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. 2017 Nov 6;2017(11):CD008727. doi: 10.1002/14651858.CD008727.pub4

Felner 2000.

Methods Study type: prospective single‐centre study
 Setting: Children's Medical Center of Dallas (University of Texas Southwestern Medical School). This information was based on additional information provided by trial authors.
Participants 10 children (mean age at diagnosis 5.3 ± 2.9 years (range 2.0 to 9.9 years); 7 boys and 3 girls) with early B‐cell lineage ALL
Interventions Induction therapy: dexamethasone, vincristine, L‐asparaginase, and daunorubicin. High‐risk therapy: 1 additional lumbar puncture with IT chemotherapy during induction
 Type of glucocorticoid therapy: induction phase: oral dexamethasone (6 mg/m2/d, divided into 2 daily doses) for 28 consecutive days
 Cumulative dexamethasone dose: 168 mg/m2 
 Duration of glucocorticoid therapy: 28 days
 Methods of cessation of glucocorticoid therapy: abrupt
No control intervention
Outcomes Specific HPA axis function test: 250 µg cosyntropin stimulation test (synthetic corticotrophin 1‐24/ACTH test) IV between 8 and 10 a.m. (Cortrosyn, Organon) (basal morning value cortisol and after 45 minutes)
Moment of testing: at diagnosis (baseline), 24 hours after completion of the dexamethasone course, and every 4 weeks thereafter until normalisation of adrenal function. Tests were performed during treatment for ALL.
 Cutoff limits defined by original studies: baseline cortisol: not defined. Low‐dose ACTH test: normal response ≥ 18 µg (≥ 500 nmol/L)
Notes 0 children were lost to follow‐up.
Length of follow‐up after glucocorticoid therapy: Children with suppressed levels underwent further testing every 4 weeks thereafter until cortisol levels were normalised. Total follow‐up duration was 8 weeks.
Funding source: National Institutes of Health grants
Declaration of interest among primary researchers: not mentioned