scholarly journals Difficulties in diagnosis of adenomas with mixed prolactin and growth hormone secretion: case presentation

2020 ◽  
Vol 17 (3) ◽  
pp. 233-240
Author(s):  
Larisa K. Dzeranova ◽  
Lizaveta A. Aboishava ◽  
Natalya S. Fedorova ◽  
Svetlana Y. Vorotnikova ◽  
Ekaterina A. Pigarova ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Hormone Secretion ◽  
Growth Hormone Secretion ◽  
Clinical Manifestations ◽  
Late Presentation ◽  
Primary Diagnosis ◽  
Pituitary Cells ◽  
Initial Examination ◽  
Symptom Complex ◽  
Periodic Evaluation

Hyperpolactinemia is a persistent excess of prolactin in the blood serum. The symptom complex of hyperprolactinemia primarily consists of disturbances in function of the reproductive system. The secretion of prolactin is under complex neuroendocrine control, which involves factors of different nature: neurotransmitters, hormones of the peripheral endocrine glands. In most cases, prolactin is secreted by pituitary cells - lactotrophs, but in some cases, hypersecretion of prolactin is combined with an excess production of growth hormone, which is typical for tumors originating from the line of progenitor cells of lactotrophs and somatotrophs of the pituitary gland, mammosomatotrophs. In this case, the symptom complex of hyperprolactinemia is accompanied by clinical manifestations of acromegaly. In patients with acromegaly, the cause of hyperprolactinemia may be pituitary stalk compression or mixed secretion of prolactin and growth hormone. Differentiation of lactotropic and somatotropic pituitary cells is determined by transcription factor Pit-1. These cell lineages are closely connected,  and this may be one of the reasons for formation of tumors with mixed secretion. Reports of late presentation of acromegaly in patients previously diagnosed with prolactinomas have also been described in literature.Clinical manifestations of hyperprolactinemia can cause the patient to seek doctor’s attention before acromegalic changes in appearance develop. Careful attention is needed both to the primary diagnosis and to the clinical course of the disease in patients with hyperprolactinemia and pituitary adenoma: full assessment of hormonal status with mandatory evaluation of IGF-1 is crucial at initial examination, during further observation it may be advised to consider periodic evaluation of IGF-1 in addition to assessment of prolactin and the size of adenoma.  Pituitary adenomas with mixed secretion may have a poorer prognosis.

Influence of catecholamines, prostaglandins and thyroid hormones on growth hormone secretion by chicken pituitary cells in vitro

1990 ◽  
Vol 7 (1) ◽  
pp. 35-42 ◽  
Author(s):  
Dan J. Donoghue ◽  
Frank M. Perez ◽  
Bruce S.A. Diamante ◽  
Sasha Malamed ◽  
Colin G. Scanes
Keyword(s):  
Growth Hormone ◽  
Thyroid Hormones ◽  
Hormone Secretion ◽  
Growth Hormone Secretion ◽  
Pituitary Cells

scholarly journals Body Image Disturbance in Acromegaly Patients Compared to Nonfunctioning Pituitary Adenoma Patients and Controls

2015 ◽  
Vol 2015 ◽  
pp. 1-8 ◽  
Author(s):  
Helen M. Conaglen ◽  
Dennis de Jong ◽  
Veronica Crawford ◽  
Marianne S. Elston ◽  
John V. Conaglen
Keyword(s):  
Growth Hormone ◽  
Body Image ◽  
Hormone Secretion ◽  
Growth Hormone Secretion ◽  
Primary Diagnosis ◽  
Body Image Disturbance ◽  
Separate Analysis ◽  
Cross Sectional Survey ◽  
Cross Sectional ◽  
The Impact

Purpose. Excess growth hormone secretion in adults results in acromegaly, a condition in which multiple physical changes occur including bony and soft tissue overgrowth. Over time these changes can markedly alter a person’s appearance. The aim of this study was to compare body image disturbance in patients with acromegaly to those with nonfunctioning pituitary adenomas (NFAs) and controls and assess the impact of obesity in these groups.Methods. A cross-sectional survey including quality of life, body image disturbance, anxiety and depression measures, growth hormone, and BMI measurement was carried out.Results. The groups did not differ with respect to body image disturbance. However separate analysis of obese participants demonstrated relationships between mood scales, body image disturbance, and pain issues, particularly for acromegaly patients.Conclusions. While the primary hypothesis that acromegaly might be associated with body image disturbance was not borne out, we have shown that obesity together with acromegaly and NFA can be associated with body image issues, suggesting that BMI rather than primary diagnosis might better indicate whether patients might experience body image disturbance problems.

GRF elevates cytosolic free calcium concentration in rat anterior pituitary cells

1987 ◽  
Vol 253 (5) ◽  
pp. E591-E594
Author(s):  
C. Schofl ◽  
J. Sandow ◽  
W. Knepel
Keyword(s):  
Growth Hormone ◽  
Anterior Pituitary ◽  
Calcium Concentration ◽  
Hormone Secretion ◽  
Growth Hormone Secretion ◽  
Free Calcium ◽  
Pituitary Cells ◽  
Maximal Increase ◽  
Anterior Pituitary Cells ◽  
Free Calcium Concentration

The effect of human growth hormone-releasing factor (GRF) on intracellular free calcium concentration ([Ca2+]i) was examined in rat anterior pituitary cells. The [Ca2+]i was monitored directly by means of the intracellularly trapped fluorescent indicator, fura-2. GRF rapidly elevated [Ca2+]i, reaching a new plateau within approximately 30 s. The half-maximally effective concentration of GRF was approximately 130 pM. GRF produced a maximal increase in [Ca2+]i by approximately 120 nM. The GRF (2 nM)-induced elevation of [Ca2+]i was abolished by removal of extracellular calcium (Ca2+ omitted, 2 mM EGTA). The GRF (2 nM)-caused rise in [Ca2+]i was largely reduced in the presence of the calcium channel blockers Mg2+ (31.2 mM) or nifedipine (1 microM). An increase in [Ca2+]i by approximately 60 nM was elicited by the addition of prostaglandin E2 (1 microM), which can stimulate growth hormone secretion independent of GRF receptors. These data indicate that GRF elevates the [Ca2+]i, possibly in somatotrophs; this GRF-induced increase in [Ca2+]i may depend on an influx of extracellular Ca2+, largely through Mg2+- and nifedipine-sensitive calcium channels.

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