ADULT GH deficiency is recognized as a specific clinical syndrome (1). Well-controlled clinical studies have shown that GH deficiency in adults is associated with a cluster of cardiovascular risk factors (2). These patients have an increased amount of body fat with an abdominal preponderance (3, 4), an increased prevalence of hypertension (5), impaired fibrinolysis (4), glucose intolerance (6), insulin resistance (7), and premature atherosclerosis (6). This cluster of cardiovascular risk factors associated with GH deficiency might explain the doubling in cardiovascular mortality observed in hypopituitary patients (8, 9). The quality of life is impaired, and there are data suggesting an increased prevalence of disability pensions among these patients (10, 11). In addition, these patients have reduced bone mineral content and density with increased prevalence of fractures (12, 13). Randomized placebo-controlled studies indicate that GH replacement therapy can reverse several of these biological changes (3, 14–18). Although these studies have been of relatively short duration, replacement therapy with GH in adults has now been approved by the regulatory authorities in Europe and the United States. The long-term experience is, however, limited.
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Bengtsson et al. (2000) studied this question.
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