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Thyroid function in children treated for acute lymphoblastic leukemia

A Mohn1, F Chiarelli, A Di Marzio

  • 1Clinica Pediatrica, Università di Chieti, Italy.

Journal of Endocrinological Investigation
|April 1, 1997
PubMed
Summary
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Childhood acute lymphoblastic leukemia survivors treated with cranial irradiation may develop thyroid dysfunction. Long-term monitoring of thyroid stimulating hormone (TSH) and thyrotropin-releasing hormone (TRH) is crucial for these patients.

Area of Science:

  • Pediatric Oncology
  • Endocrinology
  • Radiation Oncology

Background:

  • Survivors of childhood acute lymphoblastic leukemia (ALL) often face long-term health issues.
  • Cranial irradiation is a common treatment modality for ALL, potentially affecting endocrine function.

Purpose of the Study:

  • To investigate the late effects of ALL treatment, specifically cranial irradiation, on thyroid function in pediatric survivors.
  • To assess the relationship between radiation dose, time since therapy, and age at diagnosis with thyroid hypofunction.

Main Methods:

  • Plasma thyroid hormone levels and thyroid-stimulating hormone (TSH) response to thyrotropin-releasing hormone (TRH) stimulation were assessed in 24 ALL survivors.
  • Patients received 18-24 Gy cranial irradiation as part of their combination chemotherapy.

Related Experiment Videos

  • Thyroid status was evaluated a mean of 6.8 years after treatment completion.
  • Main Results:

    • Six children exhibited a blunted TSH peak following TRH stimulation, indicating potential hypofunction.
    • Three children had low basal TSH levels.
    • Thyroid hypofunction was more prevalent in patients receiving 24 Gy versus 18 Gy cranial irradiation (50% vs 14%) and in those treated more than 5 years prior.

    Conclusions:

    • Treatment for childhood ALL, including cranial irradiation, can lead to thyrotropin-releasing hormone/thyroid-stimulating hormone (TRH/TSH) axis dysfunction.
    • Long-term survivors of childhood ALL require ongoing surveillance for thyroid dysfunction.