Deposition of amyloid in the gastrointestinal tract.

Amyloid may cause widespread damage to the gastrointestinal tract. Affection of blood vessels may lead to infarction and perforation of the bowel (Brody, Wertlake, and Laster, 1964; Akbarian and Fenton, 1964) as well as to bleeding or loss of protein into the lumen of the gut (Jarnum, 1965); damage to the musculature or nervous elements may cause marked alterations in motility (Gilat and Spiro, to be published); and mucosal destruction may lead to impaired absorption (Beddow and Tilden, 1960). The presence of amyloid in a tissue does not evoke an inflammatory response and damage is apparently caused by local replacement of tissue. Knowledge of the anatomo-histological site of amyloid deposition may, therefore, help in understanding and anticipating the clinical manifestations. Perusal of reported cases of amyloidosis with gastrointestinal manifestations failed to reveal any pattern or trend: the deposition of amyloid appeared to be quite haphazard and unpredictable. The present study was, therefore, initiated to study systematically the site of amyloid deposition in the digestive tract in a large number of cases. Amyloid is an extracellular scleroprotein with a characteristic fibrillar structure as seen by electron microscopy (Cohen and Calkins, 1959; Gafni, Merker, Shibolet, Sohar, and Heller, 1966). The weight of recent evidence favours the thesis of local production (Cchen, Gross, and Shirahama, 1965; Gafni et al, 1966) apparently by reticuloendothelial cells (Cohen, 1967). The detection and localization of amyloid in histological sections has been much facilitated by the use of polarized light. When Congo red-stained sections are viewed with the polarizing microscope amyloid exhibits a typical green birefringence which allows of the detection of even minute amounts of amyloid as well as its exact localization in various histological structures (Ravid, Gafni, Sohar, and Missmahl, 1967).