scholarly journals Pituitary Hyperplasia: To Operate or Not to Operate, That Is the Question

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A599-A599
Author(s):  
Aakash Rajwani ◽  
Luma Ghalib
Keyword(s):  
Imaging Techniques ◽  
Post Partum ◽  
Hormone Replacement ◽  
Mass Effect ◽  
Primary Hypothyroidism ◽  
Absolute Increase ◽  
Pituitary Hyperplasia ◽  
Imaging Results ◽  
History Of ◽  
Pituitary Enlargement

Abstract Pituitary hyperplasia is defined as an absolute increase in the number of one or more adenohypophyseal cell subtypes, manifesting radiologically as pituitary enlargement beyond what is considered normal. It has been noted in certain physiological conditions like pregnancy however can also be seen in pathological conditions with end organ insufficiency like severe hypothyroidism. 21- year old female with a past medical history of Primary Hypothyroidism secondary to Hashimoto’s thyroiditis presented initially for evaluation of worsening headache and blurry vision. She was diagnosed with hypothyroidism at 10 years of age and had an extensive family history of hypothyroidism. At the time of presentation, she was 11 months post- partum and had been on and off her levothyroxine supplementation, having stopped it completely for a few months after delivery. MRI brain showed an 18 mm homogeneously enhancing intrasellar mass with suprasellar extension. She was referred to Neurosurgery for further evaluation. Workup revealed a TSH >100 (0.27 - 4.2 mIU/L) and FT4 <0.4 (0.8 - 2 ng/dL). In the context of severe untreated hypothyroidism and MRI findings consistent with pituitary hyperplasia with abutment but no mass effect on the optic apparatus, initial plan was to treat the hypothyroidism medically and observe closely. Patient was started on levothyroxine supplementation. Her TSH improved to 3.367 (0.550 - 4.780 uIU/mL) and FT4 to 2.00 (0.89 - 1.76 ng/dL), ηοωεϖερ she continued to have worsening of visual symptoms. Surgery was considered to decompress the optic nerve, but pre-operative MRI showed a significant decrease in size of the pituitary gland with decreased suprasellar bulging and no mass effect on the optic chiasm. Surgery was subsequently cancelled. Prolonged primary hypothyroidism leads to pituitary hyperplasia due to loss of negative feedback from lack of circulating T4 and T3, leading to excessive TRH secretion from the hypothalamus. The high TRH can lead to thyrotroph as well as lactotroph hyperplasia. Subsequently patients can present with headache, vision changes along with signs and symptoms of hypothyroidism and increased prolactin secretion. It is important to differentiate hyperplasia from other sellar lesions like pituitary macroadenoma or hypophysitis. Patients with hypothyroidism, who have pituitary enlargement diagnosed on brain imaging, should be promptly diagnosed and treated with thyroid hormone replacement. With a higher frequency and improved quality of imaging techniques, we are increasingly coming across scenarios of abnormal findings on imaging. Correlation of radiographic imaging results with a thorough history and biochemical testing is essential prior to proceeding with surgical intervention.

scholarly journals Pituitary hyperplasia: an uncommon presentation of a common disease

2015 ◽  
Vol 2015 ◽  
Author(s):  
C P Neves ◽  
E T Massolt ◽  
R P Peeters ◽  
S J Neggers ◽  
W W de Herder
Keyword(s):  
Differential Diagnosis ◽  
Thyroid Function ◽  
Hormone Replacement ◽  
Primary Hypothyroidism ◽  
Common Disease ◽  
Pituitary Hormone ◽  
List Type ◽  
Pituitary Mass ◽  
Pituitary Hyperplasia ◽  
Pituitary Enlargement

