Background: The accumulation of periodic acid Schiff (PAS)positive material
in the epithelium in microvillous atrophy (MVA) is diagnostic but unexplai
ned. It occurs earlier in the epithelial life cycle than the formation of m
icrovillous inclusions and warrants further investigation
Methods: Scanning photometry was used to assess the distribution of the PAS
-positive material within epithelial cells and to assess how this changed w
ith position on the crypt-villus axis. Thiery staining was applied to test
the PAS positivity of the secretory granules, and quantitative ultrastructu
ral morphometry was used to study secretory granule distribution in the epi
thelium.
Results: The PAS abnormality arose in upper crypt epithelium in congenital
and late-onset MVA and continued up the villus. Thiery staining demonstrate
d that the secretory granules were PAS positive. Quantitative morphometry s
howed that secretory granules in congenital MVA were predominantly present
in upper crypt and declined in the low villus. In late-onset MVA, secretory
granules arose in the upper crypt but predominated in the low villus regio
n. No evidence of secretory granule coalescence with the epical membrane wa
s seen, although evidence of crinophagy was observed. Secretory granule pro
files were seen, indicating that they formed part of a membrane-bound vesic
ular network within the cell, rather than existing simply as discrete bodie
s. The Golgi complex appeared normal.
Conclusions: The secretory granules are responsible: for the PAS-positive s
taining in upper crypt and low villus regions in MVA. They appear to form a
n intracytoplasmic vesicular network, undergo crinophagy, and decline in pr
ominence in the low to midvillous region. The absence of evidence of coales
cence with the apical membrane indicates that the secretory granules arise
from a post-Golgi block in exocytosis rather than from endocytosis of gut l
uminal contents. Periodic acid-Schiff positivity in upper villous regions a
rises from microvillous inclusions and lysosomal bodies. (C) 1999 Lippincot
t Williams & Wilkins, Inc.