تكمله العلاج
Women — Women who have hypogonadism, ie, are deficient in estradiol and progesterone, and who are not interested in fertility, can be treated with estrogen-progestin replacement therapy. (See "Preparations for postmenopausal hormone therapy"). In women over age 50, the considerations for hormone therapy are the same as for women who undergo a natural menopause. (See "Postmenopausal hormone therapy: Benefits and risks"). The choice of treatment does not differ from that in women with primary hypogonadism.

Women with secondary hypogonadism who wish to become fertile may be treated with pulsatile GnRH or gonadotropins. (See "Congenital gonadotropin-releasing hormone deficiency (idiopathic hypogonadotropic hypogonadism) in adults", section on Treatment and see "Overview of ovulation induction", sections on Gonadotropin therapy and Pulsatile GnRH therapy).

Serum androgen concentrations in women with hypopituitarism, particularly those with both gonadotropin and ACTH deficiency, are significantly lower than those in normal control women [4]. In a study of women with testosterone deficiency due to hypopituitarism, who were taking exogenous estrogen orally, testosterone replacement transdermally at doses of 150 to 300 mcg/day for one year increased the serum free testosterone into the normal range, and increased mean bone mineral density of the hip and radius, but not the spine [5]. This treatment also increased fat-free mass and thigh muscle area but not fat mass. Treatment also improved some aspects of mood, sexual function, and quality of life, as assessed by questionnaires. Cognitive function was unchanged. One third of the women receiving testosterone developed acne but no patients developed hirsutism or other hyperandrogenic side effects.

GROWTH HORMONE DEFICIENCY — The availability of several recombinant human growth hormone preparations (Humatrope®, Nutropin®, Serostim®, and Genotropin®) for treating adults with growth hormone deficiency allows physicians in the United States to prescribe this treatment. Patients with GH deficiency acquired as an adult must meet at least two criteria for therapy: a poor GH response to at least two standard stimuli; and hypopituitarism due to pituitary or hypothalamic damage. The criteria are different in children in whom GH is required for normal growth. (See "Treatment of growth hormone deficiency in children").

Patients who develop GH deficiency in adulthood have unfavorable serum lipid profiles, increased body fat, decreased muscle mass, decreased bone mineral density, and a diminished sense of well-b****. There is substantial evidence that growth hormone treatment in these patients increases muscle mass and reduces body fat. The evidence for improvement in bone mineral density is less convincing, and the evidence concerning improvements in the sense of well-b****, muscle strength, and serum lipids is conflicting. Thus, we do not recommend recombinant human growth hormone as routine treatment for all patients with adult-onset growth hormone deficiency. (See "Growth hormone deficiency in adults").

PROLACTIN DEFICIENCY — The only known presentation of prolactin deficiency is the inability to lactate after delivery (for which there is currently no available treatment).

SUMMARY — Treatment of patients with hypopituitarism is the sum of the treatments of each of the individual pituitary hormonal deficiencies detected when a patient with a pituitary or hypothalamic disease is tested. The treatments of corticotropin (ACTH), thyroid-stimulating hormone (TSH), and luteinizing hormone (LH) and follicle-stimulating hormone (FSH) deficiencies are in many ways the same as the treatments of primary deficiencies of the respective target glands, but in other ways they differ.

Lack of ACTH primarily induces cortisol deficiency. Treatment consists of the administration of hydrocortisone or other glucocorticoid in an amount and timing to mimic the normal pattern of cortisol secretion (see "ACTH deficiency" above and see "Treatment of adrenal insufficiency").
TSH deficiency, which results in thyroxine (T4) deficiency, is treated with L-thyroxine. The goal of therapy should be a normal serum T4 value. T4 should not be administered until adrenal function, including ACTH reserve, has been evaluated and either found to be normal or treated. Measurement of serum TSH cannot be used as a guide to the adequacy of L-thyroxine replacement therapy. (See "TSH deficiency" above and see "Central hypothyroidism").
In men with gonadotropin deficiency, testosterone replacement is indicated when fertility is not desired. (See "Testosterone treatment of male hypogonadism"). Men with secondary hypogonadism who wish to become fertile may be treated with gonadotropins, if they have pituitary disease or with either gonadotropins or gonadotropin-releasing hormone (GnRH) if they have hypothalamic GnRH deficiency. (See "Induction of fertility in men with secondary hypogonadism").
In women with gonadotropin deficiency, treatment depends upon the patient's goals. Estrogen and progestin replacement is indicated in women who are not pursuing fertility, while gonadotropin or pulsatile GnRH therapy may be used when ovulation induction and fertility are the goal. (See "Postmenopausal hormone therapy: Benefits and risks" and see "Overview of ovulation induction").
We currently do not recommend recombinant human growth hormone as routine treatment for all patients with adult-onset growth hormone deficiency. This issue is reviewed in detail elsewhere. (See "Growth hormone deficiency in adults").