Summary A 21-year-old woman presented with amenorrhea, bilateral galactorrhea and fatigue. Visual acuity and visual fields were normal. Laboratory examination demonstrated hyperprolactinemia. Magnetic resonance imaging (MRI) of the pituitary showed a 19×17×12-mm sellar mass with supra- and parasellar extension, causing compression of the pituitary stalk and optic chiasm. Further examinations confirmed mild hyperprolactinemia, strongly elevated TSH (>500 mU/l), low free thyroxine (FT4), hypogonadotropic hypogonadism and secondary adrenal insufficiency. Hydrocortisone and l-T4 replacement therapy was started. Three months later, the galactorrhea had disappeared, thyroid function was normalized and MRI revealed regression of the pituitary enlargement, confirming the diagnosis of pituitary hyperplasia (PH) due to primary hypothyroidism. Subsequently, the menstrual cycle returned and the hypocortisolism normalized. This case demonstrates that severe primary hypothyroidism may have an unusual presentation and should be considered in the differential diagnosis of pituitary enlargement associated with moderate hyperprolactinemia. Learning points One should always try to find one etiology as the common cause of all the clinical findings in a pathologic process. Amenorrhea, galactorrhea and fatigue may be the only presenting clinical manifestations of primary hypothyroidism. Not every patient with galactorrhea, hyperprolactinemia and a pituitary mass has a prolactinoma. Primary hypothyroidism should always be considered in the differential diagnosis of hyperprolactinemia associated with pituitary enlargement and pituitary hormone(s) deficiency(ies). When PH due to primary hypothyroidism is suspected, thyroid hormone replacement should be started and only regression of pituitary enlargement on MRI follow-up can confirm the diagnosis. Examination of thyroid function in patients with a pituitary mass may avoid unnecessary surgery.

scholarly journals Hypothyroidism presenting with development delay, failure to thrive, and pituitary adenoma

2017 ◽  
Vol 4 (5) ◽  
pp. 1906
Author(s):  
Jatinder Singh ◽  
Vaneeta Bhardwar ◽  
Daaman Mittal
Keyword(s):  
Pituitary Adenoma ◽  
Hormone Replacement ◽  
Pituitary Tumors ◽  
Failure To Thrive ◽  
Primary Hypothyroidism ◽  
Pituitary Hyperplasia ◽  
Development Delay ◽  
Pituitary Enlargement ◽  
Ct And Mri

Pituitary enlargement secondary to primary hypothyroidism (PH) is a known but uncommon occurrence, and is also difficult to distinguish on CT and MRI from primary pituitary tumors. Following adequate hormone replacement with L-thyroxine, both symptoms and pituitary hyperplasia are reported to regress within a few months. It is important to recognize this condition so as to avoid unnecessary surgery.

scholarly journals SUN-281 Pituitary Hyperplasia Secondary to Uncontrolled Primary Hypothyroidism

2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Jessica Lee Betancourt
Keyword(s):  
Pituitary Gland ◽  
Early Recognition ◽  
Hormone Replacement ◽  
Primary Hypothyroidism ◽  
Laboratory Evaluation ◽  
Complete Regression ◽  
Pituitary Macroadenoma ◽  
Free T4 ◽  
Pituitary Hyperplasia ◽  
Patient Reported

Abstract Background: There are several recognized causes of hyperplasia of the pituitary gland. These may present as sellar masses and be misdiagnosed as pituitary adenomas. Pituitary hyperplasia can occur in the presence of long standing primary hypothyroidism due to the loss of negative feedback caused by decreased secretion of thyroxine (T4) and triiodothyronine (T3) by the thyroid gland, leading to excessive thyrotropin releasing hormone (TRH) production by the hypothalamus causing Thyrotroph pituitary hyperplasia Clinical case: 51 y/o female with a past medical history that includes anxiety & depression, obesity, pre-diabetes and uncontrolled hypothyroidism due to Hashimoto’s, presented to the Endocrinology clinic for recent diagnosis of pituitary macroadenoma. Patient reported tiredness, decrease energy, myalgias, weight gain, abnormal menstrual periods and frontal headaches. On physical exam, she had a body mass index of 37.39kg/m2, blood pressure of 130/85mmHg, heart rate of 91 bpm. There was no thyromegaly noted on exam. No abdominal striae was noted. Overall, exam was unremarkable. Her neurological exam was normal and there were no obvious visual field deficits. Initial laboratory tests revealed a thyroid stimulating hormone (TSH) >150 uIU/mL (0.46–4.7 uIU/mL), free T4 0.3 ng/dL (0.7–1.3 ng/dL) and positive TPO antibodies. Other endocrine work up including ACTH, cortisol, prolactin, FSH, LH and IGF-1, were normal. An MRI of the pituitary revealed a heterogeneous enhancing mass replacing the pituitary gland in the sella that measured 16 x 17 x 11 mm. She was evaluated by Neurosurgery, for presumed diagnosis of pituitary macroadenoma. However, prompt recognition of uncontrolled primary hypothyroidism causing pituitary hyperplasia lead to medical management, first. She was started on weight based (1.6mcg/kg/day) levothyroxine at 175 mcg per day. Six weeks after thyroid replacement therapy laboratory evaluation showed improvement in thyroid function test with a TSH of 0.8mIU/mL, free T4 2.8ng/dL and total T3 307ng/dL. A repeat MRI of the pituitary showed decrease in size of the pituitary gland measuring 15 x 4 x 10 mm. Conclusion: This case illustrates the importance of early recognition of uncontrolled primary hypothyroidism during the evaluation of a pituitary mass. Complete regression of this pituitary gland abnormality can be achieved with thyroid hormone replacement avoiding the irreversible consequences of inappropriate pituitary surgery.

