scholarly journals Silent somatotroph tumour revisited from a study of 80 patients with and without acromegaly and a review of the literature

2017 ◽  
Vol 176 (2) ◽  
pp. 195-201 ◽  
Author(s):  
Laura Chinezu ◽  
Alexandre Vasiljevic ◽  
Jacqueline Trouillas ◽  
Marion Lapoirie ◽  
Emmanuel Jouanneau ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Transcription Factor ◽  
Somatostatin Receptors ◽  
Clinical Signs ◽  
Secretory Activity ◽  
Thyroid Stimulating Hormone ◽  
Lower Percentage ◽  
Review Of The Literature ◽  
Pituitary Tumours ◽  
Ki 67

Background Silent somatotroph tumours are growth hormone (GH) immunoreactive (IR) pituitary tumours without clinical and biological signs of acromegaly. Their better characterisation is required to improve the diagnosis. Materials and methods Twenty-one silent somatotroph tumours were compared to 59 somatotroph tumours with acromegaly. Tumours in each group were classified into GH and plurihormonal (GH/prolactin (PRL)/±thyroid-stimulating hormone (TSH)) and into densely granulated (DG) and sparsely granulated (SG) types. The two groups were then compared with regards to proliferation (Ki-67, p53 indexes and mitotic count), differentiation (expression of somatostatin receptors SSTR2A–SSTR5 and transcription factor Pit-1) and secretory activity (% of GH- and PRL-IR cells). Results The silent somatotroph tumours represented 2% of all tested pituitary tumours combined. They were more frequent in women than in men (P = 0.002), more frequently plurihormonal and SG (P < 0.01), with a lower percentage of GH-IR cells (P < 0.0001) compared to those with acromegaly. They all expressed SSTR2A, SSTR5 and Pit-1. The plurihormonal (GH/PRL/±TSH) tumours were mostly observed in women (sex ratio: 3/1) and in patients who were generally younger than those with acromegaly (P < 0.001). They were larger (P < 0.001) with a higher Ki-67 index (P = 0.007). Conclusions The silent somatotroph tumours are not uncommon. Their pathological diagnosis requires the immunodetection of GH and Pit-1. They are more frequently plurihormonal and more proliferative than those with acromegaly. A low secretory activity of these tumours might explain the normal plasma values for GH and insulin-like growth factor 1 (IGF1) and the absence of clinical signs of acromegaly.

scholarly journals SAT-265 An Asynchronous Double Growth Hormone Secreting Pituitary Adenoma as a Cause of Rapid Tumor Regrowth After Initially Successful Surgery

2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Malgorzata Trofimiuk-Muldner ◽  
Kluczynski Lukasz ◽  
Grzegorz Zielinski ◽  
Grzegorz Sokolowski ◽  
Maria Maksymowicz ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Pituitary Adenoma ◽  
Pituitary Tumor ◽  
Tumor Regression ◽  
Somatostatin Receptors ◽  
Ki 67 ◽  
Gh Secretion ◽  
Repeated Surgery ◽  
Double Pituitary Adenomas ◽  
Mitotic Figures

Abstract Background. Double pituitary adenomas are a rare entity, which requires clinical attention and a careful follow-up. Case report. A 37-year-old man presented with left-sided painful gynecomastia. He denied typical symptoms of excessive growth hormone (GH) secretion and did not show any acromegalic features. Due to low testosterone and LH levels with mild hyperprolactinaemia, the patient was referred to pituitary MR, which revealed an 11x13 mm right-sided sellar tumor. An increased IGF-1 was noted subsequently (1482 ng/mL; N 109-284 ng/mL), together with the lack of GH suppression in OGTT. Transphenoidal resection of pituitary tumor performed in 2012 led to biochemical (IGF-1 260 ng/mL, GH 0.08 ng/mL) and radiological remission of the disease. A histopathology report revealed a densely granulated somatotropic pituitary adenoma with mild nuclear atypia, expressing somatostatin receptors [sstr2A (+), sstr5 (+/-)]. Due to gradually increasing IGF-1 levels (with low, although rising, GH values ranging from 0.07 to 0.92 ng/mL) in subsequent years, OGTT was repeated in 2015, showing appropriate GH suppression. In 2016, however, acromegaly recurrence was confirmed both biochemically (increasingly high IGF-1 - 664 ng/mL - and unsuppressed post-OGTT growth hormone) and in MR imaging. The patient was reoperated in June 2017. The second histopathology reported an oncocytic somatotropic acidophil stem cell pituitary adenoma with Ki-67 &gt;3% and mitotic figures. Subsequent anterior pituitary lobe insufficiency (adrenal, thyroid and gonadal axis) was found and adequately treated. Complete tumor removal was confirmed by MR performed three months after repeated surgery, as well as a low GH level (0.97 ng/mL), although accompanied by borderline IGF-1 values (277 ng/mL). Eighteen months after surgery, the recurrence of acromegaly was again confirmed, with adenoma regrowth and increased GH (2.31 ng/mL) and IGF-1 (474 ng/mL) levels. Octreotide LAR was started (despite retina wrinkling which was observed when lanreotide was administered before the first surgery), which led to a normalization of GH (0.96 ng/mL) and IGF-1 levels (152 ng/mL), as well as partial pituitary tumor regression after six months therapy. Conclusion. In a case of GH-secreting pituitary adenoma recurrence after apparent successful surgery, a double pituitary tumor with more aggressive histology should be considered.

