Sclerosing encapsulating peritonitis and non-occlusive mesenteric infarction found at autopsy in a man who had undergone continuous ambulatory peritoneal dialysis: A histochemical and immunohistochemical study
T. Ohmori et al., Sclerosing encapsulating peritonitis and non-occlusive mesenteric infarction found at autopsy in a man who had undergone continuous ambulatory peritoneal dialysis: A histochemical and immunohistochemical study, PATHOL INT, 50(8), 2000, pp. 660-666
This is a report of a post-mortem histological, histochemical, and immunohi
stochemical examination of a rare case of sclerosing encapsulating peritoni
tis (SEP) and non-occlusive mesenteric infarction (NOMI), two serious compl
ications of continuous ambulatory peritoneal dialysis (CAPD), with which a
man suffering hepatitis C virus (HCV)-induced liver cirrhosis for 7 years a
nd trauma-induced paraplegia for 50 years had been treated for 1 year. The
direct cause of death was encephalopathy caused by extreme hyperammonemia (
11 250 mu g/dL in serum). The autopsy revealed that the SEP had drastically
reduced the length of the small intestine to 210 cm, 180 cm of which prese
nted acute ischemic enteritis with Gram-negative bacterial infection. Histo
logical examination of the SEP revealed that the exterior was composed of n
ormal serosal elastic lamina, but with a cocoon-like appearance remarkably
thickened by fibrosis to 3-8 times that of the normal subserosal layer and
consisting of spindle cells and blood vessels, with some infiltration of ma
st cells and lymphocytes. The immunohistochemical examination of the spindl
e cells revealed few AE1/AE3(+) cells, HHF35(+) cells, and CD34(+) cells, m
any CD117(+) cells with slight proliferative activity based on MIB-1 positi
vity (proliferation index < 1%), but no CD44(+) cells. It was concluded tha
t either the few CD34(+) and/or the many CD117(+) cells were mesenteric ste
m cells that had originated from the serosa, proliferated, then differentia
ted into myofibroblasts or fibroblasts, producing collagen and hyaluronic a
cid in the matrix, leading to the gradual formation of the SEP, which was i
nduced by the continual irritation of CAPD.