Androlog Mail
Dr. Ira Sharlip presented a difficult case of secondary infertility,
azoospermia, hyperprolactinemia & decreased testosterone associated with the
development of a seminoma, that was removed. Cranial MRI, serum FSH, LH
Pre- and post-op serum beta-HCG and alpha fetoprotein have been normal.
Tumor staging showed no metastasis.
It is known that hyperprolactinemia inhibits LH-RH release, pituitary
response to LH-RH, as well as testosterone synthesis by Leydig cells.
Intratesticular testosterone is needed for initiating spermatogenesis after
being transferred inside the seminiferous tubules by an Androgen binding
protein secreted by Sertoli cells under the influence of FSH. Thus
hyperprolactinemia may explain the low T levels and diminished or arrested
spermatogenesis.
Frequently it is difficult to diagnose the cause of hyperprolactinemia. The
control of prolactin release from the pituitary is unusual as it is
controlled primarily by tonic inhibition by dopamine rather than by a
releasing factor. Thus any lesion that interrupts the flow of dopamine from
the hypothalamus down the pituitary stalk, or deplete its stores or
interrupts its production, release, or reuptake may result in elevated
prolactin levels. Early Pituitary microadenomata may also be hard to
detect.
The puzzle is; how could this be related to the seminoma? Does the seminoma
or treatments received in relation to it, affect dopamine metabolism? Stress
may also be related to elevated prolactin levels.
Treatment using Bromocryptine with close follow up of prolactin and T levels
and possibly a repeat MRI in 6 months might be a practical approach to this
difficult case. It would be very interesting to know the progress of the
case.
Sincerely,
Hussein Ghanem, M.D.
Professor of Andrology, Sexology & STDs
Cairo University, Cairo, Egypt
hmghanem@hotmail.com
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