Background

Growth hormone (GH) deficiency (GHD) in adults (GHDA) is now fully recognized as a specific clinical syndrome (Cuneo et al., 1992). Thus, this syndrome is associated with a decreased pychological well-being (McGauley et al., 1990; Rosén et al., 1994b), an abnormal body composition (Binnerts et al., 1992; Rosén et al., 1993a), reduced bone mineral content (Rosén et al., 1993c), with an increased fracture frequency (Rosén et al., 1997), impaired cardiac function (Shahi et al., 1991), and a decrease in exercise capacity (Cuneo et al., 1991). Furthermore, GHDA has been associated with a disturbed lipoprotein pattern (Rosén et al., 1993b), impaired glucose-homeostasis (Johansson, J.-O. et al., 1995) and fibrinolysis (Johansson J.-O. et al., 1994), and increased cardiovascular mortality (Rosén & Bengtsson, 1990).

This review will address the consequences of GHDA on cardiovascular risk factors and the effects of the following rhGH treatment.

Cardiovascular mortality

Untreated GHDA seems to be associated with a premature cardiovascular and cerebrovascular mortality. In a retrospective study of 333 patients with hypopituitarism on routine replacement therapy diagnosed between 1956 and 1987, there was a twofold increase in deaths from cardiovascular disease among patients compared with controls (Rosén & Bengtsson, 1990). No relationship was found between increased death rate and variables such as age at diagnosis, calendar year, sex, time before and after diagnosis, prevalence of hypertension or diabetes mellitus. In another retrospective cohort study from southern Sweden, 344 patients with hypopituitarism, diagnosed between 1952 and 1992, the cardiovascular mortality was likewise increased in patients compared with the control population (Bülow et al., 1997).