A CLINICO.PATHOLOGICAL STUDY OF ANAL FISTULAE

Anal Fk*uh .
Revlew otLiterature
immunodeficiency (Griffiths, l98E). Ulcerations, erosions, and mucosal
hemonhage are the primary macroscopic findings. Although such lesions
may have other causes, microscopic identification of the eytomogalicell
provides evidence of tissue infection vyith CMV (see below,
"Histopathology') (Hinnant et aL 1986) Special stains for CMV antigens
aird DNA have shown that many more cells are infected than those that
have classic cytomegalic changes (Hinnnnt et aL 1986.\ many
gastrointestinal cell types can be infected in active disease, most commonly
vascular endothelial cells but fibroblasts, smooth muscle cells, and
glandular epithelium are also infected {Hinnant et aL 1986.) Figure ll.
f
The pathogenesis of intestinal lesions recently been reviewed(
Grrmdy. Igg0). it is a complex process involving mucosal CMV infection
with inflammation and tissue necrosis and vascular endothelial
involveurent with subsequent ischernic mucosal injury (Iwasaki 1987.)
vascular occlusion may be an important cause of tissue injury . however ,
surface epithelia! cells columnar, never squamous are frequently infected
at the edge of the uleerations and in nearby mucosa that is not inflamed
(Foucar, ef aL l9&I).results suggesting that vascular involvernent is not
necessarily the only or predominant cause of tissue injury. Local immune
suppression or autoimm$ne factors may play role in the pathogenesis of
gastrointestinal CMV disease (Merigutt, et al. 199A.) btrt they do not
appear to be central to the pathogenesis as they are in CMV pneumonitis in
bone marrow transplant recipients( Grundy. 1990.)
U
#
I
30