Obesity in survivors of childhood-onset craniopharyngioma - impact of parental body mass index at craniopharyngioma diagnosis?

Julia Beckhaus; Maria Eveslage; Brigitte Bison; Carsten Friedrich; Hermann Muller

doi:10.1530/endoabs.99.P110

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Endocrine Abstracts (2024) 99 P110 | DOI: 10.1530/endoabs.99.P110

ECE2024 Poster Presentations Pituitary and Neuroendocrinology (120 abstracts)

Obesity in survivors of childhood-onset craniopharyngioma – impact of parental body mass index at craniopharyngioma diagnosis?

Julia Beckhaus ^1,2 , Maria Eveslage ³ , Brigitte Bison ⁴ , Carsten Friedrich ¹ & Hermann Müller ¹

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Author affiliations

¹Carl von Ossietzky Universität Oldenburg School VI - School of Medicine and Health Sciences, Department of Pediatrics and Pediatric Hematology/Oncology, Klinikum Oldenburg AöR, Oldenburg, Germany; ²Carl von Ossietzky Universität Oldenburg School IV - School of Medicine and Health Sciences, Divison of Epidemiology and Biometry, Oldenburg, Germany; ³Institute of Biostatistics and Clinical Research, University of Münster, Münster, Germany; ⁴University of Augsburg, Faculty of Medicine, Diagnostic and Interventional Neuroradiology, Augsburg, Germany

Background: It is well known that both genetic backgroup and lifestyle influence the development of ‘general’ obesity. However, the role of parental body mass index (BMI) on the development of obesity in long-term survivors of childhood-onset craniopharyngioma (CP) is not well understood. This study aimed to analyze the correlation of patients’ BMI at diagnosis, and last visit and parental BMI at CP diagnosis and further explored potential risk factors for obesity in CP patients.

Patients and methods: 291 CP patients and their parents recruited in the German KRANIOPHARYNGEOM studies were included. Correlations between patient’s BMI SDS at CP diagnosis and last visit and parental BMI at CP diagnosis were analyzed. The associations between hypothalamic damage, maternal/paternal BMI and CP patients’ obesity at last visit were analyzed by multivariable logistic regression.

Results: After a median follow-up of 9.38 years, 52% of CP patients developed obesity (BMI>3SDS). Patient’s BMI SDS at last visit was moderately correlated with BMI-SDS at CP diagnosis (r=0.48, 95%-CI 0.38-0.58, P<0.001), and also with maternal BMI at diagnosis (r=0.28, 95%-CI 0.17-0.38, P<0.001) and paternal BMI at diagnosis (r=0.3, 95% CI-0.19-0.41, P<0.001). Hypothalamic involvement (HI) and surgical hypothalamic lesions (HL) of posterior hypothalamic structures (grade II) were independent risk factors for obesity. With increasing maternal or paternal BMI, the probabilty of developing obesity as a patient with CP increased. However, the contributing role of parental BMI to the pathogenesis of obesity was small compared to the impact of HL.

Conclusion: We conclude that besides HL, parental disposition for obesity is associated with the development of obesity in patients after CP. Hypothalamus-sparing treatment strategies are most effective in prevention of hypothalamic obesity. Our results indicate that also the family situation could have an influence on the development of obesity after CP and might be a therapeutic target.