Introduction

Growth hormone (GH) deficiency (GHD) in childhood has been recognized and treated since the 1960s. Diagnostic features include shortness of stature, slow linear growth rate, mildly delayed bone age with reduced bone density, excess adiposity with a predominantly truncal distribution, reduced lean tissue mass and fasting hypoglycaemia (Collip et al., 1973; Hopwood et al., 1975; Tanner et al., 1977; Milner et al., 1979; Parra et al., 1979; Shore et al., 1980). These effects reflect the known metabolic actions of GH (Davidson, 1987; Press, 1988); GH promotes long bone growth, anabolism and lipolysis, and has complex actions on carbohydrate metabolism which can be summarized as insulinotropic and insulin antagonistic.

While short stature provides a hallmark feature of GHD in childhood, patients with adult onset GHD have normal stature, which may have left investigators assuming GH had no role in adult medicine. The syndrome of GHD in adults may also have been overlooked because adults who developed hypopituitarism from the mass effects of a pituitary tumour or radiotherapy survived, often returning to reasonably functional lives with conventional pituitary hormone replacement therapy. With the introduction of recombinant DNA technology, availability of sufficient authentic sequence human GH (rhGH) has permitted an explosion of interest in adults with GHD starting in the 1980s. The aim of this chapter is to summarize the spectrum of characteristics of adults with GHD (Cuneo et al. 1992a; Cuneo, Salomon & Sönksen, 1996). Descriptions of GH treatment effects will only be mentioned to support conclusions based on cross-sectional studies of adults with GHD, given the extensive coverage elsewhere in this volume.