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WAYNE V. MOORE, PAULA LEPPERT, Role of Aggregated Human Growth Hormone (hGH) in Development of Antibodies to hGH, The Journal of Clinical Endocrinology & Metabolism, Volume 51, Issue 4, 1 October 1980, Pages 691–697, https://doi.org/10.1210/jcem-51-4-691
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Abstract
By measuring [125I]hGH binding in the plasma of human GH (hGH)-deficient children at 3- to 4-month intervals during hGH therapy with hGH prepared by Raben's method, we have defined three patterns of antibody formation. One group of patients developed antibodies by 3 months of therapy that persisted despite the length or type of hGH therapy. Their antibodies were characterized by a low affinity (1.49 × 109 M−1) and a high capacity (29 nmol/liter plasma). The development or presence of antibodies adversely affected the growth rate in only one patient in this group. This patient's antibodies were characterized by the highest capacity (1235 nmol/liter plasma) and lowest affinity (0.044 × 109 M−1). The capacity decreased to 134 nmol/liter plasma upon switching to a hGH preparation without aggregated hGH.
The second group developed antibodies to hGH by 6–9 months of therapy, but [125I]hGH binding by the plasma returned to control levels by 20 months of therapy. The antibodies of this group were characterized by a higher affinity (12.7 × 109 M−1) and a lower capacity (0.9 nmol/liter plasma) than the group with antibodies. This group had received hGH with less than 5% aggregated hGH.
The third group did not develop significant [125I]hGH binding in the plasma despite prolonged therapy with multiple hGH preparations.
Several patients have been treated solely with recent hGH preparations from the National Pituitary Agency which contain less than 10% aggregated hGH compared to earlier preparations containing more than 20%. The incidence (44%) of significant [125I]hGH binding by these patients' plasmas was similar to that of patients receiving hGH with aggregated hGH; however, hGH binding by the plasma of most of these patients was characteristic of that of patients with transient antibodies.
We conclude that 1) the development of antibodies to hGH during therapy is dependent on individual susceptibility and the presence of aggregated hGH in the hGH preparation, 2) the antibody response is more likely to be transient if the content of aggregated hGH is low, and 3) the eventual incidence of significant hGH binding in plasma of patients who receive hGH prepared by Raben's method without aggregated hGH will be the same as that observed in patients receiving hGH prepared by other methods.
