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  • Title: Recurrent plurihormonal bimorphous pituitary adenoma producing growth hormone, thyrotropin, and prolactin.
    Author: Felix I, Asa SL, Kovacs K, Horvath E, Smyth HS.
    Journal: Arch Pathol Lab Med; 1994 Jan; 118(1):66-70. PubMed ID: 8285835.
    Abstract:
    A 48-year-old man with visual disturbances and subtle features of acromegaly had elevated serum thyrotropin (thyroid-stimulating hormone) levels but was clinically euthyroid and initially had normal blood growth hormone (GH) levels. A computed tomographic scan documented a large pituitary tumor; he underwent incomplete transsphenoidal adenomectomy. Postoperative octreotide treatment failed to shrink the tumor. Rising GH levels necessitated repeated transsphenoidal and, subsequently, frontotemporal resection. By histology, the tumor was a chromophobic adenoma. In the first specimen, immunocytochemistry localized GH, beta-thyrotropin, and alpha-subunit of glycoprotein hormones in adenoma cells. The second specimen also contained prolactin, whereas the third contained only GH and beta-thyrotropin. By electron microscopy, the tumor was bimorphous, composed of elongated thyrotrophs and densely granulated somatotrophs. In tissue culture, the first specimen released GH, thyrotropin, and alpha-subunit and smaller quantities of prolactin; the second specimen released only GH and alpha-subunit; and the third released GH, thyrotropin, alpha-subunit, and prolactin. Incubation with somatorelin (GH-releasing hormone) variably stimulated release of all four hormones in the first and third specimens; protirelin (thyrotropin-releasing hormone) had no effect. Somatostatin consistently inhibited release of all four hormones; inhibition by bromocriptine mesylate was variable. The mild degree of clinical and biochemical acromegaly is unusual for a large macroadenoma, and the reasons for the absence of hyperthyroidism are unclear. These discrepancies may be attributed to retarded hormone release and/or synthesis due to suppression by somatostatin in vivo.
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