Abstract: MON 550
A New Hope in Management of Hypothalamic Obesity
Presenter: Sadia Ashraf
Introduction: view more
Hypothalamic obesity (HO) is intractable form of obesity syndrome that happens in patients with hypothalamic damage. It is characterized as significant polyphagia, lack of satiety and rapid weight gain not usually responsive to caloric restriction or lifestyle modification. HO has been reported in 67% of patients with craniopharyngioma (CP) resulting in increased morbidity & mortality from cardiovascular disease, diabetes mellitus, liver disease, reduction in functional capacity and quality of life. So far there have not been many effective treatment modalities for HO. Liraglutide, a Glucagon like Peptide-1 (GLP-1) analog, has recently been approved for long-term treatment of obesity. We present an interesting case of successful treatment of HO with liraglutide following resection of CP.
A 21 year old female underwent resection of CP at age 8, subsequently developed panhypopituitarism and HO. She had been adequately treated for panhypopituitarism with levothyroxine, hydrocortisone, growth hormone, desmopressin and estrogen–progesterone replacement. However, she had been complaining of poor quality of life due to weight gain from excessive hunger and lack of satiety after her surgery and was gaining an average of 1 pound per week post surgery. Her highest BMI was 35.3 kg/m2 compared to 13 kg/m2 before the surgery. A trial of Triiodothyronine (T3), and later Dextroamphetamine in addition to life style modification with low caloric diet and exercise had not had much beneficial effect. Octreotide was also considered but couldn’t be given because of insurance issues. She was complaining of significant social distress associated with her obesity when she entered college. She was started on liraglutide in August 2015, after its FDA approval for use in treatment of obesity. She noted marked improvement in polyphagia, started to have satiety after meals and was able to loose 20 pounds and BMI improved to 31 kg/m2 after seven months of therapy. She felt remarkably well both physically and emotionally. She tolerated liraglutide with no major side effects.
The pathophysiology of HO is most likely secondary to injury to ventromedial hypothalamus, which is responsible for satiety sensation. Peripheral afferent hormones such as leptin, insulin and gut hormones are unable to transduce their signals leading to perceived sense of CNS starvation. GLP-1 analogs help in weight reduction by various mechanisms, including direct and indirect effect on CNS to suppress appetite, increase energy expenditure and delay gastric emptying. The neuroanatomical distribution of GLP-1 receptor in CNS allows for multicenter, widespread impact of GLP-1 on food reward behavior that are intact in patients with HO. Our patient showed significant reduction in her weight with liraglutide and hence highlight the use of GLP-1 analogs as an excellent available option for the treatment of HO.