scholarly journals SAT-276 Co-Secreting TSH and Growth Hormone Pituitary Adenoma

2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Hatem Eid

Abstract Introduction: Secreting pituitary adenoma is exceedingly rare. Less than 15 cases having been reported. Its clinical presentation and diagnosis is challenging. We report a case of pituitary macroadenoma, with features of acromegaly and hyperthyroidism. Case report: A 75 years’ old man presented with new onset atrial fibrillation. He had high FT4 with normal TSH. His ultrasound scan of the neck showed a solitary nodule. He had ablation twice and was started on bisoprolol and anticoagulant. He had MRI scan for headaches and this showed a pituitary macroadenoma. He had high IGF-1. His oral glucose tolerance showed failure of GH suppression. His FT4 was persistently high with normal TSH and he had high a subunits. This suggested the diagnosis of TSH and GH secreting pituitary adenoma. Discussion: TSH-secreting pituitary adenomas are rare and not uncommonly, they co-secrete other pituitary hormones including growth hormones. Somatotrophs and lactotrops share common transcription factors with thyrotrophs. TSH-secreting adenomas are benign but 60% of them are locally invasive. TSH-secreting pituitary adenomas typically present with either symptoms of tumor growth like headache or visual field disturbance or symptoms of hyperthyroidism. Thyroid nodules are common in patients with TSHomas. In patients with TSH-secreting pituitary adenomas, majority will need only surgery and radiation. The medical treatment used to normalize TSH and FT4 levels is somatostatin analogs. This is effective in about 90% of patients with TSH secreting pituitary adenomas TSHoma should be differentiated from resistance to thyroid (RTH). The main difference between TSHoma and RTH is the presence of signs and symptoms of hyperthyroidism in patients with TSHoma, absence of a family history, normal thyroid hormone levels in family members, and the presence of an elevated glycoprotein α-subunit in patients with pituitary tumor. Reference: H Adams and D Adams. A case of a co-secreting TSH and growth hormone pituitary adenoma presenting with a thyroid nodule. EDM case reports 2018 [email protected]

2012 ◽  
Vol 2012 ◽  
pp. 1-5 ◽  
Author(s):  
Subramanian Kannan ◽  
Susan M. Staugaitis ◽  
Robert J. Weil ◽  
Betul Hatipoglu

Pituitary adenomas can express and secrete different hormones. Expression of pituitary hormones in nonneoplastic pituitary cells is regulated by different transcription factors. Some pituitary adenomas show plurihormonal expression. The most commonly reported plurihormonal adenomas are composed of somatotrophs, lactotrophs, thyrotrophs and gonadotrophs. Pituitary adenomas composed of both corticotroph and somatolactotroph secreting cells are not common because transcription factors regulating the expression of these hormones are different. We report a rare case of pituitary adenoma with concomitant corticotroph, prolactin, and growth hormone staining cells, review literature on similar cases, and discuss possible biological mechanisms underlying these plurihormonal tumors.


Author(s):  
Laura Hamilton Adams ◽  
Derick Adams

Summary Co-secreting TSH and growth hormone pituitary adenomas are rare. We present a case of a 55-year-old woman who presented with symptoms of neck fullness. Ultrasound revealed multiple thyroid nodules and examination revealed several clinical features of acromegaly. She was found to have a co-secreting TSH and growth hormone pituitary macroadenoma. She underwent surgical resection followed by gamma knife radiation, which resulted in complete remission of her TSH and GH-secreting adenoma. Learning points: TSH-secreting pituitary adenomas are rare and about one-third co-secrete other hormones. Thyroid nodules are common in acromegaly and can be the presenting sign of a growth hormone-secreting pituitary adenoma. In the workup of acromegaly, assessment of other pituitary hormones is essential, even in the absence of symptoms of other pituitary hormone dysfunction. Complete remission of co-secreting GH and TSH pituitary macroadenomas is possible with surgery and radiation alone.


Author(s):  
Gamze Akkus ◽  
Barış Karagun ◽  
Nuri Eralp Çetinalp ◽  
Arbil Açıkalın ◽  
Mehtap Evran ◽  
...  

