食道アカラシアの病理―発生機序からみて

The Pathology of Esophageal Achalasia: From the Viewpoint of Occurrence Mechanism

要旨　臨床経過，胸部X線，上部消化管造影所見，内視鏡所見，および内圧検査などより食道アカラシアと診断され，外科的に切除された31症例50切片を用いて，主として病理学的に検討を行った．H・E染色標本では，Auerbach神経叢の神経節細胞の消失，減少，変性が顕著であった．食道癌を合併したアカラシアでは，神経節細胞の消失は拡張部に高度であった．従来の報告どおりアカラシアでは，アセチルコリンエステラーゼ活性によるコリン作動性神経活性の分布は，Auerbach神経叢上にほとんど認められなかった．また，VIPも同部に染色されず，食道下部括約筋の弛緩不全にVIPも関与しているものと思われる．アカラシア症例では，筋層間にc-kit陽性のCajalの介在細胞の減少はみられなかったが，Cajalの介在細胞に絡み付いて存在すると言われるNO合成細胞はアカラシアで減少しており，NANC抑制神経の障害，特にCajalの介在細胞に対する作用の障害が食道アカラシアの病態に関与するものと考えられる．

　Esophagectomy specimens from 31 patients diagnosed with achalasia by clinical course, x-ray examination, endoscopic observation and esophageal manometry were examined histopathologically. In the H・E stained specimens, disappearance, decrease and degeneration of the ganglion cells of the Auerbach's plexus were remarkable. In achalasias, cholinergic activity assessed by acethylcholinesterase activity could seldom be recognized in ganglion cells and nerve fibers, neither was VIP activity observed, suggesting that loss of this activity is also involved in relaxation disorders of the esophageal lower sphincter. C-kit positive cells were not decreased, but nitric oxide synthesizing cells which twist around the interstitial cells of Cajal, were decreased in achalasia. Taken together, the functional failure of non-adrenergic non-cholinergic inhibitory nerves, and especially the failure of the interstitial cells of Cajal, seems to be involved in the pathogenesis of esophageal achalasia. In addition, in surgically resected achalasia accompanied with esophageal cancer, disappearance of the ganglion cells was severe in the proximal part of the esophagus.