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Gonadal impairment secondary to nonpituitary intrasellar and parasellar masses may recover after treatment of the lesion. The choice of treatment depends on the nature of the disease. However, surgery represents the first option in most cases. Surgical treatment generally involves trans-sphenoidal decompression of the mass, when possible, attempting to limit damage and restore normal function of the pituitary gland. Contraindications to the trans-sphenoidal approach include dumb-bell tumors and inaccessible extrasellar extension (18).

Radiotherapy is recommended for residual tumor after surgery and for brain metastases. Medical therapy is not generally performed with dysgerminomas or metastatic lesions that require radiotherapy and chemotherapy, respectively, and hamartomas producing GnRH that respond to treatment with GnRH analogs. Long-acting GnRH analogs suppress gonadotropin secretion but do not affect the tumor. However, GnRH analogs may be the logical therapeutic option if the hamartoma does not cause other complications related to mass effects, because surgery may not be curative or may result in extensive complications, including fatality (89).

When hypogonadism persists after surgical treatment or remains after conventional treatment, androgen replacement therapy is used to restore physiologic serum concentrations of testosterone. If fertility is desired, Leydig cell function is stimulated by the

Table 4

Nontumorous Causes of Acquired Hypogonadotropic Hypogonadism

Pituitary apoplexy

Empty sella syndrome


Pituitary abscess



Giant cell granuloma

Lymphocitic hypophysitis

Histiocytosis X


Arachnoid cyst


Postsurgery/irradiation Head trauma administration of hCG. Spermatogenesis may be restored; however, human follicle-stimulating hormone (hFSH) is sometimes necessary as well (19). In patients with hypopituitarism, adequate replacement therapy further improves gonadal function.

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