Background: Silent pituitary adenomas are clinically found to be non-functional (i.e., without clinically evident pituitary hormone production). Introduction: The aim of this study was to investigate subjects with silent pituitary adenomas for possible variations in their clinical status. Methods: A total of 102 patients who had undergone surgery for pituitary adenoma and had been diagnosed with silent pituitary adenoma was included in the study. The patients’ preoperative and postoperative hormonal parameters and magnetic resonance imaging (MRI) features were collected, and pathological specimens were re-evaluated. Results: Immunohistochemistry results of the 102 patients were as follows: hormone-negative adenomas (n=35) 35.5%; FSH+LH-positivity (n=32) 31.3%; ACTH-positivity (n=11) 10.7%; α-subunit-positivity (n= 9) 8.8%; prolactin-positivity (n=8) 7.8%; GH-positivity (n=6) 5.4%; and plurihormonal adenoma (n=1). The mean sizes of SGA, SGHA, and SCA were 28.0±12.7, 30.0±16.0, and 27.7±8.9mm (p>0.05), respectively. With the exception of silent gonadotroph adenomas (SGAs), female gender dominance was shown in patients with silent growth hormone adenoma (SGHA) and silent corticotroph adenoma (SCA). Although no clinical relevance was observed in relation to hormonal excess, preoperative GH (4.21±4.6,vs 0.27±0.36 p=0.00) was slightly more elevated in SGHA than in GH-negative adenomas. Additionally, preoperative basal ACTH values (47.3±28.7 vs 23.9±14.4, p=0.003) were also higher in SCA compared to the other types. Our findings revealed SCAs to be more aggressive behaviour than SGHAs and SGAs due to invasiveness in radiological imaging, their elevated re-operation and postoperative ACTH values. Conclusion: Silent pituitary adenomas represent a challenging diagnostic tumour group. Careful initial evaluation of patients with pituitary adenomas should consider any mild signs and symptoms of functionality, particularly in cases of GH- and ACTH-secreting adenomas.


2021 ◽  
Vol 15 (1) ◽  
Author(s):  
Ebtesam Allehaibi ◽  
Mussa H. AlMalki ◽  
Imad Brema

Abstract Background Plurihormonal pituitary adenomas are a unique type of pituitary adenomas that secrete two or more pituitary hormones normally associated with separate cell types that have different immunocytochemical and ultrastructural features. Although they represent 10–15% of all pituitary tumors, only a small fraction of plurihormonal pituitary adenomas clinically secrete multiple hormones. The most common hormone combinations secreted by plurihormonal pituitary adenomas are growth hormone, prolactin, and one or more glycoprotein hormones. The most common hormonal symptom is acromegaly (50%). The aim of this case report is to bring awareness about this rare type of pituitary adenomas and to describe the unique presentation of our patient, even though plurihormonal pituitary adenomas are known mostly as a clinically silent tumors. Case presentation Herein, we describe an unusual case of plurihormonal pituitary adenoma with triple-positive staining for adrenocorticotropic hormone, growth hormone, and prolactin. The patient is a 65-year-old Egyptian woman who presented with mass effect symptoms of the pituitary tumor, which primarily manifested as severe headache and visual field defects. She also presented with some cushingoid features, and further analysis confirmed Cushing’s disease; slightly high prolactin and normal growth hormone levels were observed. She underwent transsphenoidal surgery and has been in remission thus far. Only a few cases have been reported in the literature, but none has exhibited silent acromegaly or mass effect symptoms as the initial presentation. Conclusion This case highlights an unusual plurihormonal pituitary adenoma case with a rare combination of secreted hormones; mass effect symptoms were dominant, as were uncommon visual field defects. Our case further proves that immunohistochemical analyses of all pituitary hormones are needed to ensure correct diagnosis and to alert clinicians to the need for more rigorous follow-up due to the higher morbidity of these patients. Our case report approval number Federal Wide Assurance NIH, USA is FWA00018774 IRB registration number with OHRP/NIH is IRB00010471.


