scholarly journals Reversible thyrotroph hyperplasia with hyperprolactinemia: A rare presenting manifestation of primary hypothyroidism

2012 ◽  
Vol 16 (6) ◽  
pp. 1037 ◽  
Author(s):  
Rajesh Rajput ◽  
Ashish Sehgal ◽  
Deepak Gahlan
2020 ◽  
Vol 35 (2) ◽  
pp. 238-243
Author(s):  
Satyam Chakraborty ◽  
◽  
Mona Tiwari ◽  
Rajan Palui ◽  
Kajari Bhattacharya ◽  
...  

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.


Author(s):  
John D. Farley ◽  
Ellen L. Toth ◽  
Edmond A. Ryan

ABSTRACT:We report the case of a young boy being considered for pituitary surgery because of pituitary enlargement found during assessment of growth delay. There was no goitre but he was hypothyroid clinically and biochemically. The finding of an elevated TSH suggested primary thyroid disease with thyrotroph hyperplasia. Treatment with L-thyroxine resulted in prompt resolution of his pituitary enlargement and improvement in his visual fields.


2015 ◽  
Vol 21 ◽  
pp. 221
Author(s):  
Abbas Mansour ◽  
H. Jawad ◽  
Ahmed Ahmed ◽  
N.A. Zainab ◽  
A.L. Emara

1974 ◽  
Vol 75 (2) ◽  
pp. 274-285 ◽  
Author(s):  
A. Gordin ◽  
P. Saarinen ◽  
R. Pelkonen ◽  
B.-A. Lamberg

ABSTRACT Serum thyrotrophin (TSH) was determined by the double-antibody radioimmunoassay in 58 patients with primary hypothyroidism and was found to be elevated in all but 2 patients, one of whom had overt and one clinically borderline hypothyroidism. Six (29%) out of 21 subjects with symptomless autoimmune thyroiditis (SAT) had an elevated serum TSH level. There was little correlation between the severity of the disease and the serum TSH values in individual cases. However, the mean serum TSH value in overt hypothyroidism (93.4 μU/ml) was significantly higher than the mean value both in clinically borderline hypothyroidism (34.4 μU/ml) and in SAT (8.8 μU/ml). The response to the thyrotrophin-releasing hormone (TRH) was increased in all 39 patients with overt or borderline hypothyroidism and in 9 (43 %) of the 21 subjects with SAT. The individual TRH response in these two groups showed a marked overlap, but the mean response was significantly higher in overt (149.5 μU/ml) or clinically borderline hypothyroidism (99.9 μU/ml) than in SAT (35.3 μU/ml). Thus a normal basal TSH level in connection with a normal response to TRH excludes primary hypothyroidism, but nevertheless not all patients with elevated TSH values or increased responses to TRH are clinically hypothyroid.


1984 ◽  
Vol 105 (2) ◽  
pp. 179-183 ◽  
Author(s):  
Ståle Skare ◽  
Harald M. M. Frey ◽  
Ragnvald Konow-Thorsen

Abstract. Five patients are described, who developed primary hypothyroidism between 25 and 57 years of age. They were all adequately treated with l-thyroxine. Graves' disease developed six months to 34 years later. Two had TSH binding inhibiting immunoglobulin (TBII) in their serum at this stage. All were treated with carbimazole, and 3 have experienced relapse upon withdrawal. Our patients are discussed in relation to the 16 cases previously reported. The pathogenesis of this condition is open to speculation.


1986 ◽  
Vol 111 (4) ◽  
pp. 516-521
Author(s):  
Nina Clausen ◽  
Per-Eric Lins ◽  
Ulf Adamson ◽  
Bertil Hamberger ◽  
Suad Efendić

Abstract. Hypothyroidism has been alleged to modulate insulin action and influence the secretion of growth hormone and catecholamines. We recently investigated the influence of hypothyroidism on glucose counterregulatory capacity and the hormonal responses to insulin-induced hypoglycaemia in 6 patients with primary hypothyroidism (age 32–52 years, TSH-values 66–200 mU/l). Hypoglycaemia was induced in the hypothyroid state and again when the subjects were euthyroid. After an overnight fast a constant rate infusion of insulin (2.4 U/h) was given for 4 h. Glucose was measured every 15 min and insulin, C-peptide, glucagon, epinephrine, norepinephrine, growth hormone and cortisol every 30 min for 5 h. During insulin infusion somewhat higher concentrations of the hormone were obtained in the hypothyroid state and simultaneously glucose levels were 0.5 mmol/l lower. As expected, basal norepinephrine levels were higher in hypothyroidism. However, no increase in circulating norepinephrine during hypoglycaemia was registered in the two experiments. The responses of counterregulatory hormones showed an enhanced response of cortisol, similar responses of growth hormone and epinephrine while the glucagon response was paradoxically impaired. Our findings suggest that hypothyroidism alters insulin metabolism, and that the glucagon response to hypoglycaemia is impaired in this condition.


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