RECURRENT PLURIHORMONAL BIMORPHOUS PITUITARY-ADENOMA PRODUCING GROWTH-HORMONE, THYROTROPIN, AND PROLACTIN

A 48-year-old man with visual disturbances and subtle features of acro megaly had elevated serum thyrotropin (thyroid-stimulating hormone) le vels but was clinically euthyroid and initially had normal blood growt h 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, fr ontotemporal resection. By histology, the tumor was a chromophobic ade noma. In the first specimen, immunocytochemistry localized GH, beta-th yrotropin, and alpha-subunit of glycoprotein hormones in adenoma cells . The second specimen also contained prolactin, whereas the third cont ained only GH and beta-thyrotropin. By electron microscopy, the tumor was bimorphous, composed of elongated thyrotrophs and densely granulat ed somatotrophs. In tissue culture, the first specimen released GH, th yrotropin, and alpha-subunit and smaller quantities of prolactin; the second specimen released only GH and alpha-subunit; and the third rele ased GH, thyrotropin, alpha-subunit, and prolactin. Incubation with so matorelin (GH-releasing hormone) variably stimulated release of all fo ur 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 u nusual for a large macroadenoma, and the reasons for the absence of hy perthyroidism are unclear. These discrepancies may be attributed to re tarded hormone release and/or synthesis due to suppression by somatost atin in vivo.