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NEW EVIDENCE CONCERNING THE CAUSE OF OESOPHAGEAL SMOOTH MUSCLE ATROPHY IN SCLERODERMA
Dysphagia and reflux are common features of scleroderma that, in the past, have been attributed to ischaemia and secondary fibrosis. However, this substantial study of an archival database containing 74 patients suggests otherwise. There was marked atrophy of circular smooth muscle (see fig), most obvious distally in 93% of patients compared with 5% of controls. However, there was no evidence of fibrosis. Although vascular intimal hyperplasia was noted in 38% of patients compared with 5% of controls, this did not correlate with smooth muscle atrophy. Furthermore, there was atrophy of circular smooth muscle even when it was interdigitated with skeletal muscle, a feature incompatible with an ischemic basis. They found no significant increase of inflammatory cells in the myenteric plexus but did find reduced staining for the interstitial cells of Cajal (ICCs), although these data are preliminary as there were only three patients with tissue available for this stain. The authors speculate that the smooth muscle atrophy may be secondary to damage to ICCs, a novel hypothesis which is worthy of further exploration.
See p 1697
Central atrophy (a) of circular smooth muscle from the distal oesophagus in scleroderma. Peripheral smooth muscle (m) is normal.
USE OF TISSUE-ENGINEERED CELL SHEET GRAFTS TO PREVENT STRICTURE FORMATION AFTER ENDOSCOPIC MUCOSAL RESECTION
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