title: Adrenal axis function after high-dose steroid therapy for childhood acute lymphoblastic leukemia.
abstract: BACKGROUND
  A 4-week course of high-dose glucocorticoids may cause prolonged adrenal suppression even after a 9-day tapering phase. In this study, adrenal function and signs and symptoms of adrenal insufficiency were prospectively assessed in children with acute lymphoblastic leukemia (ALL) after induction treatment including high-dose prednisone (PDN) or dexamethasone (DXM).
  
  
  METHODS
  Sixty-four children with ALL, treated according to the AIEOP ALL 2000 Study protocol, underwent low dose ACTH (LD-ACTH) stimulation 24 hr after the last tapered steroid dose. In those with impaired cortisol response, additional LD ACTH tests were performed every 1-2 weeks until cortisol levels normalized. Signs and symptoms of adrenal insufficiency were recorded during the observation period.
  
  
  RESULTS
  All patients had normal basal cortisol values at diagnosis. Twenty-four hours after last glucocorticoid dose, morning cortisol was reduced in 40/64 (62.5%) patients. LD-ACTH testing showed adrenal suppression in 52/64 (81.5%) patients. At the following ACTH test 7-14 days later, morning cortisol values were reduced in 8/52 (15.4%) patients and response to the test was impaired in 12/52 (23%). Adrenal function completely recovered in all patients within 10 weeks. No difference was found between patients treated with PDN or DXM. Almost 35% of children with impaired cortisol values at the first test developed signs or symptoms of adrenal insufficiency. One child developed a severe adrenal crisis during adrenal suppression.
  
  
  CONCLUSIONS
  High-dose glucocorticoid therapy in ALL children may cause prolonged adrenal suppression and related clinical symptoms. Laboratory monitoring of cortisol levels and steroid coverage during stress episodes may be indicated.
authors.affiliation: Department of Pediatric Endocrinology, Regina Margherita Children's Hospital, Turin, Italy. silvein@libero.it
authors.forename: Silvia
authors.initials: S
authors.lastname: Einaudi
authors.forename: Nicoletta
authors.initials: N
authors.lastname: Bertorello
authors.forename: Nicoletta
authors.initials: N
authors.lastname: Masera
authors.forename: Loredana
authors.initials: L
authors.lastname: Farinasso
authors.forename: Elena
authors.initials: E
authors.lastname: Barisone
authors.forename: Carmelo
authors.initials: C
authors.lastname: Rizzari
authors.forename: Andrea
authors.initials: A
authors.lastname: Corrias
authors.forename: Alessia
authors.initials: A
authors.lastname: Villa
authors.forename: Francesca
authors.initials: F
authors.lastname: Riva
authors.forename: Paola
authors.initials: P
authors.lastname: Saracco
authors.forename: Guido
authors.initials: G
authors.lastname: Pastore
mesh_terms: D000302:Adrenal Cortex / Q000187:drug effects; D000309:Adrenal Insufficiency / Q000139:chemically induced* / Q000188:drug therapy; D000324:Adrenocorticotropic Hormone; D000971:Antineoplastic Combined Chemotherapy Protocols / Q000627:therapeutic use*; D002648:Child; D003907:Dexamethasone / Q000008:administration & dosage / Q000009:adverse effects* / Q000494:pharmacology; D004305:Dose-Response Relationship, Drug; D004334:Drug Administration Schedule; D005260:Female; D015725:Fluconazole / Q000008:administration & dosage; D006801:Humans; D006854:Hydrocortisone / Q000378:metabolism* / Q000627:therapeutic use; D008297:Male; D010913:Pituitary-Adrenal System / Q000187:drug effects / Q000503:physiopathology; D054198:Precursor Cell Lymphoblastic Leukemia-Lymphoma / Q000188:drug therapy* / Q000503:physiopathology; D011241:Prednisone / Q000008:administration & dosage / Q000009:adverse effects* / Q000494:pharmacology; D013312:Stress, Physiological / Q000503:physiopathology; D013375:Substance Withdrawal Syndrome / Q000209:etiology / Q000503:physiopathology*