Clinically nonfunctioning pituitary adenomas (NFPAs) represent approx 25-30% of pituitary tumors and are the most commonly encountered macroadenomas (78-80). Hypogonadism is present in approximately half of the patients with NFPA, 50% of whom have mild hyperprolactinemia (31), reflecting stalk compression that might contribute to impaired gonadal function.
The majority of nonfunctional tumors are inefficiently secreting rather than nonse-creting. They usually synthesize and immunostain for FSH and/or LH and/or free a-subunits and P-subunits. The gonadal dysfunction in males with NFPA is primarily related to intrasellar expansion of the tumor with compression of residual glandular tissue (31). In fact, NFPAs usually are macroadenomas, causing hypopituitarism by both direct compression of the portal vessels that limits delivery of hypothalamic releasing factors and focal ischemic necrosis of the normal pituitary tissue. LH secretion is impaired in approx 53% of NFPAs (78,81,82). However, disruption of ACTH, thyroid-stimulating hormone (TSH), and GH secretion may further inhibit gonadal function. In fact, corticotropin releasing factor (CRF)/ACTH/cortisol, thyroid hormones, and GH/IGF-1 modulate spermatogenesis and steroidogenesis.
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