BACKGROUND: GH deficiency (GHD) and spine irradiation (SI) have been implicated in the mechanism of reduced adult height (AH) in childhood survivors of medulloblastoma. However, growth dynamics after tumor diagnosis and the effectiveness of rhGH on AH in comparison with rhGH-untreated survivors have not been reported. AIM: To follow height (H) SDS (HSDS) since tumor diagnosis and the effect of rhGH in GHD patients, comparing with GH-untreated GHD patients. METHODS: 14 patients received rhGH treatment until AH (medulloblastoma GH-treated group, MGHGr). 19 patients refused rhGH therapy (GH-untreated control medulloblastoma group, MCGr). Standing H and sitting H (SitH) were measured. RESULTS: In MGHGr, mean +/- SD HSDS decreased from 0.09 +/- 0.63 at tumor diagnosis to -1.38 +/- 0.91 at diagnosis of GHD, and to -1.90 +/- 0.72 at the onset of rhGH, p < 0.01, but it remained unchanged during rhGH (AH -2.12 +/- 0.55). MCGr HSDS (-0.25 +/- 0.88) was not different from MGHGr at tumor diagnosis, but it was -3.40 +/- 0.88 at AH, significantly lower than in MGHGr, p = 0.001. SitH SDS at AH (-4.56 +/- 0.82) was significantly lower than at the onset of rhGH (-2.86 +/- 0.75), p = 0.003, and it was not different from MCGr (-4.85 +/- 1.77). CONCLUSIONS: rhGH treatment improves AH in GH-deficient childhood medulloblastoma survivors but not spinal growth. Copyright (c) 2010 S. Karger AG, Basel.
BACKGROUND:GH deficiency (GHD) and spine irradiation (SI) have been implicated in the mechanism of reduced adult height (AH) in childhood survivors of medulloblastoma. However, growth dynamics after tumor diagnosis and the effectiveness of rhGH on AH in comparison with rhGH-untreated survivors have not been reported. AIM: To follow height (H) SDS (HSDS) since tumor diagnosis and the effect of rhGH in GHD patients, comparing with GH-untreated GHD patients. METHODS: 14 patients received rhGH treatment until AH (medulloblastoma GH-treated group, MGHGr). 19 patients refused rhGH therapy (GH-untreated control medulloblastoma group, MCGr). Standing H and sitting H (SitH) were measured. RESULTS: In MGHGr, mean +/- SD HSDS decreased from 0.09 +/- 0.63 at tumor diagnosis to -1.38 +/- 0.91 at diagnosis of GHD, and to -1.90 +/- 0.72 at the onset of rhGH, p < 0.01, but it remained unchanged during rhGH (AH -2.12 +/- 0.55). MCGr HSDS (-0.25 +/- 0.88) was not different from MGHGr at tumor diagnosis, but it was -3.40 +/- 0.88 at AH, significantly lower than in MGHGr, p = 0.001. SitH SDS at AH (-4.56 +/- 0.82) was significantly lower than at the onset of rhGH (-2.86 +/- 0.75), p = 0.003, and it was not different from MCGr (-4.85 +/- 1.77). CONCLUSIONS: rhGH treatment improves AH in GH-deficient childhood medulloblastoma survivors but not spinal growth. Copyright (c) 2010 S. Karger AG, Basel.