Guidelines for Complications of Cancer Treatment Vol VIII Part B

development after brain tumor therapy, with reductionin height due to accelerated bone maturation. In medulloblastoma, after CSI dose of 36 Gy, 75% hadhormone axis impairment with majority (70%) havingGH axis deficit while cortisol and thyroid axis wereusually preserved. Younger patients had significantlyhigher GH deficiency after RT. Laughton et al., hadshowed 93% (±4%) deficit in GH axis, 65% (±7%)thyroid axis deficiency and 38% (±6%) patient hadcortisol axis deficiency at 4 year follow up after CSI. It seems HP axis deficiency is dose dependent and lowerradiation dose is associated significantly less hormoneaxis deficiency. In a prospective study , GH axis deficiency was observedin 41% of pediatric brain tumor patients treated withchemotherapy and surgery (Clarson et al). There were further significant impairment in both GHand thyroid axis after treatment with CSI. Few otherstudies on medulloblastoma/PNET patients treated withCSI (±chemotherapy) had shown to be associated withdecline in endocrine function. After whole brain RT in metastatic brain tumor, 50%patient developed hormone axis deficit in at least oneaxis. In patients receiving prophylactic cranial RT, higherRT dose is associated with significantly more endocrinedysfunction. Studies have also shown correlationbetween the endocrine dysfunction and severity ofneurocognitive impairment after RT. Prospective evaluation of endocrine function after focalRT is sparse. There are evidences of ‘dose-effect’relationship between RT dose and HP axis deficit. Withfocal RT as HP axis is expected to be spared, it is assumed351