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Growth Hormone Deficiency in Adults

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Growth Hormone Deficiency in Adults ROUNDTABLE PROCEEDINGS Clinical Presentation and Diagnosis: Growth Hormone Deficiency in Adults Gary Owens, MD; Donald Balfour, MD, FACP; Beverly MK Biller, MD; Jay Cohen, MD, FACE; Michael Jacobs, RPh; Michael Lease, MS, PharmD, FASCP; Rajendra Ratnesar, MD; Kenneth L. Schaecher, MD; and David E. Wilcox, MD, FACEP n the United States, growth hormone mammary glands to stimulate milk produc- deficiency (GHD) affects 50 000 adults, tion; adrenocorticotropic hormone, which Iwith 6000 new cases yearly.1 Patients targets the adrenal cortex to cause glucocor- with GHD have decreased or absent growth ticosteroid production; thyrotropin influ- hormone (GH) production as a result of ences the production of thyroid hormones; hypothalamic or pituitary disorders result- thyroid stimulating hormone (TSH) targets ing in underactive pituitary gland function the thyroid; and, finally, GH (also called (ie, hypopituitarism). GHD is distinct from somatotropin), which targets many tissues to somatopause, a term that describes the grad- promote growth and control protein, lipid, ual decline in GH production through nor- and carbohydrate metabolism. Of all the mal adulthood. Adults with hypopituitarism anterior pituitary hormones, only GH and routinely receive replacement cortisol, thy- PRL act independently and not through a tar- roid hormone, and gonadal hormone get endocrine gland. The effects of an excess replacement therapy. Until the past decade, or deficiency in hormone production are list- GH replacement therapy had been primarily ed in Table 1. The typical managed care reserved for pediatric use. GHD in adults, organization formulary includes drug thera- however, represents a serious clinical disor- pies for all of the hormone deficiency states, der, which is distinct from pediatric GHD and for several of the hormone excess states. and can be treated with recombinant human The pituitary is the master gland, but it is GH replacement therapy. also controlled by hormones originating in GH is produced in the pituitary gland, the hypothalamus, an area of the brain just which is located at the base of the brain above the pituitary. Anatomically linked to behind the sphenoid sinus in a small bony the pituitary through a funnel-shaped struc- cavity called the sella turcica (Figure 1). The ture called the infundibulum, the hypothala- pituitary gland secretes hormones from 2 mus controls pituitary function by secretion distinct lobes, each derived from different of releasing and inhibiting factors. GH re- embryonic tissue (Figure 2). These hor- lease is stimulated by GH-releasing hormone mones affect numerous body systems. (GHRH) and inhibited by somatostatin. The posterior lobe of the pituitary gland, During a 24-hour period, pulses of GHRH an extension of the hypothalamus, secretes and somatostatin stimulate or inhibit the 2 hormones: arginine vasopressin (also pituitary to release GH in discrete bursts, called antidiuretic hormone), which stimu- with a distinct diurnal phase resulting in lates the kidney to reduce urine output, and most of the 24-hour GH secretion during oxytocin, which causes uterine contrac- sleep. Most healthy individuals, therefore, tions. The anterior lobe secretes 6 hor- have little measurable GH secreted during mones: luteinizing hormone, which much of the daylight hours. Measurement of stimulates the secretion of sex steroids from a single blood sample for GH is therefore not the gonads; follicle-stimulating hormone, helpful in making the diagnosis of GH excess which stimulates ovulation and sperm pro- or deficiency. When GH deficiency is con- duction; prolactin (PRL), which targets the sidered, stimulation testing (sometimes S424 THE AMERICAN JOURNAL OF MANAGED CARE OCTOBER 2004 Clinical Presentation and Diagnosis: Growth Hormone Deficiency in Adults Figure 1. Pituitary Gland Pituitary Gland Pituitary Gland Source: Acromegaly by AG Harris, 2001. Figure 2. Hypothalamic-pituitary Hormone Relationships Pituitary Target Principal Hormone Organ Effect TSH Thyroid Hormone Production ACTH Cortisol Production Anterior Pituitary Somatotropin (Adenohypophysis) (GH) Growth, Glucose Production TRH Prolactin CRH Milk Production GHRH Dopamine GnRH FSH/LH Estrogen, Progesterone, Testosterone Hypothalamus Oxytocin Uterine Posterior Pituitary Contractions (Neurohypophysis) Milk Let-down ADH Water Balance TRH indicates thyrotropin-releasing hormone; CRH, corticotropin-releasing hormone; GHRH, growth hormone releasing hormone; GnRH, gonadotropin-releasing hormone, TSH, thyroid-stimulating hormone; ACTH, adrenocorti- cotropic hormone; FSH, follicle-stimulating hormone; LH, luteinizing hormone; ADH, antidiuretic hormone. Adapted from Acromegaly by AG Harris, 2001. VOL. 