Lavin Chapter 12

Chapter 12 • Growth Hormone in Adults   133

Symptomatology and Physical Stigmata in Growth Hormone– Deficient Adults

TABLE 12-3

Symptoms

Signs

1. Systemic: fatigue, limited exercise capacity 2. Psychological: impaired mood and social outlook; reduced memory, well- being, and concentration; apathy 3. Sexual: diminished libido and sexual activity

1. Dyslipidemia: elevated LDL and total cholesterol; variably increased TG and reduced HDL 2. Osteopenia/osteoporosis 3. Increased (visceral) body fat; mild insulin resistance 4. Sarcopenia/muscle weakness; thinning skin 5. Reduced extracellular fluid space; less sweating 6. Diminished renal blood flow; low cardiac output; diastolic dysfunction 7. Mild anemia

HDL, high-density lipoprotein; LDL, low-density lipoprotein; TG, thyroglobulin.

J. Problems with sleep quality K. Decreased social contact L. Decreased libido M. Weight gain N. Psychological symptoms 1. Shyness 2. Withdrawal from others 3. Nervousness or anxiety 4. Sadness or depression 5. Feelings of helplessness

IX. PATHOGENESIS A. Experimental animal infarction models suggest that IGF-1 may promote survival of myocytes exposed to ischemic injury, in part by advancing glucose uptake. B. IGF-1 has also been identified as a neuroprotective agent. Low-normal levels of IGF-1 may predict increased risk of ischemic heart disease and ischemic stroke which may be associated with pituitary dysfunction, particularly GHD/gonadotropin deficiency. The higher IGF-1 levels observed in patients with better outcomes suggest a possi- ble neuroprotective role of IGF-1. Circulating IGF-1 levels may predict functional performance during rehabilitation and ischemic stroke outcome. C. The cardiovascular profile in patients with GHD demonstrated increased incidence of plaque formation, increased intima-media thickness, decreased production of nitrous oxide, abnormal lipid profile, inflammatory markers, and development of insulin resistance. Several studies demonstrated an increased stiffness of arteries in comparison with controls. Böger et al. demonstrated that GH was responsible for endothelial nitric oxide production. Nitric oxide is not only a potent vasodilator but also an inhibitor of LDL oxidation. 1. GHD may result in impaired cardiac performance manifested by a reduction in the left ventricular mass and ejection fraction, but data are inconsistent. 2. Atherosclerosis is an inflammatory process, and inflammation markers such as CRP or interleukin 6 are highly sensitive indicators of atherosclerosis. In patients with GHD, CRP may be increased. 3. Adults with GHD demonstrate alterations in plasma fibrinolytic balance, includ- ing elevated levels of plasminogen activator inhibitor 1 with decreased tissue plasminogen activator activity. These changes may contribute to the increased cardiovascular morbidity in AGHDS. 4. Some articles conclude that the beneficial effects of GH on the cardiovascular system are strongly suggestive but not completely proven.