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The immunoprofile of 76 human pituitary adenomas was studied with particular reference to the occurrence of entrapped, non-neoplastic pituitary cells. This phenomenon was defined as unevenly distributed, usually peripherally located cells forming less than 1% of the total cell population. The stellate contour of such passively incorporated cells departed from the more rounded shape of most principal, neoplastic cells. Thirty-six of the adenomas studied comprised one or more types of entrapped elements. According to the hormone produced, prolactin-(PRL-)cells most commonly occurred as a minor "foreign" component (seen in 23 of the adenomas), whereas growth hormone-(GH-) and adrenocorticotropic hormone-(ACTH-)cells rarely were trapped (seen in 5 and 4 of the adenomas. Entrapped follicle stimulating hormone-(FSH-), luteinizing hormone-(LH-), and thyroid-stimulating hormone-(TSH-)cells assumed an intermediate position (seen in 14, 17 and 15 of the adenomas, respectively).

Silent pituitary adenomas were compared with hormonally active tumors taking into account the size, number, and ultrastructural characteristics of secretory granules (SG). The study group (a total of 79 primary pituitary adenomas) comprised 27 silent, 21 growth hormone (GH)-producing-, 16 prolactin (PRL)-producing-, 5 GH-PRL-producing- and 10 adrenocorticotropic hormone (ACTH)-producing adenomas. The SG of silent adenomas were significantly smaller than SG in endocrine active adenomas. All hormonally inactive tumors also contained small (mean, 94 nm) specific cytoplasmic granules, designated "silent adenoma granules" (SIG). The fine structural features of the SIG included: a flocculent, granular material occupying an eccentric position in a larger vesicle limited by a double membrane. In the silent adenomas this particular granule was present in up to 90% of the adenoma cells and constituted approximately 10 to 50% of the granules in each cell. These granules were not seen in hormonally active tumors and considered therefore diagnostic of silent pituitary adenomas.

A 54-year-old man with a long-lasting left-sided headache and biochemical evidence of hyperprolactinemia was found to have a large chromophobe pituitary adenoma, which concurred with a granulomatous hypophysitis. The mechanism of the inflammatory reaction is discussed and the immunohistochemical and ultrastructural findings of this hitherto undescribed combination of lesions are presented.

Thirty cases of silent pituitary adenomas were studied clinico-morphologically and classified into 4 groups according to their fine structural characteristics. Tumors poor in organelles (7 cases) and typical oncocytomas (6 cases) produced pituitary insufficiency significantly more frequently than did tumors with moderately oncocytic changes (10 cases) and non-oncocytic, organelle-rich adenomas (7 cases). The latter 2 groups were more prone to proliferate suprasellarly. Postoperative, short-term follow-up studies showed that intrasellar disease was common in all groups, whereas suprasellar disease was more frequent among the latter 2 than in the former 2 types of adenomas. Hence, it seems possible from the fine structure to deduce a subgrouping of clinical significance.

Light bodies are large cytoplasmic granules originally described in the gonadotrophic cells of the rat pituitary gland. In order to determine whether similar bodies occur in the human anterior pituitary gland, 89 pituitary adenomas and periadenomatous tissue from 20 cases were examined by transmission electron microscopy. Double membrane bound bodies with filamentous internal structure identical to rodent light bodies were identified in 10 hormone-producing adenomas: 5 PRL, 1 PRL-GH, 2 GH, and 2 ACTH-producing tumours. No light bodies were found in the remaining 79 tumours nor in the pituitary cells in periadenomatous tissue from 20 cases. These results show that some human pituitary adenomas may contain light bodies identical to those seen in gonadotrophs of rat pituitary.

Thirty-eight human pituitary adenomas (24 endocrine active and 14 endocrine inactive tumors) were studied immunohistochemically for the presence of the basement membrane component, laminin, and ultrastructurally for the presence of basement membrane. Immunoreactivity of laminin delineated staining of epithelial and endothelial basement membranes, the reaction product being confined mostly to the perivascular zones. Moreover, a hitherto undescribed presence of intercellular laminin-positive droplets was observed in ten of the active adenomas (nine patients with hyperprolactinemia and/or acromegalia and one patient with Cushing's syndrome). Concurrently, at the ultrastructural level, bunches of basement membrane-like material intermingled between the adenoma cells were demonstrated in seven of these ten active adenomas. Furthermore, secretory granules were entrapped occasionally in this intercellular matrix, indicating a mutual dependence between excessive hormone extrusion and an increase of "misplaced" deposits of basement membrane components, e.g., laminin.