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Superoxide anion release from neutrophils in growth hormone deficient adults before and after replacement therapy
N Reinisch1, P Schratzberger, G Finkenstedt
1Department of Internal Medicine, University of Innsbruck, Austria.
Insights
Growth hormone deficiency impairs neutrophil function in adults, but replacement therapy restores superoxide anion release. Monocyte function remained unaffected in these patients.
Area of Science:
- Immunology
- Endocrinology
Background:
- Growth hormone (GH) influences leukocyte biology.
- GH deficiency in children is linked to impaired leukocyte function.
- Leukocyte function in adults with GH deficiency is not well understood.
Purpose of the Study:
- To investigate leukocyte function in adults with GH deficiency.
- To assess the impact of recombinant human growth hormone (rhGH) replacement therapy on neutrophil and monocyte function.
Main Methods:
- Studied superoxide anion release from neutrophils and monocyte chemotaxis in 15 adult GH-deficient patients.
- Compared patient function before and after 6 months of rhGH therapy to age/sex-matched controls.
- Ensured patients received adequate thyroid, adrenal, and gonadal hormone replacement.
Main Results:
- Neutrophil superoxide anion release was significantly suppressed (~40%) in GH-deficient patients before treatment compared to controls.
- Following 6 months of rhGH therapy, neutrophil superoxide anion release normalized in patients.
- No significant differences in monocyte migration were observed between patients and controls, either before or after rhGH treatment.
Conclusions:
- Adult-onset GH deficiency alters neutrophil function, specifically suppressing the respiratory burst.
- Growth hormone replacement therapy can restore neutrophil function to near-normal levels.
- Monocyte chemotaxis appears unaffected by GH deficiency in adults.
Abstract:
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 hormone levels may be responsible for to the functional impairment of leukocytes observed in growth hormone deficient children. Whether leukocyte function is impaired in growth hormone deficient adults is not known as yet. We therefore studied superoxide anion release from neutrophils and chemotaxis of monocytes in 15 patients with adult-onset growth hormone deficiency before and after a period of 6 months of replacement therapy with recombinant human growth hormone. Analyses were performed by comparing functions of the leukocytes from these patients with those from age and sex-matched healthy control subjects. Before growth hormone treatment, patients received appropriate replacement therapy with thyroid, adrenal and gonadal hormones. The dose of recombinant human growth hormone was 0.25-0.5 U/kg/week (0.013-0.026 mg/kg/day) throughout the whole period of replacement therapy. In growth hormone deficient subjects, formylpeptide-triggered release of superoxide anions from neutrophils was significantly suppressed by about 40% before treatment as compared to healthy control subjects. After 6 months of replacement therapy, neutrophil superoxide anion release was similar in patients and healthy individuals. Neither before nor after replacement therapy, however, was there a difference in monocyte migration between control and growth hormone deficient subjects. These data indicate that neutrophil function is somehow altered in growth hormone deficient patients, even when receiving appropriate therapy with thyroid, adrenal and gonadal hormones, but that neutrophil function can be restored to near normalcy by growth hormone replacement therapy. This would suggest that suppressed neutrophil respiratory burst is due to the deficiency in growth hormone.