2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A581-A582
Author(s):  
Ivan Augusto Rivera Nazario ◽  
Kyomara Hernandez Moya ◽  
Arnaldo Nieves Ortiz ◽  
Jose Ayala Rivera ◽  
Arnaldo Rojas Figueroa ◽  
...  

Abstract Acromegaly is an uncommon clinical syndrome that results from excessive secretion of growth hormone with an annual incidence of 6 to 8 cases per 1 million of individuals with a mean age of diagnosis between 40-45 years. Pituitary adenomas can be the principal reason for an overgrowth of the anterior pituitary somatotroph cells, and account for approximately one-third of all hormone-secreting pituitary adenomas with a prevalence of about 38-69 cases per 1 million and an incidence of 3-4 cases per 1 million individuals. The onset of acromegaly is insidious, and its progression is usually very slow. At the moment of diagnosis, approximately 75% of patients have presence of macro adenomas, but most cases are diagnosed after several laboratory workups and incidental brain imaging. A characteristic clinical presentation of pituitary adenomas could be secondary to mass effect. Metabolic presentation such as diabetes is one of the most common related conditions preceding the diagnosis of acromegaly. Clinical presentation with abrupt onset of DKA could be a determining factor on disease progression due to higher GH levels correlating with an increased prevalence of insulin resistance. We present a rare case of a 28y/o female G5P3A2 without previous PMHx who presented to ER with abdominal pain, general malaise, slurred speech, headache and gait difficulty of 3 days of evolution. Upon initial evaluation at ER patient was found with hyperglycemia of 317mg/dL, low central bicarbonate, high anion gap and positive serum ketones suggestive of DKA de novo. Based on neurological complaints, head CT performed showed an incidental parasellar/suprasellar/temporal hyperdense mass measuring 2.5cm x 2.6cm with optic chiasm compression features. Upon further specific questioning patient referred amenorrhea for the past 3 years, bitemporal hemianopsia, galactorrhea and marked facial feature changes, frontal bossing, weight gain, and acanthosis nigricans, for the past year. Pituitary adenoma workup revealed low prolactin levels (1.38), markedly increased growth hormone (501) and IGF-1 (893) suggesting diagnosis of acromegaly, most likely secondary to a functioning macroadenoma. Patient initially treated with Cabergoline, uncontrolled diabetes was managed and was referred to Neurosurgery service for further evaluation and tumor removal. Based on current literature, the incidence of acromegaly cases is low, more specifically when presenting with new onset diabetic ketoacidosis, insulin resistance and secondary to functioning macroadenomas. Medical awareness should be promoted to assess for careful consideration of signs and symptoms, workup, management and treatment to assess and minimize further health complications and physical burdens acromegaly and pituitary adenomas could pose for affected individuals.


2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Siroj Dejhansathit ◽  
Subhanudh Thavaraputta ◽  
Genevieve LaPointe ◽  
Ana Marcella Rivas Mejia

