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The Pathogenesis and Management of Achalasia: Current Status and Future Directions.

Ates F, Vaezi MF - Gut Liver (2015)

Bottom Line: Pneumatic dilation and surgical myotomy are the only definitive treatment options for patients with achalasia who can undergo surgery.Botulinum toxin injection into the lower esophageal sphincter should be reserved for those who cannot undergo definitive therapy.Close follow-up is paramount because many patients will have a recurrence of symptoms and require repeat treatment.

View Article: PubMed Central - PubMed

Affiliation: Division of Gastroenterology, Hepatology, and Nutrition, Center for Swallowing and Esophageal Disorders, Vanderbilt University Medical Center, Nashville, TN, USA.

ABSTRACT
Achalasia is an esophageal motility disorder that is commonly misdiagnosed initially as gastroesophageal reflux disease. Patients with achalasia often complain of dysphagia with solids and liquids but may focus on regurgitation as the primary symptom, leading to initial misdiagnosis. Diagnostic tests for achalasia include esophageal motility testing, esophagogastroduodenoscopy and barium swallow. These tests play a complimentary role in establishing the diagnosis of suspected achalasia. High-resolution manometry has now identified three subtypes of achalasia, with therapeutic implications. Pneumatic dilation and surgical myotomy are the only definitive treatment options for patients with achalasia who can undergo surgery. Botulinum toxin injection into the lower esophageal sphincter should be reserved for those who cannot undergo definitive therapy. Close follow-up is paramount because many patients will have a recurrence of symptoms and require repeat treatment.

No MeSH data available.


Related in: MedlinePlus

Both lower esophageal sphincter (LES) smooth muscle and the inhibitory neurons of the myenteric plexus have cholecystokinin receptors. (A) In a normal esophagus, administration of cholecystokinin-octapeptide (CCK-OP) results in LES relaxation because the inhibitory neurons override the direct excitation of the LES smooth muscle. (B) However, in achalasia, the LES smooth muscle excitation is unopposed due to the loss of the inhibitory neurons in the myenteric plexus. As a result, CCK-OP causes LES contraction.
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f2-gnl-09-449: Both lower esophageal sphincter (LES) smooth muscle and the inhibitory neurons of the myenteric plexus have cholecystokinin receptors. (A) In a normal esophagus, administration of cholecystokinin-octapeptide (CCK-OP) results in LES relaxation because the inhibitory neurons override the direct excitation of the LES smooth muscle. (B) However, in achalasia, the LES smooth muscle excitation is unopposed due to the loss of the inhibitory neurons in the myenteric plexus. As a result, CCK-OP causes LES contraction.

Mentions: However, unlike the intact excitatory innervation, many physiologic studies show either absent or abnormal inhibitory innervation in achalasia. Dodds et al.34 performed a case-control study in which 24 patients with achalasia received intravenous bolus doses of cholecystokinin-octapeptide (CCK-OP). The control group consisting of seven volunteers and 32 patients without evidence of idiopathic achalasia who were referred for esophageal manometry also received CCK-OP. In the control group, excitation of both inhibitory neurons and LES smooth muscle using CCK-OP produced the net effect of LES relaxation. This is because the inhibitory neurons override the direct stimulation of the LES smooth muscle. However, in patients with achalasia, administration of CCK-OP caused paradoxical increase in LES pressure due to the absence of inhibitory neurons resulting in unopposed direct excitatory effect of CCK-OP on the LES smooth muscle (Fig. 2), again, highlighting the absence of inhibitory neurons in achalasia patients. Hence, this test can be clinically used in patients with dysphagia postfundoplication suspected of having achalasia. If CCK-OP administration in this group results in increased resting LES pressure, it is likely that the patient has achalasia.34


The Pathogenesis and Management of Achalasia: Current Status and Future Directions.

Ates F, Vaezi MF - Gut Liver (2015)

Both lower esophageal sphincter (LES) smooth muscle and the inhibitory neurons of the myenteric plexus have cholecystokinin receptors. (A) In a normal esophagus, administration of cholecystokinin-octapeptide (CCK-OP) results in LES relaxation because the inhibitory neurons override the direct excitation of the LES smooth muscle. (B) However, in achalasia, the LES smooth muscle excitation is unopposed due to the loss of the inhibitory neurons in the myenteric plexus. As a result, CCK-OP causes LES contraction.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4477988&req=5

f2-gnl-09-449: Both lower esophageal sphincter (LES) smooth muscle and the inhibitory neurons of the myenteric plexus have cholecystokinin receptors. (A) In a normal esophagus, administration of cholecystokinin-octapeptide (CCK-OP) results in LES relaxation because the inhibitory neurons override the direct excitation of the LES smooth muscle. (B) However, in achalasia, the LES smooth muscle excitation is unopposed due to the loss of the inhibitory neurons in the myenteric plexus. As a result, CCK-OP causes LES contraction.
Mentions: However, unlike the intact excitatory innervation, many physiologic studies show either absent or abnormal inhibitory innervation in achalasia. Dodds et al.34 performed a case-control study in which 24 patients with achalasia received intravenous bolus doses of cholecystokinin-octapeptide (CCK-OP). The control group consisting of seven volunteers and 32 patients without evidence of idiopathic achalasia who were referred for esophageal manometry also received CCK-OP. In the control group, excitation of both inhibitory neurons and LES smooth muscle using CCK-OP produced the net effect of LES relaxation. This is because the inhibitory neurons override the direct stimulation of the LES smooth muscle. However, in patients with achalasia, administration of CCK-OP caused paradoxical increase in LES pressure due to the absence of inhibitory neurons resulting in unopposed direct excitatory effect of CCK-OP on the LES smooth muscle (Fig. 2), again, highlighting the absence of inhibitory neurons in achalasia patients. Hence, this test can be clinically used in patients with dysphagia postfundoplication suspected of having achalasia. If CCK-OP administration in this group results in increased resting LES pressure, it is likely that the patient has achalasia.34

Bottom Line: Pneumatic dilation and surgical myotomy are the only definitive treatment options for patients with achalasia who can undergo surgery.Botulinum toxin injection into the lower esophageal sphincter should be reserved for those who cannot undergo definitive therapy.Close follow-up is paramount because many patients will have a recurrence of symptoms and require repeat treatment.

View Article: PubMed Central - PubMed

Affiliation: Division of Gastroenterology, Hepatology, and Nutrition, Center for Swallowing and Esophageal Disorders, Vanderbilt University Medical Center, Nashville, TN, USA.

ABSTRACT
Achalasia is an esophageal motility disorder that is commonly misdiagnosed initially as gastroesophageal reflux disease. Patients with achalasia often complain of dysphagia with solids and liquids but may focus on regurgitation as the primary symptom, leading to initial misdiagnosis. Diagnostic tests for achalasia include esophageal motility testing, esophagogastroduodenoscopy and barium swallow. These tests play a complimentary role in establishing the diagnosis of suspected achalasia. High-resolution manometry has now identified three subtypes of achalasia, with therapeutic implications. Pneumatic dilation and surgical myotomy are the only definitive treatment options for patients with achalasia who can undergo surgery. Botulinum toxin injection into the lower esophageal sphincter should be reserved for those who cannot undergo definitive therapy. Close follow-up is paramount because many patients will have a recurrence of symptoms and require repeat treatment.

No MeSH data available.


Related in: MedlinePlus