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Acquired hypothalamic obesity (aHO) presents as rapid, clinically relevant, and persistent weight gain due to hypothalamic damage, and leads to significant morbidity/mortality and decreased quality of life. Causes include craniopharyngioma and other space-occupying lesions, neurosurgical intervention, irradiation, and traumatic brain injury. This review summarizes the evidence and provides expert opinion on diagnostic criteria for aHO. Eight experts in neuroendocrinology and neurosurgery from Japan and Europe participated in a multidisciplinary meeting at the 57th Annual Meeting of the Japanese Society for Pediatric Endocrinology, Yokohama, Japan, 2024. Thereafter, three experts from Korea joined the discussion. Data were sourced from a search of the databases Web of Science, MEDLINE/PubMed, and Embase for reports published since 2000. Expert opinion of the authors was used substantially when no published data were available. The consensus on diagnostic criteria for aHO included: a.) traumatic event or (oncological) disease leading to hypothalamic lesions/damage detectable on MRI; b.) rapid (occurring during the first 12 months after surgery/diagnosis), persisting (for 24 months after surgery), and clinically significant increase in BMI (≥5% BMI increase in adult; ≥1.0 SDS BMI increase in pediatric patients) starting during the first 12 months following the onset of hypothalamic damage under clinical and anthropometric monitoring at 3 months intervals; c.) obesity of a certain level (BMI SDS ≥+2.0 SD in pediatric; BMI ≥25 kg/m2 or BMI ≥30 kg/m2 in adult patients), depending on racial and ethnic characteristics.
Müller et al. (Mon,) studied this question.