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CASE REPORTS
JOURNAL ARTICLE
Treatment of acromegaly with pegvisomant during pregnancy: maternal and fetal effects.
Journal of Clinical Endocrinology and Metabolism 2007 September
OBJECTIVE: Our objective was to describe the first case of the successful use of pegvisomant during pregnancy in a woman with acromegaly.
DESIGN: We present the case of a 26-yr-old female with acromegaly who had failed surgical and subsequent medical therapy but whose disease was well controlled on pegvisomant. She then conceived and was continued on pegvisomant throughout pregnancy. We then collected both maternal and cord blood samples at parturition, and later analyzed her breast milk.
RESULTS: Maternal IGF-I was well controlled during gestation. Fetal GH and IGF-I were within the normal range. Maternal pegvisomant levels were consistent with a 25-mg daily dosage. Fetal pegvisomant levels were minimal and near the range detected in untreated acromegalic patients, likely representing minimal cross-reactivity from endogenous GH or spurious contamination by maternal blood. GH variant levels in the maternal blood and the cord blood were both within the normal ranges. Pegvisomant levels in breast milk were below the lower limit of quantification of the assay and similar to those observed when analyzing breast milk samples from normal mothers in the same assay. Fetal growth parameters were normal; the baby was healthy and showed no adverse signs.
CONCLUSIONS: Pegvisomant therapy during gestation was safe and effective in our patient. Transplacental passage of pegvisomant is either absent or minimal, with a concentration highly unlikely to convey any significant pharmacodynamic effects on the fetal GH and IGF-I system. In addition, there is no evidence of substantial secretion of pegvisomant into breast milk.
DESIGN: We present the case of a 26-yr-old female with acromegaly who had failed surgical and subsequent medical therapy but whose disease was well controlled on pegvisomant. She then conceived and was continued on pegvisomant throughout pregnancy. We then collected both maternal and cord blood samples at parturition, and later analyzed her breast milk.
RESULTS: Maternal IGF-I was well controlled during gestation. Fetal GH and IGF-I were within the normal range. Maternal pegvisomant levels were consistent with a 25-mg daily dosage. Fetal pegvisomant levels were minimal and near the range detected in untreated acromegalic patients, likely representing minimal cross-reactivity from endogenous GH or spurious contamination by maternal blood. GH variant levels in the maternal blood and the cord blood were both within the normal ranges. Pegvisomant levels in breast milk were below the lower limit of quantification of the assay and similar to those observed when analyzing breast milk samples from normal mothers in the same assay. Fetal growth parameters were normal; the baby was healthy and showed no adverse signs.
CONCLUSIONS: Pegvisomant therapy during gestation was safe and effective in our patient. Transplacental passage of pegvisomant is either absent or minimal, with a concentration highly unlikely to convey any significant pharmacodynamic effects on the fetal GH and IGF-I system. In addition, there is no evidence of substantial secretion of pegvisomant into breast milk.
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