Development of Antibodies to Human Growth Hormone (Hgh) in Children of Short Stature Treated With HGH

Waldhäusl, W.; Rath, F

doi:10.1530/acta.0.0680345

Cited by 19 publications

(4 citation statements)

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“…The incidence of antibody development in these studies varied from 30 to 60% of treated patients. This is the same as the incidence observed in several smaller groups of patients receiving hormone prepared in the same fashion (32,34,40,42,99,100). Resistance to hGH treatment is seen in few patients who develop antibodies.…”

Section: Antibodies To Human Growth Hormonesupporting

confidence: 81%

Human Pituitary Growth Hormone (hGH) Therapy in Growth Hormone Deficiency

1983

Endocrine Reviews

153

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This review has attempted to answer a number of questions regarding human growth hormone therapy in growth hormone deficiency. I believe that the available data support several conclusions which form a suggested current approach to the clinical use of hGH. While these conclusions are derived from data obtained using pituitary growth hormone, it is likely that they are applicable to growth hormone manufactured by recombinant DNA technology, as well. Treatment should be begun as early as the diagnosis can be made in anticipation of a better initial and long-term response in younger patients. Growth hormone should be administered on the basis of body weight in an initial dose of 0.06-0.10 unit/kg 3 times a week. Growth hormone may be administered either intramuscularly or subcutaneously. Therapy should be continuous whenever possible. Treatment should be given until there is no further response which generally will reflect closure of the epiphyses. Associated hormone deficiencies should be adequately treated, and patients should be periodically evaluated for the development of additional deficiencies. Concomitant therapy is not indicated unless deficiencies are clearly demonstrated. Thyroid replacement should be at full dosage, while glucocorticoid replacement should probably not exceed 10-15 mg/m2 x day. Gonadal steroids should be used at the bone age when puberty is expected, and hGH should be continued during pubertal development. There is no general indication for giving anabolic/androgenic steroid in combination with hGH in prepubertal patients. If a waning effect of therapy is observed, the dose of hGH should be incrementally increased, and/or the addition of anabolic/androgenic steroid therapy should be considered. While most reports have focused on the effect of hGH on linear growth, changes in weight, bone age, body proportions, and body composition have also been observed. The effect on bone age is variable, but there is greater enhancement of linear growth than of epiphyseal development in the majority of treated patients. Bone age must be monitored during hGH administration whether or not anabolic/androgenic steroids are used concurrently. Growth hormone administration is remarkably free of side effects. However, neutralizing antibodies to hGH may develop and they should be sought in patients in whom an unexplained decrease in response is observed. Certainly the available incomplete data allow for different conclusions. The expanding supply of hGH should lead to a more systematic evaluation and provide more definite answers to the questions which this review has considered.

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Section: Antibodies To Human Growth Hormonesupporting

confidence: 81%

Human Pituitary Growth Hormone (hGH) Therapy in Growth Hormone Deficiency

1983

Endocrine Reviews

153

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“…Only one of nine patients receiving P-hGH has antibodies typical of patients with persistent antibodies. This indicates that the eventual incidence of antibodies to hGH prepared by the method of Raben but purified to remove aggregated hGH will be consistent with that observed in patients receiving hGH prepared by Roos' method (8,12,13). The problem ROLE OF AGGREGATED hGH 697 of antibody formation should be significantly modified by the use of recent P-hGH preparations without significant quantities of aggregated hGH.…”

Section: Characterization Of Hghsupporting

confidence: 62%

“…4). The P-hGH and monomeric hGH samples contained between 5-10% antibodies to hGH (1,2,(9)(10)(11)(12). This has been contrasted to treatment with hGH prepared by the method of Roos (13), under which 5% of the children developed antibodies to hGH.…”

Section: Characterization Of Hghmentioning

confidence: 99%

Role of Aggregated Human Growth Hormone (hGH) in Development of Antibodies to hGH*

Moore

Leppert

1980

The Journal of Clinical Endocrinology & Metabolism

222

106

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By measuring [ 125 I]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 x 10 9 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 x 10 9 M~"). 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 [ 125 I]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 x 10 9 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 ['"' r 'I]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 [ 125 I]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. (J Clin Endocrinol Metab 51: 691, 1980)

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“…(Growth hormone was estimated according to a modified method of Boden and Soeldner[6] as reported by Waldhs and Rath[7]. During the insulin test hypoglycemia occurred.…”

mentioning

confidence: 99%

Weill-Marchesani syndrome

Götz¹,

Schenk²

1973

Z. Kinder-Heilk.

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Marehesani syndrome consists essentially of shortness of stature, spherophakia and other eye abnormalities and brachydactyly. It is probably an inherited disease of unknown etiology manifesting itself in organs of mesodermal origin.Investigations of a patient with the full picture of the syndrome revealed normal growth hormone levels following insulin and glucagon stimulation as well as normal thyroid function. Karyotypy was also normal. Intelligence was average for the patient's age.

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Development of Antibodies to Human Growth Hormone (Hgh) in Children of Short Stature Treated With HGH

Cited by 19 publications

References 0 publications

Human Pituitary Growth Hormone (hGH) Therapy in Growth Hormone Deficiency

Human Pituitary Growth Hormone (hGH) Therapy in Growth Hormone Deficiency

Role of Aggregated Human Growth Hormone (hGH) in Development of Antibodies to hGH*

Weill-Marchesani syndrome

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