Abstract
The aim of this study was to clarify the relationship between the histological features of GH-producing adenomas surgically resected at the Toranomon Hospital and the clinical features of the patients. Histological examinations, including immunohistochemistry for anterior pituitary hormones and cytokeratin (CK), were performed on 242 consecutively excised GH-producing pituitary adenomas. Immunohistochemistry showed 45% of the adenomas to be monohormonal and 55% to be plurihormonal, producing GH-PRL (77%), GH-TSH (13%), and GH-PRL-TSH (10%). One-fourth of the monohormonal GH adenomas had a dot-like pattern of CK immunoreactivity in the majority of the tumor cells (>80%); they were significantly more common in female or younger patients and usually tended to be larger and more invasive than monohormonal GH adenomas with perinuclear CK. Interestingly, CK-immunonegative adenomas were found in only 5% of the patients; they also showed a tendency to be larger, suggesting that they are a distinct type of GH adenoma with clinically aggressive features. Serum hormone levels correlated well with tumor size only in GH-producing adenomas with a perinuclear pattern of CK immunoreactivity. Each histological subtype of adenoma, classified according to the pattern of CK immunoreactivity, was associated with distinct clinical characteristics. This information is useful for understanding the pathophysiology of acromegaly-causing GH-producing adenomas.
Highlights
Is a syndrome caused by overproduction of growth hormone (GH), which is secreted, in majority of the patients, from GH-producing pituitary adenomas [1]
We examined pathological features of pituitary adenomas surgically resected from 242 patients with clinical symptoms of acromegaly. e adenomas were subcategorized according to hormone secretion and CK distribution assessed by immunostaining
Plurihormonality is commonly observed in GHproducing adenomas, around half of which are reported to contain PRL [8]
Summary
Is a syndrome caused by overproduction of growth hormone (GH), which is secreted, in majority of the patients, from GH-producing pituitary adenomas [1]. It is well known that GH-producing pituitary adenomas o en coexpress prolactin (PRL) and, less frequently, thyroid stimulating hormone (TSH) [1]. Production of anterior pituitary hormones in nonneoplastic as well as neoplastic cells is controlled by several transcription factors and cofactors [2]. Accumulating evidence supports the hypothesis that normal and adenoma cells expressing GH, PRL, and TSH are regulated by the pituitary-speci c transcription factor-1 (Pit1) and, belong to the Pit-1 cell lineage [2,3,4,5,6,7]. Monohormonal GH-producing adenomas are classi ed in two subtypes, densely granulated (DG) and sparsely granulated (SG), based on the density of secretory granules in the cytoplasm of the adenoma cells [1, 8, 9].
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