Effect of Sms 201-995, a long-acting somatostatin analog, on the morphology of a growth hormone-secreting pituitary adenoma causing acromegaly: A histologic, immunohistochemical, ultrastructural and morphometric study

1986 ◽  
Vol 44 ◽  
pp. 318-319
Author(s):  
K. Kovacs ◽  
E. Horvath ◽  
S.L. Asa ◽  
D. Lietz ◽  
S.R. George ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Somatostatin Receptors ◽  
Clinical Signs ◽  
Signs And Symptoms ◽  
Somatostatin Analog ◽  
Morphometric Study ◽  
Cell Adenoma ◽  
Clinical Signs And Symptoms ◽  
Long Acting ◽  
Therapy Treatment

Treatment of acromegalic patients with somatostatin is a logical approach, since growth hormone (GH) cell adenomas possess somatostatin receptors and somatostatin is known to inhibit GH release. Because of short duration of its action, therapy with natural somatostatin is ineffective in patients with acromegaly. I has been shown recently that SMS 201-995, a long-acting somatostatin analog, reduces blood GH levels and ameliorates clinical signs and symptoms in GH excess. We report here morphologic findings in a pituitary GH cell adenoma removed by surgery from a 36-year-old acromegalic woman after 10 days of SMS 201-995 therapy. Treatment resulted in reduction of blood GH levels.

Thyrotropin-secreting pituitary adenoma in an 11-year-old boy with type 1 autoimmune polyglandular syndrome

2016 ◽  
Vol 29 (2) ◽  
Author(s):  
Nadia Mazerkina ◽  
Yuri Trunin ◽  
Sergey Gorelyshev ◽  
Andrey Golanov ◽  
Boris Kadashev ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Radiation Therapy ◽  
Pituitary Adenoma ◽  
Clinical Signs ◽  
Thyroid Stimulating Hormone ◽  
Hormone Deficiency ◽  
Endocrine Diseases ◽  
Autoimmune Polyglandular Syndrome ◽  
First Case

AbstractThyrotropinomas (TSHomas) are rare pituitary adenomas, particularly in childhood. We present here the case of an 11-year-old boy with type 1 autoimmune polyglandular syndrome (APS1) and TSHoma which was diagnosed by elevated thyroid – stimulating hormone and thyroid hormones levels without evident clinical signs of hyperthyroidism. He was underwent partial resection of the tumor via transsphenoidal approach and subsequently radiation therapy. Consequently, 1 year after radiotherapy, the patient developed growth hormone deficiency, three and half years after radiation became euthyroid, and five and half years after treatment – hypothyroid. This is the first case of the coexistence of these two rare endocrine diseases in one patient.

Molecular pathogenesis of pituitary tumours

2011 ◽  
pp. 112-121
Author(s):  
Ines Donangelo ◽  
Shlomo Melmed
Keyword(s):  
Growth Hormone ◽  
Pituitary Adenomas ◽  
Single Cells ◽  
Hormone Secretion ◽  
Cell Types ◽  
Pituitary Tumour ◽  
Thyroid Stimulating Hormone ◽  
Gene Products ◽  
Pituitary Tumours ◽  
Secretory Products

