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Reduced pulsatile growth hormone secretion in children after therapy for acute lymphoblastic leukemia
Insights
Children treated for acute lymphoblastic leukemia (ALL) show significantly reduced growth hormone (GH) secretion. This impaired GH release may explain growth problems in ALL survivors.
Area of Science:
- Pediatric Endocrinology
- Neuroendocrinology
- Oncology
Background:
- Standard therapy for acute lymphoblastic leukemia (ALL) can impact endocrine function.
- Growth disturbances are a known complication in long-term survivors of childhood ALL.
Purpose of the Study:
- To investigate spontaneous pulsatile growth hormone (GH) secretion in long-term survivors of childhood ALL.
- To compare GH secretion patterns between ALL survivors and healthy children.
Main Methods:
- Measured basal GH levels every 20 minutes over 24 hours in 8 ALL survivors and 13 controls.
- Analyzed total GH output (AUC), pulse amplitude, and frequency.
- Assessed diurnal variation in GH secretion.
Main Results:
- ALL survivors had significantly lower total GH output (median 43 vs. 341 units, P < 0.001).
- Reduced GH pulse amplitude (6.9 vs. 32 ng/ml, P < 0.001) and frequency (4.6 vs. 8.5, P < 0.05) were observed in ALL survivors.
- The normal nocturnal surge in GH secretion was absent in 3 of the 8 ALL survivors.
Conclusions:
- Perturbations in spontaneous pulsatile GH secretion are common in children treated for ALL.
- Impaired GH secretion may be a sensitive indicator of therapy-related neuroendocrine damage.
- Blunted GH secretion could contribute to growth abnormalities in ALL survivors.
Abstract:
Basal growth hormone levels were measured every 20 minutes over 24 hours in eight long-term survivors of acute lymphoblastic leukemia and in 13 age- and pubertal stage-matched normal children. Among the patients, the median total basal growth hormone output (AUC) was 43 units, compared with 341 units in the normal control group (P less than 0.001). In the patients, mean pulse amplitude (6.9 ng/ml) and frequency (4.6) over 24 hours also were reduced, compared with the control values (32 ng/ml and 8.5, P less than 0.001 and P less than 0.05, respectively). In addition, normal children secreted more GH at night (median AUC 280) than during the day (113, P less than 0.001). However, this diurnal pattern was absent in three of the patients studied. These data suggest that perturbations of spontaneous pulsatile GH secretion are common after standard therapy for ALL and may be a sensitive means of detecting therapy-related neuroendocrine damage. Blunting of spontaneous pulsatile GH secretion may contribute to the abnormalities in growth seen in children with ALL.