Abstract Background: Unlike nonfunctioning gonadotroph pituitary adenomas, functioning gonadotroph pituitary adenomas (FGA) are an uncommon type of pituitary tumors that secrete biologically active gonadotropins (LH, FSH, or both). Clinical Case: A 23-year-old man with no previous medical history presented to the emergency department with three months history of progressive decreased vision and decreased libido. He denied headache, seizure, erectile dysfunction, or weakness. On physical examination, his visual acuity was significantly reduced on the right eye and was only able to perceive light. He had a visual field narrowing on the left eye. Gynecomastia was noted bilaterally and testicles were found to be enlarged (Orchidometer >25 mL). Complete blood count was significant for hemoglobin of 19.2 g/dL (N, 13.7-17.5 g/dL), and hematocrit of 57.0% (N, 40.1-51.0%). Pituitary function tests were as follow: FSH >200.0 mIU/mL (N, 1.5-12.4 mIU/mL), LH 17.0 mIU/mL (N, 1.7-8.6 mIU/mL), total testosterone 41.3 nmol/L (N, 8.6-29.0 nmol/L), free testosterone 1.263 nmol/L (N, 0.148-0.718 nmol/L), and bioavailable testosterone 29.609 (N, 2.110-8.920 nmol/L). Prolactin, TSH, GH, and ACTH were all within the normal range. Magnetic resonance imaging (MRI) showed a sellar mass involving the planum sphenoidal measuring 5.8 x 5.2 x 5.6 cm with optic chiasm displaced superiorly, in addition, subfalcine herniation with mild hydrocephalus was also noted. The patient underwent orbitozygomatic approach resection of the pituitary tumor. Histological examination was consistent with a pituitary adenoma. Cells stained positive for transcription factor steroidogenic factor 1 (SF 1), FSH, LH, and alpha-subunit consistent with a gonadotroph adenoma. They were negative for transcription factor Pit 1 stain and the remaining pituitary hormones including ACTH, GH, prolactin, and TSH stain. Postsurgical hormone assessment showed a significant decline in FSH and LH to 2.3 and 0.4 mIU/mL, respectively and testosterone level decreased to < 0.087 nmol/L on postoperative day 18. The patient’s vision improved postoperatively prior to discharge but he lost follow up thereafter. Conclusion: Most patients with functioning gonadotroph pituitary adenoma present with large tumors that are detected based on the occurrence of symptoms of compression that result from the enlarging sellar mass. Most patients, particularly men and postmenopausal women, do not develop symptoms of hormone excess and the lack of symptomatology results in delay in diagnosis. Our patients presented with significant polycythemia which resulted from excess testosterone and could have prompted earlier tumor detection if he had presented in an earlier stage. The incidence of polycythemia in male patients with functioning gonadotroph pituitary adenoma has previously been described in the literature in a few case reports.


2010 ◽  
Vol 29 (4) ◽  
pp. E5 ◽  
Author(s):  
Peter G. Campbell ◽  
Erin Kenning ◽  
David W. Andrews ◽  
Sanjay Yadla ◽  
Marc Rosen ◽  
...  

Object Using strict biochemical remission criteria, the authors assessed surgical outcomes after endoscopic transsphenoidal resection of growth hormone (GH)–secreting pituitary adenomas and identified preoperative factors that significantly influence the rate of remission. Methods A retrospective review of a prospectively maintained database was performed. The authors reviewed cases in which an endoscopic resection of GH-secreting pituitary adenomas was performed. The cohort consisted of 26 patients who had been followed for 3–60 months (mean 24.5 months). The thresholds of an age-appropriate, normalized insulin-like growth factor–I concentration, a nadir GH level after oral glucose load of less than 1.0 μg/l, and a random GH value of less than 2.5 μg/l were required to establish biochemical cure postoperatively. Results Overall, in 57.7% of patients undergoing a purely endoscopic transsphenoidal pituitary adenectomy for acromegaly, an endocrinological cure was achieved. The mean clinical follow-up duration was 24.5 months. In patients with microadenomas (4 cases) the cure rate was 75%, whereas in patients harboring macroadenomas (22 cases) the cure rate was 54.5%. Cavernous sinus invasion (Knosp Grades 3 and 4) was associated with a significantly lower remission rate (p = 0.0068). Hardy Grade 3 and 4 tumors were also less likely to achieve biochemical cure (p = 0.013). The overall complication rate was 11.5% including 2 incidents of transient diabetes insipidus and 1 postoperative CSF leak, which were treated nonoperatively. Conclusions A purely endoscopic transsphenoidal approach to GH-secreting pituitary adenomas leads to similar outcome for noninvasive macroadenomas compared with traditional microsurgical techniques. Furthermore, this approach may often provide maximal visualization of the tumor, the pituitary gland, and the surrounding neurovascular structures.


2016 ◽  
Vol 141 (1) ◽  
pp. 104-112 ◽  
Author(s):  
William C. McDonald ◽  
Nilanjana Banerji ◽  
Kelsey N. McDonald ◽  
Bridget Ho ◽  
Virgilia Macias ◽  
...  

