Introduction

The importance of growth hormone (GH) deficiency (GHD) in adulthood as a disease entity first became apparent in the late 1980s when clinical studies, facilitated by the ready availability of recombinant human GH (rhGH), demonstrated the beneficial effects of GH replacement in GH-deficient adults (Jørgensen, et al., 1989; Salomon et al., 1989). It has subsequently been shown that GH-deficient adults have several abnormal clinical features including increased adiposity (Hoffman et al., 1995), reduced muscle strength and exercise capacity (Cuneo et al., 1990; Rutherford et al., 1991), reduced sweating (Juul et al., 1993) and impaired psychological well-being (McGauley et al., 1990; Rosén et al., 1994). Although such clinical characteristics have become recognized as a clinical syndrome of adult GHD (see Chapter 8), the syndrome and its components are not sufficiently distinctive to enable a confident diagnosis. Some of these features are a normal accompaniment of ageing, in particular the reduction in lean tissue mass and increase in fat mass (Forbes, 1987). In view of the non-specific clinical features of adult GHD specific biochemical criteria remain necessary for diagnosis.

There are three conventional approaches to the evaluation of GHD. These are measurement of: (i) peak GH response to provocative stimuli; (ii) measurement of spontaneous GH secretion derived from repetitive sampling over extended periods; and (iii) biological markers of integrated GH action including serum insulin-like growth factor-I (IGF-I) and IGF binding protein-3 (IGFBP-3). An evaluation of the extensive paediatric experience demonstrates poor concordance between the various tests (Bercu et al., 1986; Rose et al., 1988; Lee et al., 1990) and this has resulted in a long standing controversy as to which is the most accurate test for the diagnosis of GHD.