[The role of diffuse endocrine system and colonocytes cellular renovation in formation of clinical variants of irritable colon syndrome in young persons].
60 patients with irritable colon syndrome (ICS) were examined. They were divided into 2 groups. Group 1 included 30 patients who had ICS with dominating constipation (ICSc). Group 2 consisted of 30 patients with ICS and dominating diarrhea (ICSd). 12 practically healthy persons composed control group. The patients were being observed in dynamics (in periods of aggravation and remission), under uniform program including clinical, endoscopic, morphologic and immunohistochemical methods. It was established that ICSc development related to hyperplasia and hyperfunction serotonin producing cells together with decrease of number and functional activity of VIP-producing cells and mast cells. It was detected significant increase of colonocytes proliferative activity, shown throw number of immunopositive to cycline Dl epithelial cells, and compensatory increase of apoptosis activity. In patients with ICSd it was registered increase of number and functional activity of general population of apudocytes, serotonin-, melatonin- and VIP-produsing cells and mast cells. It was detected decrease of number of colonocytes immunopositive to cycline D1 and proliferating cell nuclear antigen, and growth of colon epithelial cells apoptosis activity. More significant changes of diffuse endocrine system in patients with ICSd set conditions for progress of changes of cell renovation with frequent colon mucous tunic atrophy, acting as a background for carcinogenesis.
Osadchuk
A M
AM
Osadchuk
M A
MA
Balashov
A V
AV
Kvetnoĭ
I M
IM
D001078:APUD Cells / Q000378:metabolism*; D017667:Adipocytes / Q000378:metabolism*; D000328:Adult; D019938:Cyclin D1 / Q000378:metabolism*; D004759:Enterochromaffin Cells / Q000378:metabolism*; D005260:Female; D006801:Humans; D043183:Irritable Bowel Syndrome / Q000378:metabolism* / Q000503:physiopathology*; D008297:Male; D012075:Remission, Spontaneous
D019938:Cyclin D1