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Boekstegers, Ann; Schmidt, Heinrich; Kurzay, Mathias; Vallée, Tanja; Jung, Eva; Dubinski, Ilja; Maxwell, Rebecca; Schmid, Irene (2023): Cortisol response in children with cancer and fever during chemotherapy: A prospective, observational study using random serum cortisol levels. Cancer Medicine, 12 (8). pp. 9247-9259. ISSN 2045-7634

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Abstract

Background
Glucocorticoids are crucial components of the treatment of leukemia and lymphoma. High doses can lead to suppression of the hypothalamic–pituitary–adrenal (HPA) axis and be causative for an impaired stress response during infection. This study aims to evaluate the cortisol response in pediatric oncologic patients during febrile episodes.

Methods
Totally, 75 children and adolescents (5 months—18 years) with fever during chemotherapy were consecutively enrolled in this study. In total, 47 patients received glucocorticoids as part of their treatment. Random serum cortisol and adrenocorticotropic hormone (ACTH) were analyzed in every patient. A low cortisol response (LCR) was defined as a cortisol level < 14.6 μg/dL.

Results
In total, 52 (69%) patients had a cortisol level < 14.6 μg/dL during fever. There was no significant difference between patients who received glucocorticoids and those who did not. Significantly lower cortisol levels were measured ≤7 days after last glucocorticoid intake compared to later time points. Nearly all patients treated with dexamethasone or prophylactic posaconazole demonstrated a LCR under stress (fever).

Conclusion
The incidence of an impaired HPA axis in pediatric cancer patients might be underestimated since 69% of the children in our study had a LCR during fever. Intake of dexamethasone, posaconazole and a time period of ≤7 days from the last glucocorticoid intake were additional risk factors for an LCR. However, we could not confirm that patients with a LCR fared worse than patients with a high cortisol response (HCR). Therefore, a different cortisol threshold may be necessary for defining an impaired HPA axis in febrile oncologic patients without concomitant symptoms of AI.

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