Electron microscopic studies of esophageal wall structures in patients with achalasia: casting more light on unresolved aspects of pathogenesis.

Background/aims: Previous investigations of esophageal tissue and serum probes failed to identify a common etiologic agent predisposing to, triggering or causing achalasia. In order to further examine the detailed pathologic processes resulting in achalasia we performed electron-microscopic studies of muscle biopsies taken from the LES high pressure zone in patients undergoing surgery--either Heller myotomy or esophageal resection.

Methodology: Smooth muscle biopsies with a 20 x 15-mm longitudinal segment of the myenteric plexus from the distal esophagus (lower border of the esophageal incision) in patients undergoing Heller myotomy for achalasia were taken.

Reduction of interstitial cells of Cajal (ICC) associated with neuronal nitric oxide synthase (n-NOS) in patients with achalasia.

Background: The etiology of achalasia is still unknown. The current theories of chronic inflammation leading to autoimmune response with destruction and loss of the inhibitory myenteric ganglion cells enlighten its pathogenesis in a limited way only. Interstitial cells of Cajal (ICC) have been shown to be involved in nitrergic neurotransmission of the lower esophageal sphincter (LES).

Spectrum of histopathologic findings in patients with achalasia reflects different etiologies.

Background: The etiology of achalasia is still unknown. The aim of the present study was to elucidate its underlying pathologies and their chronology by investigation of esophageal specimens in patients undergoing surgery (esophageal resection or myotomy) for achalasia.

Methods: In 17 patients with achalasia, histopathologic examinations of the esophageal wall focussing on the myenteric plexus were performed.