this assessment of endocrine status. Any disruption in such an axis can cause alterations in trophic and target hormone pairs. High concentration of a target gland hormone coupled with low concentration of the corresponding trophic hormone (e.g., pituitary hormone) suggests autonomous secretion by the target endocrine organ, as is typical in primary hyperthyroidism, e.g., high thyroxine (T4), suppressed thyroid stimulating hormone (TSH). Elevated concentrations of both members of a hormone pair usually indicate autonomous secretion of the trophic hormone, either from the normal site or from a tumor in an “ectopic” (extraglandular) location. For example, excess cortisol production driven by a high plasma adrenocorticotropic hormone (ACTH) level may be due to the secretion of pituitary ACTH or secretion of ACTH by lung tumors. Alternatively, the combined elevation of trophic and target endocrine gland hormones can result from resistance to the action of the target endocrine gland hormone e.g., elevated luteinizing hormone (LH) and testosterone in androgen resistance. Autonomous hypersecretion of the trophic hormone typically results in clinical evidence of target gland hormone excess, whereas resistance to the target gland hormone leads to manifestations of hormone deficiency. Hormones circulating in the plasma were first detected by in vivo bioassays, in which plasma or extracts of plasma were injected into animals and biological responses were measured. Unfortunately, most in vivo bioassays lack the precision, sensitivity, and specificity required to measure the low concentrations of many hormones in plasma, and the assays are cumbersome and impractical for routine use in clinical chemistry laboratories. Great progress in measuring plasma hormone concentrations came with the development of radioimmunoassays (RIAs) in the late 1950s. An unknown concentration of hormone in plasma is estimated by allowing competition with a labeled hormone or analog for specific binding sites on an antibody.


1990 ◽  
Vol 11 (2) ◽  
pp. 386-398 ◽  
Author(s):  
J. C. PRIOR
Keyword(s):  

Digestion ◽  
1990 ◽  
Vol 47 (1) ◽  
pp. 11-16 ◽  
Author(s):  
J.H. Walsh
Keyword(s):  

1984 ◽  
Vol 247 (5) ◽  
pp. G457-G462 ◽  
Author(s):  
P. S. Oates ◽  
N. W. Bruce ◽  
R. G. Morgan

We studied the effect of raw soya flour (RSF) given as a single gavage or for long-term periods on pancreatic blood flow. These effects were compared with the response to treatment with cholecystokinin (CCK) since it has been suggested that RSF feeding releases CCK. In acute experiments total pancreatic blood flow was significantly increased after infusion of CCK (60 Ivy dog units X kg-1 X h-1) and after gavage with preparations of RSF or heated soya flour (HSF). When expressed as flow per 100 g pancreatic weight, the greatest increase was seen after gavage with RSF. In separate chronic studies, total pancreatic blood flow was significantly increased in rats fed RSF for 4 wk compared with rats fed HSF, but because of pancreatic enlargement in rats fed RSF flow per 100 g pancreatic weight was similar in the two groups. When rats fed RSF for 4 wk were changed to standard rat cubes for 48 h before study, pancreatic blood flow (ml/min and ml X min-1 X 100 g pancreas-1) and total pancreatic DNA decreased significantly compared with rats fed RSF continuously. However, when CCK was infused intravenously during the 48-h period on cubes, pancreatic blood flow and DNA remained significantly increased and were not significantly different from values in rats fed RSF continuously. These results show that the effects of RSF feeding and CCK treatment on pancreatic growth and blood flow are similar and are consistent with the postulated role of CCK as the trophic hormone released by RSF feeding.


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