Neural autoantibody profile of primary achalasia

Robert E. Kraichely, Gianrico Farrugia, Sean J Pittock, Donald O. Castell, Vanda A Lennon

Research output: Contribution to journalArticle

36 Citations (Scopus)

Abstract

The etiology and pathogenesis of primary achalasia are both unknown. Postulated mechanisms include autoimmune, viral-immune, and central neurodegenerative. The aim of this study is to investigate the serum profile of neural autoantibodies in patients with primary achalasia. Coded sera from 70 patients with primary achalasia and 161 healthy control subjects, matched in sex, age, and smoking habits, were screened for antibodies targeting neuronal, glial, and muscle autoantigens. No specific myenteric neuronal antibody was identified. However, the overall prevalence of neural autoantibodies in patients with primary achalasia was significantly higher than in healthy control subjects (25.7 vs. 4.4%, P < 0.0001). Most noteworthy was the 21.4% frequency of glutamic acid decarboxylase-65 antibody in patients with achalasia (versus 2.5% in control subjects), in the absence of diabetes or companion antibodies predictive of type 1 diabetes. This profile of autoantibodies suggests an autoimmune basis for a subset of primary achalasia.

Original languageEnglish (US)
Pages (from-to)307-311
Number of pages5
JournalDigestive Diseases and Sciences
Volume55
Issue number2
DOIs
StatePublished - Feb 2010

Fingerprint

Esophageal Achalasia
Autoantibodies
Antibodies
Healthy Volunteers
Glutamate Decarboxylase
Autoantigens
Serum
Type 1 Diabetes Mellitus
Neuroglia
Habits
Smoking
Muscles

Keywords

  • Achalasia
  • Autoimmune
  • Autoimmune gastrointestinal dysmotility
  • Glutamic acid decarboxylase-65
  • Neural autoantibodies

ASJC Scopus subject areas

  • Physiology
  • Gastroenterology

Cite this

Neural autoantibody profile of primary achalasia. / Kraichely, Robert E.; Farrugia, Gianrico; Pittock, Sean J; Castell, Donald O.; Lennon, Vanda A.

In: Digestive Diseases and Sciences, Vol. 55, No. 2, 02.2010, p. 307-311.

Research output: Contribution to journalArticle

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