Biomedical subjects

Randi E Schreiber

Publications and source records attributed to Randi E Schreiber.

3 recordsLinked to original sources

PubMed2005

ACTH deficiency in childhood cancer survivors.

BACKGROUND: Adrenocorticotropin deficiency (ACTHD) can be clinically subtle, but life-threatening if not recognized. We assessed the prevalence of ACTHD in survivors of childhood cancer according to tumor diagnosis/therapy. PROCEDURE: Chart review of endocrine/oncology history was performed in 310 childhood cancer survivors. Patients were referred to endocrine clinic because of slow growth, fatigue, or abnormal pubertal timing. Evaluation of growth hormone (GH), thyrotropin (TSH), ACTH, luteinizing hormone (LH), and follicle-stimulating hormone (FSH) was performed. Low response to metyrapone and/or low dose ACTH test defined ACTHD. RESULTS: ACTHD was identified in 56 (18%), [44 of 182 (24%) central nervous system (CNS) tumors, 3 of 18 (17%) non-CNS cranial tumors, 9 of 97 (9%) hematologic malignancies]. Of the 56 with ACTHD, 53 (95%) had received cranial irradiation (mean 45.5 Gy, range 14-70 Gy); three had not: one each with craniopharyngioma, hypothalamic astrocytoma, and brain stem glioma. All but one also had GH deficiency and/or central hypothyroidism. CONCLUSIONS: Childhood cancer survivors with greatest risk for ACTHD had craniopharyngioma, other suprasellar tumor, or medulloblastoma or > or =24 Gy cranial irradiation. We recommend annual testing for ACTHD for 10-15 years and continued lifelong surveillance after CNS tumor or cranial irradiation, in patients with other hypothalamic-pituitary deficiencies or symptoms of ACTHD.

Adrenocorticotropic Hormone↗

PubMed2004

Hypothalamic dysfunction after chemotherapy.

Cranial irradiation with or without chemotherapy can cause hypothalamic-pituitary dysfunction. Chemotherapy without cranial irradiation has not been thought to cause such deficiency. In order to determine whether chemotherapy without cranial irradiation can lead to hormonal deficiency, we reviewed the medical records of 362 childhood cancer patients who underwent full hypothalamic-pituitary evaluation because of altered growth and development after oncological therapy (1987-2002). Of these, 31 received chemotherapy but no cranial or total body irradiation and had no CNS tumor: 18 had hematological malignancy and 13 had a solid tumor of the torso or extremity. Duration of follow-up was 13.0 +/- 4.1 years (mean +/- SD). Growth hormone deficiency (GHD) was identified in 15 (48%), central hypothyroidism (TSH-D) in 16 (52%), and pubertal abnormalities in 10 (32%). Pubertal abnormalities included precocious puberty in two (6%), gonadal failure in five of 27 who were old enough to assess puberty (19%), and gonadotropin deficiency in three of 27 (11%). GHD and TSH-D were co-existent in eight patients (26%). Overall, 81% (n = 25) had GHD, TSH-D, precocious puberty, and/or gonadotropin deficiency. None had ACTH or ADH deficiency or primary hypothyroidism. Of note, this was not a study of prevalence, but rather an evaluation of clinically referred patients. In conclusion, hypothalamic dysfunction may occur in survivors of non-CNS tumors who receive chemotherapy but do not receive cranial irradiation. We recommend at least annual observation of growth rate and pubertal development of all children treated for pediatric malignancies, with evaluation for GHD, TSH-D, pubertal abnormalities, and other hypothalamic dysfunction in all poorly-growing cancer survivors, even those not treated with cranial irradiation.

Adolescent↗

PubMed2003

Octreotide therapy of pediatric hypothalamic obesity: a double-blind, placebo-controlled trial.

Hypothalamic obesity is a devastating complication in children surviving brain tumors and/or cranial irradiation. These subjects are thought to exhibit autonomic dysregulation of the beta-cell, with insulin hypersecretion in response to oral glucose tolerance testing (OGTT). We report the results of a randomized, double-blind, placebo-controlled trial of octreotide therapy for pediatric hypothalamic obesity. Eighteen subjects [weight, 100.6 +/- 5.6 kg; body mass index (BMI), 37.1 +/- 1.3 kg/m(2)] received octreotide (5-15 microg/kg x d s.c.) or placebo for 6 months. With octreotide, Delta weight (mean +/- SEM) was +1.6 +/- 0.6 vs. +9.1 +/- 1.7 kg for placebo (P < 0.001). Delta BMI was -0.2 +/- 0.2 vs. +2.2 +/- 0.5 kg/m(2), respectively (P < 0.001). OGTT documented Delta insulin response (peak - basal) of -417 +/- 304 pM after octreotide vs. +216 +/- 215 pM after placebo (P = 0.034). Improvement in physical activity by parent report was noted with octreotide, but not placebo (P = 0.03). For the octreotide group, changes in quality of life positively correlated with changes in insulin response (P = 0.041). Complications and adverse events were mild and self-limited. These data demonstrate the beneficial effects of octreotide in pediatric hypothalamic obesity. Octreotide suppressed insulin, and stabilized weight and BMI. Improved quality of life correlated with the degree of insulin suppression. Octreotide was safe and well tolerated.

Adolescent↗