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Content available remote Increased aortic stiffness in ulcerative colitis
Only a few studies reveal immunological changes in breast milk after the intake of probiotic and none focus on secretory IgA (sIgA). The aim our report was to investigate the levels of sIgA in human breast milk and stools before and after 4 weeks of probiotic intake in a patient with ulcerative colitis (UC) and a control. The study included 2 lactating women: 1 with UC and 1 control. Both received daily 3.75 billion viable Lactobacillus bulgaricus for 28 days. SIgA was measured in breast milk and stools before and after the probiotic intake. The concentration of sIgA in breast milk before the probiotic intake in UC was 408.5 vs 137.4 µg/ml in contol. Fecal sIgA in UC was 420 vs 274 µg/ml in control. After 28 days of probiotic intake there was a decrease in breast milk sIgA in UC but an increase in control - 266.7 vs 914 µg/ml respectively. There was an increase in fecal sIgA both in UC and control - 674.4 vs 1033 µg/ml. It is tempting to speculate that the different sIgA secretion towards the probiotic may be a result of an altered mucosal immune response in UC.
Ulcerative colitis and Crohn's disease are chronic diseases of the gastrointestinal tract, which are usually grouped together as inflammatory bowel disease (IBD). Despite many researches, the etiology is still unknown, but it is believed that IBD is caused by a combination of genetic and environmental factors that interact with the immunological system. Many people worldwide (around 4 million) suffer from a form IBD and the incidence of Crohn's disease is still increasing. Aminosalicylates, corticosteroids, immunomodulators, biologic medicines reduce the inflammation, relieve symptoms, prevent flare-ups, but new, more effective drugs with smaller amount of side effects are wanted and examined.
Purpose: Recent literature data indicate a key role of apoptosis in the pathogenesis of inflammatory bowel disease. The aim of the study was to evaluate the expression of Bax, Bid, Bcl-2 and Bcl-xl in non-dysplastic and dysplastic epithelium in inflamated mucosa of patients with ulcerative colitis. Methods: The study consists of 18 patients with diagnosed ulcerative colitis. The expression of proteins was determined immunohistochemically. Results: Lack of Bax expression in normal epithelium of the inflamed intestinal mucosa (94.4%) and a weak expression of this protein were found in dysplastic glandular cells (67%). The Bax expression of dysplastic epithelium correlates with reduced severity of chronic inflammation (p<0.005). Bid expression in non-dysplastic glands was found in 67% of cases vs. 16% in dysplastic epithelium that was associated with the occurrence of epithelial erosions or ulcers (p<0.05). Moderate cytoplasmic expression of Bcl-xl was noted in 27.7% of patients in normal epithelium and in 66.1% within dysplastic lesions. Bcl-xl expression in dysplastic glandular cells correlated with the presence of neutrophils in the lamina propria (p <0.05). Conclusions: The immunohistochemical expressions of Bax, Bcl-2 and Bcl-xl increase and Bid protein expression decreases in dysplastic glandular tubes as compared to non-dysplastic intestinal epithelium in inflamed mucosa, which may suggest an imbalance of controlled cell death in ulcerative colitis.
The risk of carcinoma increases in patients with a 10-year or longer duration of ulcerative colitis (UC). To search for a more objective parameter to assess epithelial dysplasia. The study comprised 25 cases of longstanding UC: 7 cases with regenerative atypia, 7 with low grade dysplasia, 7 with high grade dysplasia, and 4 cases indefinite for dysplasia. The colonic biopsies obtained during endoscopy were stained with H&E to identify the aforementioned categories. Seventy-five sections from biopsy specimens were stained immunohistochemically to detect differences in the frequency and pattern of nuclei positive for the proliferation marker Ki67 and p53. In high grade dysplasia, the distribution of Ki67 positive cells was diffuse throughout the full length of the crypt, whereas low grade dysplasia and epithelium indefinite for dysplasia, as well as regenerative epithelium, showed an expanded basal zone. None of the regenerative atypia cases showed strong intensity p53 staining compared to dysplasia cases. None of the high grade dysplasia cases showed restricted p53 staining to the lower two thirds of the crypt. All the cases of HGD showed extension of Ki67 and p53 staining above the basal two thirds of the crypt. Ki67 and p53 immunostained cell assessment combined with routine histological evaluation of colorectal mucosa can improve the diagnostic accuracy, as well as the assessment of malignant transformation risk.
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