10, NO. 13, SUP. THE AMERICAN JOURNAL OF MANAGED CARE S425 ROUNDTABLE PROCEEDINGS gies for GHD in adults. Table 2 describes the Table 1. Pituitary Dysfunction causes of pituitary or hypothalamic damage Hormone Excess Hormone Deficiency that results in a decrease in GH secretion. The majority of patients with pituitary hor- ■ Hyperprolactinoma ■ Absence of postpartum lactation mone abnormalities present initially with a ■ Acromegaly ■ Hypogonadism (GnRH or LH/FSH) pituitary tumor or other sellar lesions. ■ Cushings disease ■ GHRH or GH deficiency (GH/IGF-I) Pituitary tumors may secrete an excess of 1 ■ Hyperthyroidism ■ Hypoadrenalism (cortisol) pituitary hormone or be clinically nonfunc- ■ Syndrome of Inappropriate (CRH or ACTH) tioning, producing clinical problems by mass ■ Antidiuretic Hormone Hypothyroidism (thyroxine) effect, such as headaches or visual field (SIADH) (TRH or TSH) abnormalities accused by compression of ■ Diabetes insipidus (AVP) the optic chiasm. Pituitary hormone defi- ciencies may be secondary to compression GnRH indicates gonadotropin-releasing hormone; LH, luteinizing hormone; of the normal gland by a cyst or tumor, or FSH, follicle-stimulating hormone; GHRH, growth hormone releasing hor- from treatment of the tumor, which may mone; GH, growth hormone; IGF-1, insulin-like growth factor 1; CRH, cor- include surgery and radiation. Hypopitui- ticotropin-releasing hormone; ACTH, adrenocorticotropic hormone; TRH, tarism may also result from other causes, thyrotropin-releasing hormone; TSH, thyroid-stimulating hormone; AVP, such as head trauma, infiltrative hypothala- arginine vasopressin. mic disorders, or infection. In addition, for termed “provocative testing” or “dynamic some children with GHD, the disorder per- hormone testing”) is usually performed. sists in adulthood. When GH enters the circulatory system it In adults, GHD can produce metabolic dis- attaches to GH receptors in virtually all body turbances that may compromise the patient’s tissue to produce and stimulate local insulin- health and quality of life and increase cardio- like growth factor 1 (IGF-1) production. At vascular (CV) risk. The most salient features the tissue level, many of the effects of GH of GHD in adults include decreased lean body are mediated by IGF-1. In addition, regula- mass, increased visceral fat and subcutaneous tion of GH production by the pituitary is fat, decreased bone mass, and hyperlipi- controlled by negative feedback from IGF-1. demia.2 GHD has been linked to a higher risk The level of GH production normally of bone fractures, an increase in carotid varies among individuals and groups of artery intimal thickness, and elevations in individuals. For example, premenopausal certain markers of CV risk, among them C- women produce more GH, and, as people reactive protein and homocysteine. It has age, production of GH gradually declines. been shown that the degree of elevation in Further, the extent of excessive visceral fat lipid level3 and the severity of bone mineral is negatively correlated with GH production, loss correlate with the severity of GHD.4 whereas exercise appears to be positively Epidemiologic studies have clearly shown correlated.2 There are many different etiolo- that adults with hypopituitarism, including GHD, display an increased risk for CV and cerebrovascular disease and premature mor- Table 2. Etiology of Adult GHD tality (Figure 3).5,6 In the transitional patient, GHD can ■ Pituitary disease induce deleterious metabolic events similar • Tumors, sellar masses/cysts • Post irradiation to those in adults. A 2-year, placebo-con- • Post surgery trolled trial examined 64 young adults • Apoplexy (mean age, 23 years) who had pediatric ■ Hypothalamic disease GHD, current GH levels of less than 5 µg/L, and were not taking GH for an average of 5.6 ■ Craniopharyngioma years.7 At baseline, 22% of these patients ■ Head trauma demonstrated evidence of below average ■ Childhood-onset bone mineral density, 59% were overweight or obese, and 45% had total cholesterol lev- GHD indicates growth hormone deficiency. els of more than 200 mg/dL. S426 THE AMERICAN JOURNAL OF MANAGED CARE OCTOBER 2004 Clinical Presentation and Diagnosis: Growth Hormone Deficiency in Adults For the clinician, diagnosing GHD can be a daunting process. Because GH is secreted Figure 3. Hypopituitarism and Mortality in a diurnal pulsatile manner and has a short 120 half-life of only 19 minutes, it is frequently Observed undetectable in blood samples without Expected provocative testing. Numerous pharmaco- 100 logic agents can be used to assess GH pro- 80 duction and secretion by the pituitary in adults (Table 3). These include insulin, argi- 60 nine, levodopa (L-dopa), arginine plus L- 40 dopa, arginine plus GHRH, and the glucagon of Deaths No. test. None display perfect sensitivity
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