SUPEROXIDE ANION RELEASE FROM NEUTROPHILS IN GROWTH-HORMONE DEFICIENTADULTS BEFORE AND AFTER REPLACEMENT THERAPY WITH RECOMBINANT HUMAN GROWTH-HORMONE

The observations that growth hormone primes neutrophils and stimulates various activities of monocytes suggested that it plays a role in the regulation of leukocyte biology. The in vivo reduction of growth horm one levels may be responsible for to the functional impairment of leuk ocytes observed in growth hormone deficient children. Whether leukocyt e function is impaired in growth hormone deficient adults is not known as yet. We therefore studied superoxide anion release from neutrophil s and chemotaxis of monocytes in 15 patients with adult-onset growth h ormone deficiency before and after a period of 6 months of replacement therapy with recombinant human growth hormone. Analyses were performe d by comparing functions of the leukocytes from these patients with th ose from age and sex-matched healthy control subjects. Before growth h ormone treatment, patients received appropriate replacement therapy wi th thyroid, adrenal and gonadal hormones. The dose of recombinant huma n growth hormone was 0.25-0.5 U/kg/week (0.013-0.026 mg/kg/day) throug hout the whole period of replacement therapy. In growth hormone defici ent subjects, formylpeptide-triggered release of superoxide anions fro m neutrophils was significantly suppressed by about 40% before treatme nt as compared to healthy control subjects. After 6 months of replacem ent therapy, neutrophil superoxide anion release was similar in patien ts and healthy individuals. Neither before nor after replacement thera py, however, was there a difference in monocyte migration between cont rol and growth hormone deficient subjects. These data indicate that ne utrophil function is somehow altered in growth hormone deficient patie nts, even when receiving appropriate therapy with thyroid, adrenal and gonadal hormones, but that neutrophil function can be restored to nea r normalcy by growth hormone replacement therapy. This would suggest t hat suppressed neutrophil respiratory burst is due to the deficiency i n growth hormone.