Human growth hormone is now readily available, thanks to recombinant DNA technology. Growth hormone therapy is being advocated by some physicians for adults with growth deficiency. To determine the validity of this treatment, the following four questions must be addressed: (1) Does a growth hormone deficiency syndrome in adults exist? (2) Does growth hormone deficiency actually cause the signs and symptoms of this syndrome? (3) Is growth hormone safe and does it reduce morbidity and mortality from this syndrome? (4) Is growth hormone treatment cost-effective? Isley reviewed the current knowledge about growth hormone deficiency syndrome in adults and offers thoughts about the questions involved in adult therapy.

Hypopituitarism has been associated with increased mortality, especially from cardiovascular disease. Patients with growth hormone deficiency syndrome generally have increased fat mass and decreased lean body mass. Insulin resistance, dyslipidemia, and other factors associated with increased atherogenesis have also been associated with this syndrome. Thus, a clinical growth hormone deficiency syndrome does seem to exist. It is less clear whether this syndrome is specifically due to growth hormone deficiency or results from hypopituitarism generally. Other hormonal deficiencies and hormone replacement issues may have an impact on this syndrome and increased resultant mortality. Overtreatment of multiple hormonal imbalances can cause central obesity and atherogenic and metabolic abnormalities. It is premature to conclude that growth hormone deficiency alone is responsible for growth hormone deficiency syndrome.

Growth hormone treatment can improve body mass composition when concomitant hormone deficiencies are also treated. Observed improvements in triglyceride and high-density lipoprotein levels have been less consistent. Improved survival and long-term safety of prolonged growth hormone therapy have yet to be studied. Many of the other positive results of growth hormone treatment can be achieved with conventional methods, including statins, antiplatelet therapy, and angiotensin-converting enzyme inhibitors. Altered body composition might be more cost-effectively achieved through supervised exercise training.

The author concludes that although growth hormone deficiency syndrome probably exists, it is uncertain that growth hormone deficiency is primarily the cause of the syndrome. Further studies are needed to determine the safety of treatment and whether more cost-effective approaches to the treatment of this syndrome can be identified.

In a related article in the same journal, Cook discusses the positive value of growth hormone treatment for hypopituitarism in improving bone density and the immune system, enhancing quality of life, and improving exercise tolerance. Effort on the part of the physician is required to determine testing, dosing, and monitoring guidelines for growth hormone therapy.

In an editorial in the same journal, Frohman points out some of the remaining questions and encourages further long-term research on the efficacy of growth hormone supplementation in reducing morbidity and mortality. He concludes that growth hormone therapy is probably indicated for use in patients with severe growth hormone deficiency, but other treatments may initially be more appropriate for use in patients with less severe signs and symptoms.