scholarly journals SUN-290 Pituitary Hyperplasia Due to Uncontrolled Primary Hypothyroidism: Case Series and Literature Review

2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Juan Pablo Godoy Alonso ◽  
Germán González de la Cruz ◽  
Marlon Vladimir Vázquez-Aguirre ◽  
Andrea Rocha Haro ◽  
Karla Krystel Ordaz Candelario ◽  
...  
Keyword(s):  
Pituitary Gland ◽  
Feedback Inhibition ◽  
Case Series ◽  
Optic Chiasm ◽  
Primary Hypothyroidism ◽  
Autoimmune Hypothyroidism ◽  
Hormonal Replacement ◽  
Pituitary Hyperplasia ◽  
History Of

Abstract Background: Pituitary hyperplasia secondary to primary hypothyroidism results from the loss of thyroxine feedback inhibition and the subsequent overproduction of TSH. Case 1: A 18-year-old female presented with a chronic history of spontaneous galactorrhea, headache and malaise. Autoimmune primary hypothyroidism was diagnosed, with elevated TSH of 490 mIU/L (0.3-5) and low fT4 of 0.33 ng/dL (0.63-1.34). Pituitary MRI showed an enlarged pituitary with compression of the optic chiasm. Hormonal replacement with levothyroxine 75 mcg qd was started. Five months later she was asymptomatic, and normal TSH (1.64 mIU/L) and fT4 (0.9 ng/dL) levels. A new MRI revealed normal size of pituitary gland, with no compression of the optic chiasm and an intact infundibulum. Case 2: A 24-year-old female with type 1 diabetes and autoimmune primary hypothyroidism, presented with a five-year history of galactorrhea and oligomenorrhea. She was treated with insulin glargine 20U qd, and levothyroxine 200 mcg/day. However, patient’s adherence was bad. She consulted a primary health physician who suspected a prolactinoma after high prolactin levels (77.65, normal 2.64-13.13 ng/mL). Cabergoline was started without any clinical improvement. She then was referred to our service for follow-up. TSH results showed 500 mIU/L, with low fT4 (0.08 ng/dL). Prolactin levels was normal. Pituitary MRI revealed diffuse enlargement of the gland, with compression of infundibulum and optic chiasm. Treatment was modified to levothyroxine/liothyronine 100/20mcg 1 ½ tablet qd. After 7 months, we confirmed normal TSH (0.76 mIU/L) and fT4 (1.23 ng/dL), and the patient was asymptomatic. After 17 months, new MRI showed normal pituitary gland without any compression. Case 3: A 23-year-old female with a history of Addison′s disease and hypothyroidism diagnosed at age 17 presented with a 6-month history of somnolence, fatigue, headache and amenorrhea. She was previously treated with hydrocortisone 25mg/day, fludrocortisone 0.1mg/day, and levothyroxine 200mcg/day. Patient’s adherence was bad, and multiple hospitalizations because of adrenal crises were reported. Her initial hormonal evaluation revealed high TSH of 460 mIU/L and low fT4 of 0.25 ng/dL, mild hyperprolactinemia (32.16 ng/mL), and very high ACTH levels (2,700 pg/mL, normal 10-100). Pituitary MRI revealed an enlarged pituitary with mild compression of the optic chiasm. Hormonal replacement was modified to fasting levothyroxine alternating 200mcg and 300mcg qd. Her last follow-up showed normal TSH (0.53 mIU/L) and fT4 (1.18 ng/dL) levels. New MRI showed normal pituitary size Conclusion: We presented three young women, with autoimmune hypothyroidism, who developed pituitary hyperplasia and responded to proper hormonal replacement normalizing pituitary size. Reference: Endocrinol Diabetes Metab Case Rep. 2015; 2015: 150056.

scholarly journals MON-058 Precocious Puberty and Hypothyroidism in a Pediatric Case

2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Jessica L Sea ◽  
Michael J Head ◽  
Harvey Kenn Chiu
Keyword(s):  
Precocious Puberty ◽  
Mass Effect ◽  
Optic Chiasm ◽  
Large Mass ◽  
Primary Hypothyroidism ◽  
Serum Prolactin ◽  
Free T4 ◽  
Pituitary Hyperplasia ◽  
Suprasellar Extension

