Adiposogenital dystrophy pathophysiology: Difference between revisions
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{{Adiposogenital dystrophy}} | {{Adiposogenital dystrophy}} | ||
{{CMG}} [[Ogechukwu Hannah Nnabude, MD]] | |||
==Overview== | ==Overview== | ||
The pathogenesis of adiposogenital dystrophy is believed to result from damage to the [[hypothalamus]] which links the [[nervous system]] to the [[endocrine system]] through the pituitary gland. | The pathogenesis of [[adiposogenital dystrophy]] is believed to result from damage to the [[hypothalamus]] which links the [[nervous system]] to the [[endocrine system]] through the pituitary gland. This leads to a disruption of hormone production. This occurs regardless of the cause of [[adiposogenital dystrophy]]. | ||
==Pathophysiology== | ==Pathophysiology== | ||
[[Adiposogenital dystrophy]] is an acquired disorder that result from lesions that damage the infundibulo-tuberal region in the floor of the third ventricle. Such lesions affect the hypothalamus. Possible causes include tumors such as [[craniopharyngioma]], [[encephalitis]], [[Friedreich Ataxia]] or demyelinating diseases. If a tumor is involved, symptoms such as vision impairment and headache can occur. Regardless of the cause, hypothalamic dysfunction and hypopituitarism is observed and majorly affects the somatotropic hormones and the [[gonadotropins]] leading delayed puberty and [[hypogonadism]]. <ref> "Babinski-Fröhlich Syndrome." Syndromes: Rapid Recognition and Perioperative Implications, 2e Eds. Bruno Bissonnette, et al. McGraw Hill, 2019, https://accesspediatrics.mhmedical.com/content.aspx?bookid=2674§ionid=220521811</ref>. It has also been postulated that leptin and insulin disruption due to hypothalamic injury may be a possible factor in the development of hypothalamic obesity. <ref name="pmid9461323">{{cite journal| author=Roth C, Wilken B, Hanefeld F, Schröter W, Leonhardt U| title=Hyperphagia in children with craniopharyngioma is associated with hyperleptinaemia and a failure in the downregulation of appetite. | journal=Eur J Endocrinol | year= 1998 | volume= 138 | issue= 1 | pages= 89-91 | pmid=9461323 | doi=10.1530/eje.0.1380089 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9461323 }} </ref>. However, the levels of [[ghrelin]], an appetite stimulating hormone produced in the gut, is at similar levels to those seen in individuals with common obesity <ref name="pmid15687345">{{cite journal| author=Goldstone AP, Patterson M, Kalingag N, Ghatei MA, Brynes AE, Bloom SR | display-authors=etal| title=Fasting and postprandial hyperghrelinemia in Prader-Willi syndrome is partially explained by hypoinsulinemia, and is not due to peptide YY3-36 deficiency or seen in hypothalamic obesity due to craniopharyngioma. | journal=J Clin Endocrinol Metab | year= 2005 | volume= 90 | issue= 5 | pages= 2681-90 | pmid=15687345 | doi=10.1210/jc.2003-032209 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15687345 }} </ref> <ref name="pmid15769982">{{cite journal| author=Kanumakala S, Greaves R, Pedreira CC, Donath S, Warne GL, Zacharin MR | display-authors=etal| title=Fasting ghrelin levels are not elevated in children with hypothalamic obesity. | journal=J Clin Endocrinol Metab | year= 2005 | volume= 90 | issue= 5 | pages= 2691-5 | pmid=15769982 | doi=10.1210/jc.2004-2175 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15769982 }} </ref>. Also, patients with [[adiposogenital dystrophy]] have a lower postprandial ghrelin response in comparison to healthy patients of similar body mass index and total body fat <ref name="pmid15972581">{{cite journal| author=Daousi C, MacFarlane IA, English PJ, Wilding JP, Patterson M, Dovey TM | display-authors=etal| title=Is there a role for ghrelin and peptide-YY in the pathogenesis of obesity in adults with acquired structural hypothalamic damage? | journal=J Clin Endocrinol Metab | year= 2005 | volume= 90 | issue= 9 | pages= 5025-30 | pmid=15972581 | doi=10.1210/jc.2004-1874 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15972581 }} </ref>. | |||
==References== | ==References== | ||
{{reflist|2}} | {{reflist|2}} | ||
[[Category:Disease]] | [[Category:Disease]] | ||
[[Category:Endocrinology]] | [[Category:Endocrinology]] | ||
[[Category:Genetic disorders]] | [[Category:Genetic disorders]] | ||
Latest revision as of 07:27, 29 December 2021
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Ogechukwu Hannah Nnabude, MD
Overview
The pathogenesis of adiposogenital dystrophy is believed to result from damage to the hypothalamus which links the nervous system to the endocrine system through the pituitary gland. This leads to a disruption of hormone production. This occurs regardless of the cause of adiposogenital dystrophy.
Pathophysiology
Adiposogenital dystrophy is an acquired disorder that result from lesions that damage the infundibulo-tuberal region in the floor of the third ventricle. Such lesions affect the hypothalamus. Possible causes include tumors such as craniopharyngioma, encephalitis, Friedreich Ataxia or demyelinating diseases. If a tumor is involved, symptoms such as vision impairment and headache can occur. Regardless of the cause, hypothalamic dysfunction and hypopituitarism is observed and majorly affects the somatotropic hormones and the gonadotropins leading delayed puberty and hypogonadism. [1]. It has also been postulated that leptin and insulin disruption due to hypothalamic injury may be a possible factor in the development of hypothalamic obesity. [2]. However, the levels of ghrelin, an appetite stimulating hormone produced in the gut, is at similar levels to those seen in individuals with common obesity [3] [4]. Also, patients with adiposogenital dystrophy have a lower postprandial ghrelin response in comparison to healthy patients of similar body mass index and total body fat [5].
References
- ↑ "Babinski-Fröhlich Syndrome." Syndromes: Rapid Recognition and Perioperative Implications, 2e Eds. Bruno Bissonnette, et al. McGraw Hill, 2019, https://accesspediatrics.mhmedical.com/content.aspx?bookid=2674§ionid=220521811
- ↑ Roth C, Wilken B, Hanefeld F, Schröter W, Leonhardt U (1998). "Hyperphagia in children with craniopharyngioma is associated with hyperleptinaemia and a failure in the downregulation of appetite". Eur J Endocrinol. 138 (1): 89–91. doi:10.1530/eje.0.1380089. PMID 9461323.
- ↑ Goldstone AP, Patterson M, Kalingag N, Ghatei MA, Brynes AE, Bloom SR; et al. (2005). "Fasting and postprandial hyperghrelinemia in Prader-Willi syndrome is partially explained by hypoinsulinemia, and is not due to peptide YY3-36 deficiency or seen in hypothalamic obesity due to craniopharyngioma". J Clin Endocrinol Metab. 90 (5): 2681–90. doi:10.1210/jc.2003-032209. PMID 15687345.
- ↑ Kanumakala S, Greaves R, Pedreira CC, Donath S, Warne GL, Zacharin MR; et al. (2005). "Fasting ghrelin levels are not elevated in children with hypothalamic obesity". J Clin Endocrinol Metab. 90 (5): 2691–5. doi:10.1210/jc.2004-2175. PMID 15769982.
- ↑ Daousi C, MacFarlane IA, English PJ, Wilding JP, Patterson M, Dovey TM; et al. (2005). "Is there a role for ghrelin and peptide-YY in the pathogenesis of obesity in adults with acquired structural hypothalamic damage?". J Clin Endocrinol Metab. 90 (9): 5025–30. doi:10.1210/jc.2004-1874. PMID 15972581.