Hypersecretion of LH and FSH by a Pituitary Adenoma

Snyder, Peter J.; Sterling, Francis H.

doi:10.1210/jcem-42-3-544

Cited by 94 publications

(24 citation statements)

References 23 publications

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“…The present study confirms and extends previous reports (3,6,34) in that a large proportion of pituitary tumors have been shown to contain more titan one hormone. However, tumors associated with Cushings's disease contained only ACTH cells and not all tumors contained 0-LPH.…”

Section: Discussionsupporting

confidence: 93%

Multihormonal Pituitary Adenomas

Heitz¹

1979

Horm Res

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66 pituitary tumors detected at autopsy were investigated for the presence of corticotropin, β-lipotrophin, growth hormone, prolactin, thyrotropin and gonadotropins by immunocytochemistry. 56 tumors contained hormone-producing cells; 45 were found to contain 2 or more hormones. This finding confirms and extends previous morphologic and clinical observations. The majority of pituitary tumors are mixed and they probably arise from impaired regulation at the hypothalamic and/or pituitary level.

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Section: Discussionsupporting

confidence: 93%

Multihormonal Pituitary Adenomas

Heitz¹

1979

Horm Res

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“…In our patient, the ®nding of LH immunologically within the tumour tissue and in the adenoma cell culture suggest that LH was produced and probably secreted by the tumour (13). The paradoxical response of LH to TRH stimulation in vivo is further evidence that supports LH secretion by the gonadotroph adenoma (14,15). Following LHRH administration, a markedly increased LH response was seen.…”

Section: Discussionsupporting

confidence: 61%

Evolution of clinical symptoms in a young woman with a recurrent gonadotroph adenoma causing ovarian hyperstimulation

Pentz-Vidovic

Škorić

Grubišić

et al. 2000

European Journal of Endocrinology

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Objective: To demonstrate the clinical course in a young female with gonadotroph adenoma causing ovarian stimulation. Patient and methods: Our patient was a 23-year-old woman with a history of oligomenorrhea who had previously undergone bilateral ovarian wedge resection owing to the clinical appearance of polycystic ovaries. Two years later, she sought treatment for headache, galactorrhea, history of spotting and lower abdominal distension. FSH, LH, b-LH, inhibin A and B, estradiol, prolactin (PRL), and bchorionic gonadotrophin (b-CG) were measured, and the responses of FSH, LH and b-LH to thyrotrophin-releasing hormone (TRH) were documented. Immunohistochemical analysis of the tumor tissue was performed after surgery. Five years after the trans-sphenoidal surgery, the patient again became oligomenorrheic. A large recurrent adenoma was diagnosed on CT one year later. Transvaginal ultrasound showed ovaries of normal size with multiple small cystic formations simulating a polycystic pattern, While the patient was awaiting surgery, a pituitary apoplexy occurred. Emergency decompressive surgery was performed and the patient fully recovered. Results: Enlarged ovaries were found on ultrasound examination simulating a hyperstimulationlike pattern. At that time, elevated levels of FSH (13.4 IU/l) and marginally elevated levels of b-LH (1.43 ng/ml) were found, whereas the level of LH (0.5 IU/l) was subnormal. Plasma estradiol was markedly supranormal (6150 pmol/l). Levels of inhibin A and B were elevated (326 pg/ml and 588 pg/ml respectively). The prolactin level (70 ng/ml) was increased, whereas b-chorionic gonadotrophin (b-CG) was normal. Signi®cantly increased FSH, LH, and b-LH responses to TRH stimulation were documented. Pituitary macroadenoma was found on MRI scan and removed by trans-sphenoidal surgery. Immunohistochemical examination showed high positivity for b-CG and LH, and slight positivity for FSH. Five years after the surgery, estradiol was elevated (1160 pmol/l), whereas basal levels of LH (4.65 IU/l) and FSH (3.98 IU/l) were not suppressed. After the second operation, immunostaining of the adenoma tissue con®rmed the previous ®ndings. Conclusions: Measurement of gonadotrophins in our case did not prove to be a method for identifying a large recurrent gonadotroph pituitary adenoma. The sonographic ovarian imaging varied from a polycystic-to an ovarian hyperstimulation-like pattern during the evolution of the tumour.

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“…In several of the adenomas, hormones other than those increased in the serum were also detected, as reported elsewhere [3,7,10,27], However, this was the case in only a few cells and might explain why these hormones were not found to be elevated in serum above the upper limit of the normal range. It must also be considered that these cells cannot release their hormonal content, at least not in such a way that it reaches the circulating blood.…”

Section: Discussionsupporting

confidence: 66%

Immunohistochemical Examination of Pituitary Adenomas

et al. 1985

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A comparison was made with the data of 62 cases of pituitary adenoma, evaluated pre- and postoperatively, including as well the results of immunohistochemical hormone examination (also for calcitonin). Prolactin was found in 18 of the 21 adenomas carrying the preoperative diagnosis of prolactinoma, whereas cells containing other hormones (growth hormone, LH, FSH, TSH, ACTH, β-endorphin), were only occasionally present. The growth hormone was strongly positive in the adenoma tissue in 16 of the 17 cases of acromegaly. 5 of these adenomas were accompanied by a marked hyperprolactinemia and also contained many prolactin cells. 6 of the 19 adenomas diagnosed as being ‘inactive’ contained hormone-positive cells, but only a very small number of cells. ACTH was found in 3 of the 4 pituitary adenomas of patients with Cushing’s disease. 2 of these were also positive for β-endorphin. The tissue of 1 gonadotrophic adenoma (with elevated FSH in serum) gave positive results with an anti-LH antiserum. Calcitonin was not found in any adenoma. The preoperative serum prolactin levels did not quantitatively correlate with the percentage of prolactin-positive cells.

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Hypersecretion of LH and FSH by a Pituitary Adenoma

Cited by 94 publications

References 23 publications

Multihormonal Pituitary Adenomas

Multihormonal Pituitary Adenomas

Evolution of clinical symptoms in a young woman with a recurrent gonadotroph adenoma causing ovarian hyperstimulation

Immunohistochemical Examination of Pituitary Adenomas

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