Abstract Background: Hypothyroidism with secondary sellar/suprasellar mass is rarely associated with precocious puberty. Here we describe a rare case of pediatric hyperprolactinemia and precocious puberty secondary to hypothyroidism, marked TSH elevation, and pituitary hyperplasia. Clinical Case: A 9-year-old female, with onset of thelarche and menses occurring at age 7 and 8 respectively, presented with primary hypothyroidism (Free T4 <0.11; n=4.9-11.4mcg/mL), elevated TSH (1620.0mU/mL; n=0.3-4.7mU/mL), hyperprolactinemia (108.6ng/mL; n=3.0-23.1ng/mL), and elevated serum estradiol (37.6pg/mL; n=10pg/mL). The patient had coarse scaly skin, diminished energy, and poor growth lasting 1 year. There were no associated gastrointestinal issues, temperature intolerance, nor visual impairments noted during this time. Magnetic resonance imaging revealed a large mass (1.48cm) with suprasellar extension and a mass effect on the optic chiasm. The patient was then started on Levothyroxine and Cabergoline, to reduce serum prolactin levels. However, upon follow-up two months later, the patient had hypoprolactinemia (2.0ng/mL; n=3.0-23.1ng/mL). The patient was referred to neurosurgery for resection of the sellar mass. Endocrinology was also consulted, at which point Cabergoline was discontinued and Levothyroxine was gradually increased. Follow up 4 months later showed prolactin levels had normalized to 11.4ng/mL (3.0-23.1ng/mL). Serum LH and FSH were within normal ranges (1.2mIU/mL and 4.2mIU/mL, respectively). TSH, though still elevated (47.35mU/mL; n=0.3-4.7mU/mL), was significantly reduced compared to the prior measurement (1620mU/mL). Serum levels of Free T4 increased to 1.06mcg/mL (n=4.9-11.4mcg/mL). Levothyroxine was titrated up and a repeated pituitary MRI demonstrated a significant decrease in the size of the mass with resolution of the suprasellar extension and mass effect on the optic chiasm. Further, the patient’s menses ceased and thelarche resolved upon correction of T4 and regression of the pituitary mass. Conclusions: While rare, primary hypothyroidism and TSH-driven pituitary hyperplasia can result in a large mass effect with suprasellar extension, causing secondary hyperprolactinemia by a mass effect and central precocious puberty. This case highlights the benefits for evaluating underlying hypothyroidism as a cause for hyperprolactinemia and sellar/suprasellar mass.

scholarly journals Dome-Shaped Pituitary Enlargement in Primary Hypothyroidism: Avoiding Neurosurgical Interventions

2020 ◽  
Vol 35 (2) ◽  
pp. 238-243
Author(s):  
Satyam Chakraborty ◽  
◽  
Mona Tiwari ◽  
Rajan Palui ◽  
Kajari Bhattacharya ◽  
...  
Keyword(s):  
Case Reports ◽  
Pituitary Surgery ◽  
Primary Hypothyroidism ◽  
Hormone Deficiency ◽  
Homogeneity Analysis ◽  
Imaging Characteristic ◽  
Pituitary Hyperplasia ◽  
Pituitary Enlargement ◽  
Levothyroxine Treatment ◽  
Thyrotroph Hyperplasia

We describe three cases of primary hypothyroidism which presented initially to neurosurgery department with pituitary hyperplasia. We have found a novel pattern of ‘dome shaped’ enlargement of pituitary in MRI of these patients. Out of these 3 patients, in two of them, the planned surgery was deferred when endocrinologists were consulted and the pituitary hyperplasia completely resolved with levothyroxine treatment. In the third case, pituitary surgery was already performed before endocrinology consultation and histopathology revealed thyrotroph hyperplasia. The hyperplastic lesions described typically have a homogenous symmetrical ‘dome’ shaped architecture unlike the non-functioning pituitary adenoma (NFPA), which usually might often be of varying shapes and homogeneity. Analysis of pituitary images from similar case reports published in literature, also showed this typical ‘dome’ shaped pituitary enlargement. This imaging characteristic can be a clue to look for underlying hormone deficiency, especially in primary hypothyroidism. Therefore, a thorough endocrine evaluation especially looking for primary hypothyroidism in such dome shaped pituitary lesions are mandatory to prevent unwarranted neuro-surgical intervention as treatment of primary hypothyroidism may result in resolution of the abnormal enlargement.

scholarly journals Pituitary hyperplasia: case series and literature review of an under-recognised and heterogeneous condition

2015 ◽  
Vol 2015 ◽  
Author(s):  
Sunita M C De Sousa ◽  
Peter Earls ◽  
Ann I McCormack
Keyword(s):  
Polycystic Ovary ◽  
Case Series ◽  
Primary Hypothyroidism ◽  
List Type ◽  
Close Monitoring ◽  
Gnrh Analogues ◽  
Pituitary Hyperplasia ◽  
Pituitary Enlargement ◽  
And Gender ◽  
Trophic Hormone

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.