Pituitary adenomas are discovered in up to 25% of unselected autopsies, however, clinically apparent tumours are considerably less common. The pituitary gland is composed of differentiated cell types: somatotrophs, lactotrophs, corticotrophs, thyrotrophs, and gonadotrophs. Tumours may arise from any of these cell types and their secretory products depend on the cell of origin. The functional classification of pituitary tumorus is based on identification of cell gene products by immunostaining or mRNA detection, as well as measurement of circulating tumour and target organ hormone levels. Oversecretion of adrenocorticotropic hormone (ACTH) results in cortisol excess with Cushing’s disease. Growth hormone overproduction leads to acromegaly with typical acral overgrowth and metabolic abnormalities. Prolactin hypersecretion results in hypogonadism and galactorrhoea. Rarely, thyroid-stimulating hormone (TSH) hypersecretion leads to goitre and thyrotoxicosis, and gonadotropin excess results in gonadal dysfunction (1). Mixed tumours cosecreting growth hormone with prolactin, TSH, or ACTH may also arise from single cells. Clinically nonfunctional tumours are those that do not efficiently secrete their gene products, and most commonly they are derived from gonadotroph cells. Pituitary tumours are further defined radiographically as microadenomas (<1 cm in diameter) or macroadenomas (>1 cm in diameter). However, this classification does not reflect whether the pituitary tumour is amenable to total resection and limits assessment of invasive progression during serial imaging. Therefore, it is useful to apply the classification proposed by Hardy in 1973 and modified by Wilson in 1990 (Table 2.3.2.1), whereby pituitary tumours are classified into one of five grades and one of six stages, providing important preoperative information. Pituitary tumours cause morbidity by both abnormal hormone secretion as well as compression of regional structures. As a considerable proportion of patients do not achieve optimal therapeutic control of mass effects and/or hormone hypersecretion despite advances in therapeutic approaches, understanding pathogenesis and pituitary tumour growth patterns in individual patients will enable identification of subcellular treatment targets, ultimately decreasing tumour-related morbidity and mortality. Determinants of initiation and progression of pituitary adenomas are not fully understood. This chapter describes a spectrum of mechanisms implicated in pituitary tumorigenesis, including the role of pituitary plasticity, imbalances in cell cycle regulation, transcription factors, signalling pathways, and angiogenesis (Fig. 2.3.2.1). Molecular events related to tumorigenesis in human pituitary adenoma subtypes are summarized in Table 2.3.2.2. The causal role for selected genetic imbalances leading to development of pituitary tumours has been confirmed in several transgenic mouse models (Table 2.3.2.3).

scholarly journals Exploring alterations in hematological and biochemical parameters, enzyme activities and serum cortisol in Besnoitia besnoiti naturally infected dairy cattle

2021 ◽  
Vol 14 (1) ◽  
Author(s):  
Luca Villa ◽  
Alessia Libera Gazzonis ◽  
Sergio Aurelio Zanzani ◽  
Silvia Mazzola ◽  
Alessia Giordano ◽  
...  
Keyword(s):  
Enzyme Activities ◽  
Biochemical Parameters ◽  
Statistical Significance ◽  
Clinical Signs ◽  
Serum Cortisol ◽  
Lower Percentage ◽  
Besnoitia Besnoiti ◽  
Laboratory Parameters ◽  
Bovine Besnoitiosis ◽  
Hematological And Biochemical Parameters

Abstract Background Besnoitia besnoiti is an Apicomplexan protozoa causative of bovine besnoitiosis, a chronic and debilitating disease of cattle, with a variety of pathological findings that could alter some laboratory parameters. A study was conducted in a bovine besnoitiosis endemically infected dairy herd located in Italy characterized by high intra-herd seroprevalence and cattle with clinical signs of the disease. In the study, alterations in laboratory parameters, i.e. hematological and biochemical parameters, enzyme activities and serum cortisol levels, in Besnoitia besnoiti naturally infected cows were investigated in depth. Methods Laboratory parameters in 107 cows, of which 61 were seronegative and 46 were seropositive to B. besnoiti, including 27 with clinical signs of bovine besnoitiosis, were compared. Generalized linear models were used to evaluate the effect of Besnoitia infection on the considered laboratory parameters. Results Hematological analyses revealed that B. besnoiti infection determined a significant alteration to the leukocyte differential, with a higher percentage of granulocytes and a lower percentage of lymphocytes in seropositive and clinically affected animals (Mann–Whitney U-test, P = 0.022); erythrocyte and platelet counts did not show any difference between the considered groups of cows. Biochemistry tests evidenced that the parasite infection influenced serum protein values in seropositive cows and glutamate dehydrogenase values in clinically affected animals. No or only slight differences were revealed for all of the other biochemical and enzyme activity parameters in B. besnoiti-infected animals. In addition, despite the lack of statistical significance, seropositive and clinically affected cows evidenced higher concentrations of serum cortisol values compared to seronegative animals. Conclusions Although physiological, pathological and farm-related factors could have influenced the results in investigated animals, further studies involving more animals from different farms would be advisable to infer the role of B. besnoiti on these alterations, since laboratory parameters could help veterinarians in the diagnosis of bovine besnoitiosis in cattle.

