Pituitary hyperplasia in children with short stature and primary hypothyroidism

2010 ◽  
Vol 47 (10) ◽  
pp. 877-880 ◽  
Author(s):  
Aijing Xu ◽  
Tang Li
Keyword(s):  
Short Stature ◽  
Primary Hypothyroidism ◽  
Pituitary Hyperplasia

scholarly journals Low Growth Hormone Levels in Short-Stature Children with Pituitary Hyperplasia Secondary to Primary Hypothyroidism

2015 ◽  
Vol 2015 ◽  
pp. 1-6 ◽  
Author(s):  
Minghua Liu ◽  
Yanyan Hu ◽  
Guimei Li ◽  
Wenwen Hu
Keyword(s):  
Thyroid Hormones ◽  
Short Stature ◽  
Primary Hypothyroidism ◽  
Thyroid Antibodies ◽  
Gh Secretion ◽  
Pituitary Hyperplasia ◽  
Stimulation Tests ◽  
The Mean ◽  
Tsh Levels

Objective. The follow-up of GH levels in short-stature children with pituitary hyperplasia secondary to primary hypothyroidism (PPH) is reported in a few cases. We aimed to observe changes in GH secretion in short-stature children with PPH. Methods. A total of 11 short-stature children with PPH accompanied by low GH levels were included. They received levothyroxine therapy after diagnosis. Their thyroid hormones, IGF-1, PRL, and pituitary height were measured at baseline and 3 months after therapy. GH stimulation tests were performed at baseline and after regression of thyroid hormones and pituitary. Results. At baseline, they had decreased GH peak and FT3 and FT4 levels and elevated TSH levels. Decreased IGF-1 levels were found in seven children. Elevated PRL levels and positive thyroid antibodies were found in 10 children. The mean pituitary height was 14.3±3.8 mm. After 3 months, FT3, FT4, and IGF-1 levels were significantly increased (all p<0.01), and values of TSH, PRL, and pituitary height were significantly decreased (all p<0.001). After 6 months, pituitary hyperplasia completely regressed. GH levels returned to normal in nine children and were still low in two children. Conclusion. GH secretion can be resolved in most short-stature children with PPH.

Phenotypic presentation of adolescents with overt primary hypothyroidism

2018 ◽  
Vol 31 (4) ◽  
pp. 415-420 ◽  
Author(s):  
Nandini Devru ◽  
Pramila Dharmshaktu ◽  
Gaurav Kumar ◽  
Deep Dutta ◽  
Bindu Kulshreshtha
Keyword(s):  
Short Stature ◽  
Standard Deviation Score ◽  
Bone Age ◽  
Thyroid Stimulating Hormone ◽  
Periodic Paralysis ◽  
Primary Hypothyroidism ◽  
Delayed Puberty ◽  
Overt Hypothyroidism ◽  
Pituitary Hyperplasia ◽  
Severe Short Stature

AbstractBackground:The phenotypic presentation of overt hypothyroidism during adolescence is less well characterized. The aim of the study was to study the phenotypic presentation of patients with overt hypothyroidism presenting during adolescence (age 9–18 years).Methods:Records of adolescent patients with overt hypothyroidism (thyroid stimulating hormone [TSH]>10 mIU/L) were retrospectively analyzed for presenting complaints, height and pubertal status.Results:A total of 67 patients (40 females and 37 males, average age 13.2+2.3 years) with a mean TSH of 241.3±336.6 mIU/L were included. The commonest presentation was short stature in 46.2% of patients followed by neck swelling (16.4%) and weight gain (11.9%). The mean height standard deviation score (SDS) was −2.5+2.11, 43% of patients had less than 3 SDS. The height age and bone age were around 3 years less than the chronological age. The bone age significantly correlated with the height age but not with TSH levels. Three patients referred from neurology with primary complaints of headache had pituitary hyperplasia and one presented with hypokalemic periodic paralysis. Seven had delayed puberty and one patient had early periods due to huge ovarian cysts.Conclusions:In the present study, severe short stature and uncommon phenotypic presentations were a consequence of long-standing severe untreated hypothyroidism.

