Therapy

Trans-sphenoidal resection of the adenoma is the preferred and most effective treatment for symptomatic NFPA, because it may improve visual field defects and permits recovery of pituitary function (83). A two-stage procedure, craniotomy followed by trans-sphenoidal resection, is often used in patients with extremely large tumors. More than 80% of patients with microadenomas are cured by surgery. On the other hand, only 15-30% of macroadenomas are completely cured. In hypogonadism, patients with NFPAs less than 40 mm in size may experience a restoration of gonadal function (31). In these patients, the normal pituitary gland is often not destroyed, and its ability to secrete gonadotropin is regained after decompression. In NFPAs larger than 40 mm, surgery may further impair hypogonadism. In fact, with these tumors, it is common to observe a decrease in testosterone levels after surgery. This reflects the difficulty in preserving or restoring anterior pituitary function in patients with large tumors (31).

However, because of their large size, surgery alone is often not curative, and pituitary irradiation is recommended for patients who have residual tumor after surgery (80).

Somatostatin and dopamine receptors have been identified in some NFPAs. This suggests that somatostatin analogs or dopamine agonists can be useful to treat refractory NFPA. However, these drugs benefit only a minority of patients, and additional studies are needed to investigate whether subgroups of patients with NFPA will respond to medical therapy (84,85).

Gonadotropin or GnRH therapy is indicated if the patient desires spermatogenesis and fertility (see Chapter 19). If fertility is not the requested outcome, testosterone is administered to stimulate virilization, improve sexual function, and maintain bone and muscle mass (see Chapter 18). In patients with multiple pituitary hormone deficiencies, replacement therapy of all deficient hormones is required for complete improvement of gonadal function. It is worth noting that cortisol therapy (10-20 mg hydrocortisone in the early morning and 5-10 mg in the afternoon or 25-37.5 mg cortisone acetate in the early morning and 12.5-25 mg in the afternoon) should be replaced first, followed by thyroxine (1-2 ^g/kg/d) and sex steroids once the patient's condition has stabilized. This is important, because thyroxine therapy can exacerbate the features of glucocorti-coid deficiency. If indicated, GH (5-10 ^g/kg/d) can be administered as well (86).

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