The impact of chemotherapy on pituitary hormonal function in pubertal children with Hodgkin’s lymphoma

Background. Endocrine disorders are a significant long-term complication in children who have undergone anti-cancer treatment. Despite the relevance of this issue, the effects of chemotherapy (CT) on pituitary hormonal function in pubertal children with Hodgkin’s lymphoma (HL) remain poorly understood.
Aim. To evaluate the levels of pituitary hormones (somatotropic (growth) hormone (GH), thyroid-stimulating (TSH), adrenocorticotropic (ACTH), luteinizing (LH), follicle-stimulating (FSH) hormones, prolactin) in pubertal children with HL before and after chemotherapy. Materials and methods. The study included 40 pubertal children (11–17 years old, median 13.65 years) diagnosed with HL (20 (50 %) boys and 20 (50 %) girls) – main group. The control group comprised 40 conditionally healthy children of the same age range (median age 15.25 years) with equal gender distribution. Blood samples from the HL group were collected before chemotherapy and after its completion (prior to radiotherapy). Hormone levels (GH, TSH, ACTH, LH, FSH, prolactin) were measured using standard radioimmunoassay and enzyme-linked immunosorbent assay kits. Reference values were based on hormone levels in the control group. Statistical analysis was performed using Statistica 10.
Results. In girls with HL, pre-treatment levels of LH, FSH, and the LH/FSH ratio were elevated by 1.8-, 1.4-, and 1.3-fold, respectively, compared to the norm (p <0.05). GH and ACTH levels were 1.6and 3.1-fold below normal, respectively (p <0.05). After CT, LH levels decreased by 2.8-fold from baseline and by 1.5-fold relative to the norm, while FSH levels remained elevated at 1.6-fold above the norm (p <0.05). The LH/FSH ratio dropped by 2.6-fold relative to the norm and by 3.2-fold compared to baseline. Prolactin levels post-CT were 1.7-fold above the norm and 1.5-fold above baseline (p <0.05). GH levels were 7.8-fold lower than normal and 4.8-fold below baseline, whereas ACTH levels increased by 6.7-fold over baseline and were twice the normal level.
In boys with HL, pre-treatment LH levels and LH/FSH ratio were 1.5and 1.4-fold below normal, respectively (p <0.05). Prolactin was 1.8-fold higher than normal (p <0.05), and GH was 3.6-fold below normal. After CT, LH increased by 1.4-fold compared to baseline, reaching reference values (p <0.05).
Based on FSH levels, patients were divided into two subgroups: in 50 %, FSH remained within the normal range, while in the other 50 %, it increased ten-fold. The LH/FSH ratio remained normal in the first subgroup but was 11-fold below normal and 7.8-fold below baseline in the second. Post-treatment prolactin levels were 3.6-fold above normal and twice the baseline level. GH increased threefold from baseline and normalized. ACTH exceeded both normal and baseline levels two-fold. TSH levels decreased by 1.8-fold compared to both the norm and baseline (p <0.05).
Conclusion. The development of HL in pubertal children is associated with suppression of adenohypophyseal function and an imbalance in the synthesis of tropic hormones. Antitumor therapy does not generally restore normal hormone levels, which may be due to dysregulation of the central endocrine axes or the presence of extrapituitary sources of hormone production.