Primary hypothyroidism with intracranial hypertension and pituitary hyperplasia

1994 ◽  
Vol 10 (2) ◽  
pp. 166-168 ◽  
Author(s):  
Coleen Adams ◽  
Heather J. Dean ◽  
Sara J. Israels ◽  
Alice Patton ◽  
Derek H. Fewer
Keyword(s):  
Intracranial Hypertension ◽  
Primary Hypothyroidism ◽  
Pituitary Hyperplasia

Ultrasonic Morphology of Uterus and Ovaries in Girls with Pituitary Hyperplasia Secondary to Primary Hypothyroidism

2013 ◽  
Vol 45 (09) ◽  
pp. 669-674 ◽  
Author(s):  
Y. Hu ◽  
Q. Wang ◽  
G. Li ◽  
X. Sun ◽  
C. Liu
Keyword(s):  
Primary Hypothyroidism ◽  
Pituitary Hyperplasia

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) &gt;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 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 &gt;100 (0.27 - 4.2 mIU/L) and FT4 &lt;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 SUN-277 Pituitary Hyperplasia Due to Severe Primary Hypothyroidism: An Uncommon Manifestation of a Common Disease

2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Abhilasha Singh ◽  
Massiell German ◽  
Anu Sharma
Keyword(s):  
Visual Field ◽  
Negative Feedback ◽  
Brain Mri ◽  
Subsequent Development ◽  
Optic Chiasm ◽  
Primary Hypothyroidism ◽  
Serum Prolactin ◽  
Visual Field Defects ◽  
Common Disease ◽  
Pituitary Hyperplasia

Abstract Background Pituitary hyperplasia (PH) is a non-neoplastic increase in one or more cell subtype of the adenohypophysis. It is physiologically seen in pregnancy from resultant lactotroph hyperplasia and pathologically in organ dysfunctions that lead to loss of negative feedback on hypothalamus like primary hypothyroidism and primary adrenal insufficiency. Although primary hypothyroidism is common, PH is an under-recognized consequence of long-standing hypothyroidism. Case Description A 26-year-old female with class 3 obesity, type 2 diabetes mellitus, and primary hypothyroidism on replacement presented for evaluation of secondary amenorrhea. Two months prior to presentation, she underwent a brain MRI for new-onset headache which revealed diffusely enhancing homogenous pituitary tissue measuring 2.3 cm with upward lifting of the optic chiasm. Serum prolactin was elevated at 86.2 ng/ml (2.8-26 ng/ml). This was presumed to be secondary to a prolactinoma and cabergoline was started by the referring provider. Subsequent workup revealed elevated thyroid-stimulating hormone (TSH) at 494.11 mU/L (0.30- 4.00 mU/L) and a low free thyroxine (FT4) of 0.2 ng/dl (0.8-1.7 ng/dl). Other pituitary hormones were within normal limits. The visual field examination was normal. It was noted she had a persistently elevated TSH over the past five years. On further questioning, the patient ran out of levothyroxine replacement 6 months ago and had been generally non-adherent to therapy for years due to nausea. Improved medication adherence resulted in the normalization of prolactin and reduction in TSH level. Repeat MRI 2 months later revealed a reduction in her pituitary hyperplasia to 2.1 cm. Discussion In severe primary hypothyroidism, there is loss of negative feedback to the hypothalamus due to low circulating FT4 and triiodothyronine (T3) concentrations. As a result, there is stimulation of thyrotropin-releasing hormone (TRH) which promotes thyrotroph hyperplasia. A strong correlation exists between TSH concentration and the degree of pituitary hyperplasia. The typical MRI finding is a diffusely enhancing homogenous pituitary mass. Despite optic chiasm contact, physiologic pituitary hyperplasia rarely causes visual field defects. High concentrations of TRH stimulates prolactin release with resultant mild hyperprolactinemia. Although PH is reversible with therapy, rare cases with subsequent development of panhypopituitarism while on therapy have been reported in the setting of longstanding hypothyroidism. Very rarely, chronically untreated primary hypothyroidism can stimulate the growth of a thyrotroph adenoma. Long-term biochemical and radiological monitoring is therefore recommended until resolution. This case highlights the physiologic responses manifested in severe primary hypothyroidism and the fact that these changes improve with adequate replacement.

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