Incidental adenomas of the human pituitary gland.

Using conventional histological technique, we investigated 44 adenomas (31 men, 13 women) incidentally found in 36 pituitaries (25 men, 11 women) obtained from 1,117 unselected autopsies. The overall incidence of adenomas was 3.2% (men, 3.8%; women, 2.4%) without any significant sex predominance. Size, age distribution, and histological appearances of these adenomas were similar to those previously reported by others. Statistical analysis showed that the adenomas had a predilection for occurrence at the anterior margin of the gland. We further investigated 33 available adenomas with immunohistochemistry using antibodies for various adenohypophyseal hormones, S-100 protein, and glial fibrillary acidic protein, of which 6 contained growth hormone, 3 contained growth hormone and prolactin, 7 contained prolactin, 6 contained follicle-stimulating hormone, 3 contained follicle-stimulating and luteinizing hormones, 2 contained thyroid-stimulating and adrenocorticotrophic hormones (separately), and 6 contained no adenohypophyseal hormones. None of adenomas revealed neoplastic proliferation of folliculostellate cells. To investigate tumor proliferation, nucleolar organizer regions were studied in 9 adenomas using the argyrophil method. The mean number per nucleus was slightly higher than that of corresponding, nontumorous adenohypophysis at a statistically significant level. No adenoma caused symptoms of adenohypophyseal hormone abnormalities.

Immunohistochemical study of crooke's hyaline change.

Crooke's hyaline change of the human pituitary gland appears as an intracytoplasmic accumulation of fine filaments under electron microscopy. This study was attempted to identify the fine filaments by immunohistochemical methods. Twenty-eight postmortem, formalin-fixed or chrome-alum-fixed, paraffin-embedded pituitary glands revealing unequivocal Crooke's hyaline change on hematoxylin and eosin stain were selected for this study. To demonstrate Crooke's cells and fine filaments simultaneously, mirror image sections were sliced and stained with the following monoclonal antibodies using an avidin-biotin-peroxidase complex method: an antibody against synthesized adrenocorticotropic hormone 1-24, human cytokeratins (55-57 kilodalton [kd] and 68 kd), porcine vimentin (57 kd), porcine desmin (53 kd), bovine neurofilaments (70, 160, and 210 kd), human glial fibrilfary acidic protein (GFAP) (56 kd), and chicken actin. Crooke's cells showed a variable intensity of cytoplasmic staining for 55- to 57-kd cytokeratins, from focal to more even and intense staining revealing a characteristic wide brown ring around the nucleus or beneath the cell membrane. The most severely affected cells were totally replaced by dark brown reaction products with no secretory granules detectable in the cytoplasm. However, 68-kd cytokeratin could not be unequivocally demonstrated. Crooke's cells were all negative for vimentin, desmin, neurofilaments, GFAP, and actin. Thus far, it could be concluded that Crooke's hyaline change was composed of intermediate-subunit molecular weight cytokeratins that are normal constituents of the ACTH cell.

Further immunohistochemical study of crooke's hyaline change.

In a previous study, we immunohistochemically investigated Crooke's hyaline change and concluded that it was composed of cytokeratin. The present study was undertaken to further identify the cytokeratin subfamily by immunohistochemistry. Twenty-eight postmortem, routinely processed pituitary glands revealing unequivocal Crooke's hyaline change were selected. To demonstrate Crooke's cellsand cytokeratin subfamilies simultaneously, serial hori zontal sections were sliced. Using an avidin-biotin peroxidase complex method, one was stained with a monoclonal antibody against synthesized adrenocorticotropic hormone (ACTH) 1-24, and the adjacent ones were stained with one of eight test monoclonal antibodies against cytokeratin subfamilies (containing cytokeratins 1, 3, 7, 8, 13, 18, and 19, and one containing 1,5, 10, and 11, respectively). A different antibody for each type of cytokeratin was applied. Crooke's cells showed a variable intensity of cytoplasmic stainingfor antibodiesagainst cytokeratins 8 and 18 (molecular weight 52.5 and 45 kD, respectively), from focal to more even and intense staining, revealing a characteristic wide brown ring around the nucleus or under the plasmalemma. The most severely affected cells were totally replaced by dark brown reaction products with no secretory granules detectable in the cytoplasm. However, Crooke's cells did not react with other test anticytokeratin antibodies. Thus far, it can be concluded that Crooke's hyaline change was composed of low-molecular-weight cytokeratin subfamilies 8 and 18, which are found in pairs in normal ACTH cells.