Gestational diabetes mellitus: are mothers being followed-up? A retrospective study

2018 ◽  
Vol 68 (suppl 1) ◽  
pp. bjgp18X697469
Author(s):  
Rebecca Ward ◽  
Fahmy W Hanna ◽  
Ann Shelley-Hitchen ◽  
Ellen Hodgson ◽  
Adrian Heald ◽  
...  
Keyword(s):  
Gestational Diabetes ◽  
Median Time ◽  
Post Partum ◽  
Tolerance Test ◽  
Oral Glucose ◽  
Tertiary Referral Centre ◽  
Alternative Approach ◽  
Nice Guidance ◽  
History Of

BackgroundWomen with gestational diabetes (GDM) have an elevated risk of developing type 2 diabetes (T2DM). NICE Guidance recommends women who develop GDM are screened 6 weeks post-partum and annually thereafter.AimTo evaluate conformity to guidance of screening in women with GDM by 6-week post-partum fasting plasma glucose (FPG) and annual FPG and determine time between delivery and development of T2DM.MethodRecords at a tertiary referral centre were used to identify women (n = 54) diagnosed with GDM by antenatal oral glucose tolerance test between July 1999 and January 2007. Data from laboratory records were used to collect investigations of glycaemic status during the follow-up period (median follow-up 12.4 years, range 9.5–17.1 years).ResultsOf 252 women, 102 (40.2%) did not have a FPG at 6 weeks (+/−2 weeks). Of these, median time to first test was 1.2 years (range 0.04–10.8 years), with only 43.1% followed-up within 1 year. In those who had a 6-week FPG, 17 (11.3%) women had no further tests. A total of 84 (33% of those with gestational diabetes in the index pregnancy) women were diagnosed with T2DM; median time from delivery to diagnosis was 5.2 years (range 0.35–15.95). We found the only significant factor for a follow-up test at 1-year post-partum was the use of insulin.ConclusionOur data suggest an alternative approach is needed for monitoring women with a history of GDM. This needs to be appropriate for a generally healthy group in which traditional screening mechanisms may not be adequate or sufficient.

scholarly journals Estrogens and Progestogens in Triple Negative Breast Cancer: Do They Harm?

Cancers ◽  
2021 ◽  
Vol 13 (11) ◽  
pp. 2506
Author(s):  
Mark van Barele ◽  
Bernadette A. M. Heemskerk-Gerritsen ◽  
Yvonne V. Louwers ◽  
Mijntje B. Vastbinder ◽  
John W. M. Martens ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Triple Negative ◽  
Hormone Replacement ◽  
Breast Cancers ◽  
Younger Women ◽  
Alternative Pathways ◽  
Increased Risk ◽  
History Of ◽  
Hormone Sensitive

Triple-negative breast cancers (TNBC) occur more frequently in younger women and do not express estrogen receptor (ER) nor progesterone receptor (PR), and are therefore often considered hormone-insensitive. Treatment of premenopausal TNBC patients almost always includes chemotherapy, which may lead to premature ovarian insufficiency (POI) and can severely impact quality of life. Hormone replacement therapy (HRT) is contraindicated for patients with a history of hormone-sensitive breast cancer, but the data on safety for TNBC patients is inconclusive, with a few randomized trials showing increased risk-ratios with wide confidence intervals for recurrence after HRT. Here, we review the literature on alternative pathways from the classical ER/PR. We find that for both estrogens and progestogens, potential alternatives exist for exerting their effects on TNBC, ranging from receptor conversion, to alternative receptors capable of binding estrogens, as well as paracrine pathways, such as RANK/RANKL, which can cause progestogens to indirectly stimulate growth and metastasis of TNBC. Finally, HRT may also influence other hormones, such as androgens, and their effects on TNBCs expressing androgen receptors (AR). Concluding, the assumption that TNBC is completely hormone-insensitive is incorrect. However, the direction of the effects of the alternative pathways is not always clear, and will need to be investigated further.

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