title: 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.
abstract: This is a report of a post-mortem histological, histochemical, and immunohistochemical examination of a rare case of sclerosing encapsulating peritonitis (SEP) and non-occlusive mesenteric infarction (NOMI), two serious complications of continuous ambulatory peritoneal dialysis (CAPD), with which a man suffering hepatitis C virus (HCV)-induced liver cirrhosis for 7 years and 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 microg/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 presented acute ischemic enteritis with Gram-negative bacterial infection. Histological examination of the SEP revealed that the exterior was composed of normal 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 mast cells and lymphocytes. The immunohistochemical examination of the spindle cells revealed few AE1/AE3(+) cells, HHF35(+) cells, and CD34(+) cells, many CD117(+) cells with slight proliferative activity based on MIB-1 positivity (proliferation index <1%), but no CD44(+) cells. It was concluded that either the few CD34(+) and/or the many CD117(+) cells were mesenteric stem cells that had originated from the serosa, proliferated, then differentiated into myofibroblasts or fibroblasts, producing collagen and hyaluronic acid in the matrix, leading to the gradual formation of the SEP, which was induced by the continual irritation of CAPD.
authors.affiliation: Second Department of Pathology, Ehime University School of Medicine, Ehime, Japan. ohmori@m.ehime-u.ac.jp
authors.forename: T
authors.initials: T
authors.lastname: Ohmori
authors.forename: S
authors.initials: S
authors.lastname: Ohnishi
authors.forename: K
authors.initials: K
authors.lastname: Okada
authors.forename: N
authors.initials: N
authors.lastname: Arita
mesh_terms: D000368:Aged; D018952:Antigens, CD34 / Q000378:metabolism; D015415:Biomarkers; D002455:Cell Division; D017809:Fatal Outcome; D006651:Histocytochemistry; D006801:Humans; D007124:Immunoenzyme Techniques; D007238:Infarction / Q000209:etiology* / Q000378:metabolism / Q000473:pathology; D007415:Intestinal Obstruction / Q000209:etiology / Q000473:pathology; D007421:Intestine, Small / Q000378:metabolism / Q000473:pathology; D008297:Male; D008643:Mesentery / Q000098:blood supply* / Q000473:pathology; D010531:Peritoneal Dialysis, Continuous Ambulatory / Q000009:adverse effects*; D010538:Peritonitis / Q000209:etiology* / Q000378:metabolism / Q000473:pathology; D019009:Proto-Oncogene Proteins c-kit / Q000378:metabolism; D012598:Sclerosis / Q000209:etiology* / Q000378:metabolism / Q000473:pathology
chemical_list: D018952:Antigens, CD34; D015415:Biomarkers; D019009:Proto-Oncogene Proteins c-kit