P03-45 GH retesting and lipid profile in childhood-onset GHD when reaching final adult height

P03-45 GH retesting and lipid profile in childhood-onset GHD when reaching final adult height

S88 Posters / Growth Hormone & IGF Research 22 (2012) S33–S88 P03-45 GH retesting and lipid profile in childhood-onset GHD when reaching final adult h...

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S88

Posters / Growth Hormone & IGF Research 22 (2012) S33–S88

P03-45 GH retesting and lipid profile in childhood-onset GHD when reaching final adult height

P03-46 Successful pregnancy during use of octreotide and pegvisomant in an acromegalic patient

S. Wacharasindhu1,2 , S. Aroonparkmongkol1,2 , T. Sahakitrungrueng1,2 , V. Supornsilchai1,2 , C. Bongsebandhu-Phubhakdi1,2 . 1 Faculty of Medicine, Chulalongkorn University, Division of Endocrinology, Department of Pediatrics, Bangkok, Thailand; 2 Growth and Growth Monitoring Center, King Chulalongkorn Memorial Hospital, Out-Patient Department, Bangkok, Thailand

M.M. van der Klauw1 , A.N.A. van der Horst-Schrivers1 , A. Hoek2 , M. Bidlingmaier3 , B.H.R. Wolffenbuttel1 . 1 University Medical Center Groningen, University of Groningen, Endocrinology, Groningen, Netherlands; 2 University Medical Center Groningen, University of Groningen, Gynaecology and Obstetrics, Groningen, Netherlands; 3 Ludwig-Maximilians Universit¨ at, Medizinische Klinik-Innenstadt, Munich, Germany

Introduction: Previous studies showed that 20 to 80% of childhood onset GH deficiency (GHD) became normal GH secretion on GH retesting in adult life and they need no GH replacement. We investigate the percentage of childhood onset GHD subjects becoming normal GH secretion in adult life and their lipid profile. Material and Method: Twenty subjects with a mean age of 17.6±3 yr, who were treated with GH during childhood period and reached their final adult height, were recruited for GH retesting (Insulin Tolerance Test). Among 20 subjects, 13 had isolated GH deficiency (iGHD) and 7 had multiple pituitary hormone deficiency (MPHD). In iGHD subjects, 10 had idiopathic causes, 1 had small pituitary gland and 2 had GHD after surgery for tumor removal. In MPHD subjects, 6 were due to post surgical tumor removal and one had GHD and DI without any structural defect. Fasting lipid profile, serum IGF-I and IGFBP-3 were also measured. Results: On retesting, 6 of them (30%) became normal GH secretion and 14 (70%) still had GHD if we consider a peak GH cut-off at 10 ng /mL. However, if we use a peak GH cut-off at 3 ng/mL, 10 of them (50%) became normal GH secretion and 10 (50%) still had GHD. In persisting GHD subjects, 80% (8 in 10) had organic causes and 20% had idiopathic causes. Regarding the number of pituitary hormone deficiency, 70% (7 in 10) had MPHD and 30% had iGHD. Ten subject with normal GH secretion on retesting: 90% had idiopathic causes and 100% had isolated GHD. Persisting GHD subjects tend to have higher cholesterol (195.3±52.6 vs 171.1±35.9 mg/dL) and triglyceride (112.1±53.5 vs 72.6±20.8 mg/dL, p = 0.07) and lower HDL cholesterol (48.3±16.2 vs 65.6±12.6 mg/dL, p = 0.03) than those with normal GH on retesting. Additionally, serum IGF-I (129±102 vs 384±192 ng/mL, p = 0.002) and IGFBP-3 (4.0±1.6 vs 5.9±1.0 g/L, p = 0.005) levels were lower in persisting GHD subjects than those with normal GH subjects. However, all of these metabolic derangements were not demonstrated if we consider a cut-off peak GH level at 10 ng/mL on retesting. Conclusion: From this study, 50% of childhood-onset GHD became normal GH on retesting. Organic causes GHD and MPHD subjects had higher percentage of persisting GHD in adult life. When reaching the final adult height, abnormal lipid metabolism was demonstrated in persisting GHD with peak GH less than 3 ng/mL.

Introduction: Acromegaly is preferentially treated by surgery and/or radiotherapy before pregnancy, in order to avoid use of medication during pregnancy, and prevent GH excess related complications for mother and child. Only two cases of use of pegvisomant during pregnancy have been described; in one patient medication was discontinued after the first trimester, and in the other pegvisomant was used as monotherapy. Case report: A 29-year old female had been treated for acromegaly with transsphenoidal surgery. Before surgery she started with octreotide. Surgery was incomplete, and pegvisomant was added because of insufficient control. Radiotherapy was proposed, but denied by the patient. We advised against pregnancy while using pegvisomant and octreotide, but she was adamant and became pregnant at the age of 32, and was under strict medical control during pregnancy. Pregnancy was uneventful. During pregnancy, her IGF-1 levels declined from 39.8 to 19.4 nmol/l with unchanged doses of 30 mg octreotide LAR once every 3 weeks, and pegvisomant 40 mg twice weekly, as before pregnancy. A healthy child was born after a full term uneventful pregnancy. After pregnancy, IGF-1 levels rose to values consistent with those before pregnancy. The levels of octreotide and pegvisomant were measured in peripheral blood samples from the mother and in umbilical cord blood samples taken immediately after birth. Octreotide levels in the mother’s blood: 2142.790 and in umbilical cord blood: 807.106 pg/ml, pegvisomant levels in the mother’s blood: 1543 ng/ml, and in umbilical cord blood: undetectable. Conclusion: We report the first successful pregnancy in an acromegalic patient using the combination of pegvisomant and octreotide during complete pregnancy. There were no congenital malformations. Pegvisomant (80 mg weekly), was not detectable in umbilical cord blood, while detectable in the mother’s blood. Octreotide was detectable, albeit in lower levels in umbilical cord blood than in the mother’s blood.