Treatment of Hypothalamic Obesity with Dextroamphetamine: A Case Series.
Adolescent
Adult
Body Mass Index
Child
Cohort Studies
Dextroamphetamine
/ therapeutic use
Exercise
Female
Health Status
Humans
Hypothalamic Diseases
/ complications
Male
Obesity
/ drug therapy
Obesity, Morbid
/ drug therapy
Pediatric Obesity
/ drug therapy
Retrospective Studies
Treatment Outcome
Young Adult
Central nervous system stimulants
Craniopharyngioma
Dextroamphetamine
Hyperphagia
Hypothalamic obesity
Journal
Obesity facts
ISSN: 1662-4033
Titre abrégé: Obes Facts
Pays: Switzerland
ID NLM: 101469429
Informations de publication
Date de publication:
2019
2019
Historique:
received:
20
04
2018
accepted:
22
11
2018
pubmed:
8
3
2019
medline:
12
2
2020
entrez:
8
3
2019
Statut:
ppublish
Résumé
A limited number of published case reports suggest a positive effect of dextroamphetamine, an adrenergic agonist affecting both the central nervous system (CNS) and peripheral nervous system, on physical activity and weight in patients with hypothalamic obesity (intractable obesity following CNS insult). Here, we present our clinical experience with dextroamphetamine treatment for hypothalamic obesity. The clinical course of all patients started on dextroamphetamine treatment for severe hypothalamic obesity at our institution between 2010 and 2013 is reported. Dextroamphetamine administration was initiated at a single dose of 5 mg per day and titrated to effect up to a dose of 20 mg/day. BMI z-score velocity was calculated as change in BMI z-score over standardized intervals of 12 months. Parameters of treatment success and adverse events were assessed in a standardized fashion. Seven patients (2 males; mean age 17.6 years [range 12.9-24.5]) underwent individual treatment attempts with dextroamphetamine between 2010 and 2013. The primary diagnoses were craniopharyngioma (n = 4), ganglioglioma WHO I (n = 1), astrocytoma (n = 1), and neonatal meningitis (n = 1). Time from initial CNS insult to initiation of dextroamphetamine treatment averaged 5.2 years (range 2.4 months to 16.5 years). All patients demonstrated a steady increase in BMI z-score from the time of initial diagnosis until initiation of dextroamphetamine treatment. Mean baseline BMI z-score was +3.17 ± 0.93 (+1.9 to +4.4). Mean BMI z-score velocity decelerated to -0.18 ± 0.12 per year during the first year of treatment and stabilized at +0.05 ± 0.32 per year during the second year of treatment. No significant adverse events were reported. Dextroamphetamine treatment led to stabilization or reduction of BMI z-score in a cohort of 7 patients with hypothalamic obesity, with no adverse effects. Considering the projected increase in BMI z-score according to the natural course of the disease, these findings are promising and warrant further study.
Sections du résumé
BACKGROUND
A limited number of published case reports suggest a positive effect of dextroamphetamine, an adrenergic agonist affecting both the central nervous system (CNS) and peripheral nervous system, on physical activity and weight in patients with hypothalamic obesity (intractable obesity following CNS insult). Here, we present our clinical experience with dextroamphetamine treatment for hypothalamic obesity.
METHODS
The clinical course of all patients started on dextroamphetamine treatment for severe hypothalamic obesity at our institution between 2010 and 2013 is reported. Dextroamphetamine administration was initiated at a single dose of 5 mg per day and titrated to effect up to a dose of 20 mg/day. BMI z-score velocity was calculated as change in BMI z-score over standardized intervals of 12 months. Parameters of treatment success and adverse events were assessed in a standardized fashion.
RESULTS
Seven patients (2 males; mean age 17.6 years [range 12.9-24.5]) underwent individual treatment attempts with dextroamphetamine between 2010 and 2013. The primary diagnoses were craniopharyngioma (n = 4), ganglioglioma WHO I (n = 1), astrocytoma (n = 1), and neonatal meningitis (n = 1). Time from initial CNS insult to initiation of dextroamphetamine treatment averaged 5.2 years (range 2.4 months to 16.5 years). All patients demonstrated a steady increase in BMI z-score from the time of initial diagnosis until initiation of dextroamphetamine treatment. Mean baseline BMI z-score was +3.17 ± 0.93 (+1.9 to +4.4). Mean BMI z-score velocity decelerated to -0.18 ± 0.12 per year during the first year of treatment and stabilized at +0.05 ± 0.32 per year during the second year of treatment. No significant adverse events were reported.
CONCLUSION
Dextroamphetamine treatment led to stabilization or reduction of BMI z-score in a cohort of 7 patients with hypothalamic obesity, with no adverse effects. Considering the projected increase in BMI z-score according to the natural course of the disease, these findings are promising and warrant further study.
Identifiants
pubmed: 30844799
pii: 000495851
doi: 10.1159/000495851
pmc: PMC6465734
doi:
Substances chimiques
Dextroamphetamine
TZ47U051FI
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
91-102Informations de copyright
© 2019 The Author(s) Published by S. Karger AG, Basel.
Références
Neuroscience. 2005;133(3):841-51
pubmed: 15908130
J Clin Endocrinol Metab. 2004 Jul;89(7):3298-305
pubmed: 15240606
Eur J Endocrinol. 2013 May 02;168(6):845-52
pubmed: 23482594
Nat Rev Endocrinol. 2010 Nov;6(11):609-18
pubmed: 20877295
J Pediatr Endocrinol Metab. 2015 May;28(5-6):503-13
pubmed: 25781673
Pediatr Res. 2007 Apr;61(4):496-501
pubmed: 17515878
Front Endocrinol (Lausanne). 2011 Dec 14;2:78
pubmed: 22649386
Obes Rev. 2012 Sep;13(9):780-98
pubmed: 22577758
Pediatr Endocrinol Rev. 2008 Dec;6(2):220-7
pubmed: 19202508
Front Endocrinol (Lausanne). 2011 Nov 03;2:60
pubmed: 22654817
Obesity (Silver Spring). 2015 Jun;23(6):1226-33
pubmed: 25884561
Arch Pediatr Adolesc Med. 2002 Sep;156(9):887-92
pubmed: 12197795
Eur J Clin Nutr. 1990 Jan;44(1):45-60
pubmed: 2354692
Arch Dis Child. 1952 Feb;27(131):10-33
pubmed: 14904111
J Physiol. 2009 Apr 1;587(Pt 7):1607-17
pubmed: 19221126
J Clin Psychopharmacol. 2008 Jun;28(3 Suppl 2):S46-53
pubmed: 18480677
Mol Metab. 2018 Jan;7:102-118
pubmed: 29146410
J Am Acad Child Adolesc Psychiatry. 2008 Sep;47(9):994-1009
pubmed: 18580502
Int J Clin Pract. 2016 Mar;70(3):206-17
pubmed: 26811245
PLoS Biol. 2005 Apr;3(4):e101
pubmed: 15760270
Annu Rev Pharmacol Toxicol. 1993;33:639-77
pubmed: 8494354
Eur J Pediatr. 2004 Feb;163(2):99-104
pubmed: 14691718
J Clin Med. 2015 Sep 09;4(9):1774-97
pubmed: 26371051
J Pediatr Endocrinol Metab. 2006 Feb;19(2):129-34
pubmed: 16562585