Context.—Pituitary adenoma classification is complex, and diagnostic strategies vary greatly from laboratory to laboratory. No optimal diagnostic algorithm has been defined. Objective.—To develop a panel of immunohistochemical (IHC) stains that provides the optimal combination of cost, accuracy, and ease of use. Design.—We examined 136 pituitary adenomas with stains of steroidogenic factor 1 (SF-1), Pit-1, anterior pituitary hormones, cytokeratin CAM5.2, and α subunit of human chorionic gonadotropin. Immunohistochemical staining was scored using the Allred system. Adenomas were assigned to a gold standard class based on IHC results and available clinical and serologic information. Correlation and cluster analyses were used to develop an algorithm for parsimoniously classifying adenomas. Results.—The algorithm entailed a 1- or 2-step process: (1) a screening step consisting of IHC stains for SF-1, Pit-1, and adrenocorticotropic hormone; and (2) when screening IHC pattern and clinical history were not clearly gonadotrophic (SF-1 positive only), corticotrophic (adrenocorticotropic hormone positive only), or IHC null cell (negative-screening IHC), we subsequently used IHC for prolactin, growth hormone, thyroid-stimulating hormone, and cytokeratin CAM5.2. Conclusions.—Comparison between diagnoses generated by our algorithm and the gold standard diagnoses showed excellent agreement. When compared with a commonly used panel using 6 IHC for anterior pituitary hormones plus IHC for a low-molecular-weight cytokeratin in certain tumors, our algorithm uses approximately one-third fewer IHC stains and detects gonadotroph adenomas with greater sensitivity.


2012 ◽  
Vol 32 (6) ◽  
pp. E2 ◽  
Author(s):  
Grace Lam ◽  
Vivek Mehta ◽  
Gabriel Zada

Object Spontaneous and medically induced CSF leaks are uncommonly associated with pituitary adenomas. The aim of this study was to further characterize the clinical scenarios most closely associated with this phenomenon. Methods A review of the literature was conducted to identify all cases of nonsurgical CSF leaks associated with pituitary adenomas. The authors aimed to identify associated risk factors and management strategies used to treat these tumors and repair the CSF leak site. Results Fifty-two patients with spontaneous or medically induced CSF leaks in the setting of a pituitary adenoma were identified from 29 articles published from 1980 through 2011. In 38 patients (73%), CSF rhinorrhea developed following initiation of medical therapy, whereas spontaneous CSF leakage developed as the presenting symptom in 14 patients (27%). The patients' mean age was 42.8 years (range 23–68 years). There were 35 males and 17 females. Forty-two patients (81%) had a prolactinoma, with the remaining patients having the following tumors: nonfunctioning pituitary adenoma (6 patients), growth hormone–secreting adenoma (2 patients), mammosomatotroph cell adenoma (1 patient), and ACTH-secreting adenoma (1 patient). Infrasellar tumor invasion into the paranasal sinuses was specifically reported in 56% of patients. The medical agents associated with CSF leakage were dopamine agonists (97%) and somatostatin analogs (3%). The average time from initialization of medical treatment to onset of rhinorrhea was 3.3 months (range 3 days–17 months). Nonsurgical management was successful in 4 patients, including 1 who had successful resolution with a temporary lumbar drain. Forty-six patients (88%) underwent surgical intervention to treat the CSF leak and/or resect the tumor. In 2 patients, surgery was not performed due to medical contraindications or patient preference. Conclusions Nonsurgical development of CSF rhinorrhea may occur in the setting of pituitary adenomas, especially following favorable response of invasive prolactinomas to initiation of dopamine agonist therapy. Additional cases have been reported as the presenting symptom of a pituitary adenoma and are likely to be related to decreased tumor volume due to intrinsic infarction or hemorrhage, ongoing invasion, and/or increases in intracranial pressure. Surgical repair, preferentially via a transsphenoidal approach, is the recommended initial treatment for definitive repair of the CSF leak and achievement of maximal tumor resection.


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.


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