Abstract #847: Clinical Acromegaly Without Pituitary Adenoma

2017 ◽  
Vol 23 ◽  
pp. 187
Author(s):  
Mindy Griffith ◽  
Padma Raghavan ◽  
Monica Schwarcz ◽  
Michael Goldberg ◽  
Guy Valiquette ◽  
...  
Keyword(s):  
Author(s):  
Eva Horvath ◽  
Kalman Kovacs ◽  
B. W. Scheithauer ◽  
R. V. Lloyd ◽  
H. S. Smyth

The association of a pituitary adenoma with nervous tissue consisting of neuron-like cells and neuropil is a rare abnormality. In the majority of cases, the pituitary tumor is a chromophobic adenoma, accompanied by acromegaly. Histology reveals widely variable proportions of endocrine and nervous tissue in alternating or intermingled patterns. The lesion is perceived as a composite one consisting of two histogenetically distinct parts. It has been suggested that the neuronal component, morphologically similar to secretory neurons of the hypothalamus, may initiate adenoma formation by releasing stimulatory substances. Immunoreactivity for growth hormone releasing hormone (GRH) in the neuronal component of some cases supported this view, whereas other findings such as consistent lack of growth hormone (GH) cell hyperplasia in the lesions called for alternative explanation.Fifteen tumors consisting of a pituitary adenoma and a neuronal component have been collected over a 20 yr. period. Acromegaly was present in 11 patients, was equivocal in one, and absent in 3.


2016 ◽  
Vol 77 (S 01) ◽  
Author(s):  
Martin Rutkowski ◽  
Ryan Alward ◽  
Derek Southwell ◽  
Rebecca Chen ◽  
Jeffrey Wagner ◽  
...  

2016 ◽  
Vol 77 (S 02) ◽  
Author(s):  
Yuta Murakami ◽  
Shinya Jinguji ◽  
Yugo Kishida ◽  
Taku Sato ◽  
Tadashi Watanabe ◽  
...  

2016 ◽  
Vol 77 (S 02) ◽  
Author(s):  
Sivashanmugam Dhandapani ◽  
Pinaki Dutta ◽  
Tenzin Gyurmey ◽  
Reema Bansal ◽  
Ashis Pathak ◽  
...  

2016 ◽  
Vol 77 (S 02) ◽  
Author(s):  
Yoshikazu Ogawa ◽  
Kenichi Sato ◽  
Yasushi Matsumoto ◽  
Teiji Tominaga

1990 ◽  
Vol 29 (01) ◽  
pp. 40-43 ◽  
Author(s):  
W. Langsteger ◽  
P. Költringer ◽  
P. Wakonig ◽  
B. Eber ◽  
M. Mokry ◽  
...  

This case report describes a 38-year-old male who was hospitalized for further clarification of clinically mild hyperthyroidism. His increased total hormone levels, the elevated free thyroid hormones and the elevated basal TSH with blunted response to TRH strongly suggested a pituitary adenoma with inappropriate TSH incretion. Transmission computed tomography showed an intrasellar expansion, 16 mm in diameter. The neoplastic TSH production was confirmed by an elevated alpha-subunit and a raised molar alpha-sub/ATSH ratio. However, T4 distribution on prealbumin (PA, TTR), albumin (A) and thyroxine binding globulin (TBG) showed a clearly increased binding to PA (39%), indicating additional prealbumin-associated hyperthyroxinemia. The absolute values of PA, A and TBG were within the normal range. After removal of the TSH-producing adenoma, basal TSH, the free thyroid hormones and T4 binding to prealbumin returned to normal. Therefore, the prealbumin-associated hyperthyroxinemia had to be interpreted as a transitory phenomenon related to secondary hyperthyroidism (T4 shift from thyroxine binding globulin to prealbumin) rather than a genetically conditioned anomaly of protein binding.


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