Growth hormone and somatostatin gene expression in pituitary adenomas with active acromegaly and minimal plasma growth hormone elevation

1990 ◽  
Vol 122 (6) ◽  
pp. 745-752 ◽  
Author(s):  
Patrick Pagesy ◽  
Jacques Y. Li ◽  
Françoise Rentier-Delrue ◽  
Olivier Delalande ◽  
Yves Le Bouc ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Northern Blot Analysis ◽  
Secretory Activity ◽  
Ultrastructural Level ◽  
Wide Range ◽  
Igf I ◽  
Gh Gene ◽  
Basal Plasma ◽  
Active Acromegaly ◽  
Plasma Gh

Abstract. Some patients with active acromegaly have elevated plasma IGF-I concentrations with only minimal elevation of plasma GH. We compared adenomatous GH and SRIH expression in 3 such patients (patients No. 1, 2 and 3; basal plasma GH level < 4 μg/l) and in 3 acromegalic patients with high basal plasma GH level (patients No. 4, 5 and 6; 51.7 ± 16.1 μg/l, mean ± sem). By immunocytochemistry, all the tumours proved to be somatotropic adenomas. At the ultrastructural level, signs of low secretory activity were observed in adenomas from patients No. 2 and 3. Perifused adenoma cells of patients No. 1, 2 and 3 released very little GH compared with those of patients No. 4, 5 and 6 (1± 0.37 vs 51.5± 34.1 μg · (10−6 cells) · min−1, p< 0.001). Adenoma SRIH content was 65.7 and 30.6 pg/mg proteins in patients No. 1 and 2, whereas it was undetectable in the others (patients No. 4, 5 and 6). Northern blot analysis showed that the GH gene was poorly expressed in the adenomas from patients No. 1, 2 and 3 compared with the adenomas from patients No. 4, 5 and 6. SRIH mRNA was detected in all 6 adenomas. However, the signal was more intense in the adenomas from patients No. 1, 2 and 3 than in those from patients No. 4, 5 and 6. In conclusion, because of the variability of the biosynthetic and secretory potential of the somatotropic adenomas, patients harbouring this type of pituitary tumours can exhibit a wide range of plasma GH levels. In acromegaly with minimal elevation of plasma GH, the synthesis of SRIH by the adenoma cells themselves could play a role in the inhibition of GH expression.

Endocrine Aspects of Kidney Disease

2020 ◽  
Author(s):  
Marcin Adamczak ◽  
Piotr Kuczera ◽  
Andrzej Wiecek
Keyword(s):  
Chronic Kidney Disease ◽  
Growth Hormone ◽  
Kidney Disease ◽  
Kidney Diseases ◽  
Thyroid Stimulating Hormone ◽  
Normal Serum ◽  
Serum Prolactin ◽  
Clinical Consequences ◽  
Synthesis And Degradation ◽  
Insulin Like Growth Factors

Kidneys play the major role in the synthesis and degradation of several hormones. Different coexisting conditions such as inflammation, malnutrition and metabolic acidosis and applied treatment may also cause endocrine abnormalities in chronic kidney disease (CKD) patients. A tendency towards decreased thyroxin and triiodothyronine with normal serum concentrations of reversed triiodothyronine (as opposed to other chronic non-thyroid, non-kidney diseases) and thyroid stimulating hormone are observed. As far as the somatotopic axis is concerned, in CKD normal serum concentration of growth hormone and its effector – the insulin-like growth factor are observed. Nevertheless, due to the phenomenon of GH/IGF-1 “resistance” CKD patients usually present a phenotype resembling GH deficiency. Serum prolactin concentrations are often elevated in CKD women and men. This leads to the dysregulation of the pituitary-gonadal axis causing hypogonadism and it’s clinical consequences regardless of patient’s gender. The alterations in hormones of gonadal origin caused by uremia, together with hyperprolactinemia lead to the development of sexual dysfunction and infertility in men and women. The alterations of thyroid, pituitary gland and gonads associated with CKD are discussed in this chapter. This review contains 4 tables, and 64 references. Keywords: chronic kidney disease, hypothyroidism, hyperthyroidism, growth hormone, recombinant human GH, insulin-like growth factors, hemodialysis

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