scholarly journals TSH, GH, and Prolactin Producing Pituitary Adenoma: An Unusual Case Presentation

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A616-A616
Author(s):  
Helard Andres Manrique ◽  
Miguel Eduardo Pinto

Abstract Background: Pituitary adenomas are benign and frequent tumors, some of them with tendency to be recurrent or invasive e. several pituitary tumors are positive for secretion of one or more hormones of the same adenohypophysial cell lineage. However, some cases have a subclinical course and are underestimated because they have plurihormonal secretion of different adenohypophyseal cells lineage. Clinical Case: A 38 years old women with chronic headaches, who is in fertility treatment for 12 month ago presents to the clinic with unremarkable physical examination. Her laboratory studies include: Normal campimetry. T3 (triiodothyronine) 2.15 ng/m L (NR:0.8 - 2.0), TSH (thyroid stimulating hormone) 4.4 uU/mL (NR:0.27 - 4.2), T4 (tetraiodothyronine) 13.54 ug/dl, (NR:5.1 - 14.1), Free T4 2.44 ng/d (NR:0.93 - 1.7), Estradiol 60.2 pg/ml, FSH (Follicle stimulating hormone) 4.3 mUI/ml (NR:1,7-12), Cortisol (?8 am) 9.29 ug/dl (NR:4.2 - 38.4), ACTH (Corticotrophin-releasing hormone) 13.1 pg/ml (NR: 0.0 - 46.0), Somatomedin C (IGF-1) 231 .0 ng/ml (NR for age?: 57.0-241.0). Brain MRI with pituitary protocol showed in T1 an isointense lesion and slightly heterogeneous in T2 in the anterior and left aspect of the turkish saddle, of 1 x 1.1 x 1.1 cm of anteroposterior, transverse and cephalocaudal diameter, suggestive of a macroadenoma. The tumor pathology showed, possitive for a pituitary adenoma. Immunohistochemistry results were negative for: ACTH:, positive for GH, TSH: (+++) and for Prolactin:. Her post-operative findings showed a residual pituitary gland without significant findings. Her post operative pituitary axis include: Sodium 139.2 mmol/l (NR”135.0 - 145.0), Chloride 100.8 mmol/l (NR95.0 - 115.0), Potassium 3.71 mmol/l (NR3.5 - 5.1), ACTH 4.1 pg/ml(NR0.0 - 46.0), Cortisol (am) 11.11 ug/dl (NR4.2 - 38.4), Estradiol 106.5 pg/ml, FSH 5.1 mUI/ml, LH (Luteinizing Hormone) 13.53 mIU/ml, Somatomedin C (IGF-1) 134 .0 ng/m, Free T32.4 pg/ml, TSH 0.9 uU/mL Free T4 0.99 ng/dl, and Prolactin 23.4ng/ml. Patient had a satisfactory clinical course after surgery, she maintained normal pituitary function without requirement of hormonal replacement therapy. Conclusion: We present a a prolactin, TSH and GH secreting pituitary adenoma case, which is very unusual. It i is important to make a proper pituitary evaluation, and offer effective treatment to prevent complications

Author(s):  
Mingjian Shi ◽  
Ali M Manouchehri ◽  
Christian M Shaffer ◽  
Nataraja Sarma Vaitinadin ◽  
Jacklyn N Hellwege ◽  
...  

Abstract Background A genetic predisposition to lower thyroid stimulating hormone (TSH) levels associates with increased atrial fibrillation (AF) risk through undefined mechanisms. Defining the genetic mediating mechanisms could lead to improved targeted therapies to mitigate AF risk. Methods We used two-sample Mendelian randomization (MR) to test associations between TSH-associated single nucleotide polymorphisms (SNPs) and 16 candidate mediators. We then performed multivariable Mendelian randomization (MVMR) to test for a significant attenuation of the genetic association between TSH and AF, after adjusting for each mediator significantly associated with TSH. Results Four candidate mediators (free T4, systolic blood pressure, heart rate, and height) were significantly inversely associated with genetically predicted TSH after adjusting for multiple testing. In MVMR analyses, adjusting for height significantly decreased the magnitude of the association between TSH and AF from -0.12 (s.e. 0.02) occurrences of AF per standard deviation change in height to -0.06 (0.02) (p=0.005). Adjusting for the other candidate mediators did not significantly attenuate the association. Conclusions The genetic association between TSH and increased AF risk is mediated, in part, by taller stature. Thus, some genetic mechanisms underlying TSH variability may contribute to AF risk through mechanisms determining height occurring early in life that differ from those driven by thyroid hormone level elevations in later life.


