Diffuse esophageal spasm pathophysiology: Difference between revisions
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===Pathogenesis=== | ===Pathogenesis=== | ||
* The exact pathogenesis of DES is not fully understood. However, current high-resolution manometric studies suggest impairment of inhibitory myenteric plexus neurons in DES. These neurons use nitric oxide (NO) as neurotransmitter. Hence, these patients may also have dysregulation of endogenous NO synthesis or/and degradation<ref name="pmid1612326">{{cite journal| author=Yamato S, Spechler SJ, Goyal RK| title=Role of nitric oxide in esophageal peristalsis in the opossum. | journal=Gastroenterology | year= 1992 | volume= 103 | issue= 1 | pages= 197-204 | pmid=1612326 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=1612326 }}</ref>. The final result is premature and rapidly propagated or simultaneous contraction of smooth muscles of distal esophagus. | * The exact pathogenesis of DES is not fully understood. However, current high-resolution manometric studies suggest impairment of inhibitory myenteric plexus neurons in DES. Anti-ganglionic acetylcholine receptor antibodies (anti-gAChR-Abs) are reported in some cases<ref name="pmid28214088">{{cite journal| author=Morimoto N, Takahashi S, Inaba T, Takamiya M, Kageyama Y, Morimoto M et al.| title=A case of seropositive autoimmune autonomic ganglionopathy with diffuse esophageal spasm. | journal=J Clin Neurosci | year= 2017 | volume= 39 | issue= | pages= 90-92 | pmid=28214088 | doi=10.1016/j.jocn.2017.01.027 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=28214088 }}</ref>. These neurons use nitric oxide (NO) as neurotransmitter. Hence, these patients may also have dysregulation of endogenous NO synthesis or/and degradation<ref name="pmid1612326">{{cite journal| author=Yamato S, Spechler SJ, Goyal RK| title=Role of nitric oxide in esophageal peristalsis in the opossum. | journal=Gastroenterology | year= 1992 | volume= 103 | issue= 1 | pages= 197-204 | pmid=1612326 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=1612326 }}</ref>. The final result is premature and rapidly propagated or simultaneous contraction of smooth muscles of distal esophagus. | ||
==Genetics== | ==Genetics== | ||
There are reports of families with achalasia and esophageal spasm which supports the hypothesis that genetic traits may play role in pathogenesis of DES as well as association between the two disorders.<ref name="pmid3061886">{{cite journal| author=Frieling T, Berges W, Borchard F, Lübke HJ, Enck P, Wienbeck M| title=Family occurrence of achalasia and diffuse spasm of the oesophagus. | journal=Gut | year= 1988 | volume= 29 | issue= 11 | pages= 1595-602 | pmid=3061886 | doi= | pmc=1433819 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=3061886 }}</ref> However, genetic inheritance is not fully established. | There are reports of families with achalasia and esophageal spasm which supports the hypothesis that genetic traits may play role in pathogenesis of DES as well as association between the two disorders.<ref name="pmid3061886">{{cite journal| author=Frieling T, Berges W, Borchard F, Lübke HJ, Enck P, Wienbeck M| title=Family occurrence of achalasia and diffuse spasm of the oesophagus. | journal=Gut | year= 1988 | volume= 29 | issue= 11 | pages= 1595-602 | pmid=3061886 | doi= | pmc=1433819 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=3061886 }}</ref> However, genetic inheritance is not fully established. | ||
Revision as of 15:53, 3 November 2017
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Diffuse esophageal spasm Microchapters |
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Differentiating Diffuse esophageal spasm from other Diseases |
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Diffuse esophageal spasm pathophysiology On the Web |
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Madhu Sigdel M.B.B.S.[2]
Overview
The exact pathogenesis of [disease name] is not fully understood.
OR
It is thought that [disease name] is the result of / is mediated by / is produced by / is caused by either [hypothesis 1], [hypothesis 2], or [hypothesis 3].
OR
[Pathogen name] is usually transmitted via the [transmission route] route to the human host.
OR
Following transmission/ingestion, the [pathogen] uses the [entry site] to invade the [cell name] cell.
OR
[Disease or malignancy name] arises from [cell name]s, which are [cell type] cells that are normally involved in [function of cells].
OR
The progression to [disease name] usually involves the [molecular pathway].
OR
The pathophysiology of [disease/malignancy] depends on the histological subtype.
Pathophysiology
Pathogenesis
- The exact pathogenesis of DES is not fully understood. However, current high-resolution manometric studies suggest impairment of inhibitory myenteric plexus neurons in DES. Anti-ganglionic acetylcholine receptor antibodies (anti-gAChR-Abs) are reported in some cases[1]. These neurons use nitric oxide (NO) as neurotransmitter. Hence, these patients may also have dysregulation of endogenous NO synthesis or/and degradation[2]. The final result is premature and rapidly propagated or simultaneous contraction of smooth muscles of distal esophagus.
Genetics
There are reports of families with achalasia and esophageal spasm which supports the hypothesis that genetic traits may play role in pathogenesis of DES as well as association between the two disorders.[3] However, genetic inheritance is not fully established.
Associated Conditions
Gross Pathology
- On gross pathology, gross thickening of muscularis propria layer and LES which is due to hyperplasia (not hypertrophy) than normal subjects are characteristic findings of DES.[4]
Microscopic Pathology
- On microscopic histopathological analysis, degeneration of vagal fibres, inflammatory infiltration of myenteric plexus, and hyperplasia of smooth muscles are characteristic findings of DES. Data are limited due to rarity of disease and even less common need of surgery as a treatment.
References
- ↑ Morimoto N, Takahashi S, Inaba T, Takamiya M, Kageyama Y, Morimoto M; et al. (2017). "A case of seropositive autoimmune autonomic ganglionopathy with diffuse esophageal spasm". J Clin Neurosci. 39: 90–92. doi:10.1016/j.jocn.2017.01.027. PMID 28214088.
- ↑ Yamato S, Spechler SJ, Goyal RK (1992). "Role of nitric oxide in esophageal peristalsis in the opossum". Gastroenterology. 103 (1): 197–204. PMID 1612326.
- ↑ Frieling T, Berges W, Borchard F, Lübke HJ, Enck P, Wienbeck M (1988). "Family occurrence of achalasia and diffuse spasm of the oesophagus". Gut. 29 (11): 1595–602. PMC 1433819. PMID 3061886.
- ↑ Champion JK, Delise N, Hunt T (2001). "Myenteric plexus in spastic motility disorders". J Gastrointest Surg. 5 (5): 514–6. PMID 11986002.