Evidence map›Paper›PMID 23973923›Full record

ReviewGastroenterology2013

The spectrum of achalasia: lessons from studies of pathophysiology and high-resolution manometry.

Peter J Kahrilas, Guy Boeckxstaens

Registry-linked trialOpen access · bronzeAbstract readReview
In one paragraph

Review in Gastroenterology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT04798547 (Outcomes of Short-length vs Standard-length Myotomy Using Per-Oral Endoscopic Myotomy), which is not on this map. Cited by 98 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
98citing papers in PubMed, 4 pooled it
11.6field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

NCT04798547 nacompletednot on this mapstarted 2020, after this paper: background citation

Outcomes of Short-length vs Standard-length Myotomy Using Per-Oral Endoscopic Myotomy (POEM) for Achalasia: A Randomized Controlled Pilot Study

TypeinterventionalSponsorNorthwestern UniversityRan2020 to 2024Enrolled60ConditionsAchalasiaArmsShort Myotomy, Standard Length Myotomy
3 · Its place in the literature

Who cites it

98 citing papers in PubMed, 4 syntheses or guidelines pooled it, 233 citations in OpenAlex.

  1. Pooled it
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  3. Pooled it
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  5. Trial
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  19. Optimizing achalasia diagnosis in the era of high-resolution manometry: A Pakistani perspective.JGH open : an open access journal of gastroenterology and hepatology · 2025
    Article
  20. Article

38 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors at 2 institutions in 2 countries.

Peter J KahrilasDivision of Gastroenterology and Hepatology, Northwestern University Feinberg School of Medicine, Chicago, Illinois. Electronic address: p-kahrilas@northwestern.edu.
Guy Boeckxstaens
KU Leuven · BENorthwestern University · US

Funding

THE ESOPHAGOGASTRIC JUNCTION IN HEALTH AND DISEASER01DK056033 · NIDDK · NORTHWESTERN UNIVERSITY AT CHICAGO · PI KAHRILAS, PETER JAMES · 2001 to 2015
$4.1M
The mechanics of symptom generation in dysphagiaR01DK079902 · NIDDK · NORTHWESTERN UNIVERSITY AT CHICAGO · PI PANDOLFINO, JOHN E · 2009 to 2017
$2.9M
NIDDK NIH HHS R01 DK056033NIDDK NIH HHS R01 DK079902NIDDK NIH HHS R01 DK56033
6 · The paper itself

Abstract

High-resolution manometry and recently described analysis algorithms, summarized in the Chicago Classification, have increased the recognition of achalasia. It has become apparent that the cardinal feature of achalasia, impaired lower esophageal sphincter relaxation, can occur in several disease phenotypes: without peristalsis, with premature (spastic) distal esophageal contractions, with panesophageal pressurization, or with peristalsis. Any of these phenotypes could indicate achalasia; however, without a disease-specific biomarker, no manometric pattern is absolutely specific. Laboratory studies indicate that achalasia is an autoimmune disease in which esophageal myenteric neurons are attacked in a cell-mediated and antibody-mediated immune response against an uncertain antigen. This autoimmune response could be related to infection of genetically predisposed subjects with herpes simplex virus 1, although there is substantial heterogeneity among patients. At one end of the spectrum is complete aganglionosis in patients with end-stage or fulminant disease. At the opposite extreme is type III (spastic) achalasia, which has no demonstrated neuronal loss but only impaired inhibitory postganglionic neuron function; it is often associated with accentuated contractility and could be mediated by cytokine-induced alterations in gene expression. Distinct from these extremes is progressive plexopathy, which likely arises from achalasia with preserved peristalsis and then develops into type II achalasia and then type I achalasia. Variations in its extent and rate of progression are likely related to the intensity of the cytotoxic T-cell assault on the myenteric plexus. Moving forward, we need to integrate the knowledge we have gained into treatment paradigms that are specific for individual phenotypes of achalasia and away from the one-size-fits-all approach.

Indexed as

PhenotypeAlgorithmsDisease ProgressionEsophageal AchalasiaHumansManometryMuscle ContractionMuscle RelaxationPeristalsisAchalasiaDysphagiaEGJEPTEsophageal Motilityesophageal pressure topographyesophagogastric junctionherpes simplex virus 1HSV-1integrated relaxation pressureIRPLESlower esophageal sphincterPathogenesisTLESRtransient lower esophageal sphincter relaxation

Identifiers

PMID23973923
PMCPMC3835179
OpenAlexW2187796566

What OpenQuestion holds

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Registered trials

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.