2008 ◽  
Vol 04 (01) ◽  
pp. 88
Author(s):  
Sandra Pekic ◽  
Vera Popovic-Brkic

Pituitary adenomas are common benign monoclonal neoplasms— accounting for 15% of intracranial neoplasms—that may be clinically silent or secrete anterior pituitary hormones such as prolactin, growth hormone (GH), adrenocorticotrophic hormone (ACTH), or, rarely, thyroid-stimulating hormone (TSH) or gonadotrophins. Radiological studies for other reasons using high-resolution computed tomography (CT) or magnetic resonance imaging (MRI) detect incidental pituitary adenomas in approximately 20% of asymptomatic patients.1The incidence of the various types of adenoma varies;2prolactinomas are the most common pituitary adenomas. Clinically non-functioning pituitary adenomas (NFPAs), which do not secrete hormones, often cause local mass symptoms and represent one-third of pituitary adenomas. GH- and ACTH-producing adenomas each account for 10–15% of pituitary adenomas, while TSH-producing adenomas are rare. Pituitary adenomas are infrequent in childhood: fewer than 10% of pituitary adenomas are diagnosed before 20 years of age.3These adenomas can be either microor macroadenomas. The natural course of microadenomas is that a few tumors enlarge over a period of more than eight years.Although several genes and signaling pathways have been identified as important factors in the development of pituitary tumors, our understanding of pituitary tumorigenesis remains incomplete and is the focus of current research. The reason for this is that current treatment modalities fail to completely control this disorder and prevent the associated morbidity and mortality. This article reviews the advances in our understanding of pituitary adenoma, especially in the field of pathogenesis of pituitary tumors, and the possibility of new therapeutic approaches.


2019 ◽  
Vol 65 (2) ◽  
pp. 101-106
Author(s):  
Ludmila I. Astafyeva ◽  
Pavel L. Kalinin ◽  
Tatyana A. Kienia ◽  
Valentin V. Fadeyev

Cases of thyrotoxicosis associated with a previous case of secondary hypothyroidism are extremely rare. This article presents a rare clinical case of Graves disease manifestation in a patient with secondary hypothyroidism after radiosurgical treatment of acromegaly. A 38-year old woman presented with acromegaly and endo-supra-laterosellar pituitary adenoma. After non-radical removal of the pituitary adenoma, radiosurgical treatment of the of the residual tissue of the pituitary tumor in the cavernous sinus area was performed. After 14 months of radiation therapy, the acromegaly was in remission; after 24 months of radiation therapy, panhypopituitarism developed (secondary hypothyroidism, adrenal insufficiency, hypogonadism, and growth hormone deficiency). Furthermore, 1.5 years after the panhypopituitarism was diagnosed, the manifestation of Graves disease was also noted, requiring thyrostatic and radioactive iodine treatments. Diagnostic criteria for secondary hypothyroidism are low levels of the thyroid hormones free T4 and free T3, with a reduced, normal or slightly elevated level of thyroid stimulating hormone (TSH). The criterion for the development of thyrotoxicosis in the context of the secondary hypothyroidism was the persistent increase in the level of free T4 despite adequate drug therapy with levothyroxine. In the case report, the patients diagnosis of Graves disease was confirmed by the presence of a high level of antibodies to the TSH receptor.


2000 ◽  
Vol 85 (2) ◽  
pp. 545-548 ◽  
Author(s):  
A. F. Muller ◽  
A. Verhoeff ◽  
M. J. Mantel ◽  
F. H. de Jong ◽  
A. Berghout

Controlled ovarian hyperstimulation could lead to opposing effects on thyroid function. Therefore, in a prospective study of 65 women undergoing controlled ovarian hyperstimulation, thyroid hormones, T4-binding globulin, TPO antibodies, gonadotropins, estradiol, and PRL were measured before and after controlled ovarian hyperstimulation. After ovarian stimulation (mean ± se of mean): free T4 decreased, 14.4 ± 0.2 vs. 12.9 ± 0.2 pmol/L (P < 0.0001); thyroid-stimulating hormone increased, 2.3 ± 0.3 vs. 3.0 ± 0.4 mU/L (P < 0.0001); T4-binding globulin increased, 25.2 ± 0.7 vs. 33.9 ± 0.9 mg/L (P < 0.0001); total T4 increased, 98.1 ± 2.3 vs. 114.6 ± 2.5 nmol/L (P < 0.0001); total T3 increased, 2.0 ± 0.04 vs. 2.3 ± 0.07 nmol/L (P < 0.0001); TPO antibodies decreased, 370 ± 233 U/mL vs. 355 ± 224 U/mL (P < 0.0001); LH decreased, 8.1 ± 1.1 vs. 0.4 ± 0.1 U/L (P < 0.0001); FSH did not change, 6.5± 0.6 vs. 7.9 ± 0.9 U/L (P = 0.08); human CG increased, <2 ± 0.0 vs. 195 ± 16 U/L (P < 0.0001); estradiol increased, 359.3 ± 25.9 pmol/L vs. 3491.8 ± 298.3 pmol/L (P < 0.0001); and PRL increased, 0.23 ± 0.02 vs. 0.95 ± 0.06 U/L (P < 0.0001). Because low maternal free T4 and elevated maternal thyroid-stimulating hormone levels during early gestation have been reported to be associated with impaired psychomotor development in the offspring, our findings indicate the need for additional studies in the children of women who where exposed to high levels of estrogens around the time of conception.


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