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Small bowel capsule endoscopy (CE) was first introduced 15 years ago, and a large amount of literature has since been produced, focused on its indication, diagnostic yields, and safety. Guidelines that have made CE the primary diagnostic tool for small bowel disease have been created. Since its initial use in the small bowel, CE has been used for the esophagus, stomach, and colon. The primary indications for small bowel CE are obscure gastrointestinal bleeding, unexplained iron deficiency anemia, suspected Crohn's disease, small bowel tumors, nonsteroidal anti-inflammatory drug enteropathy, portal hypertensive enteropathy, celiac disease, etc. Colon CE provides an alternative to conventional colonoscopy, with possible use in colorectal cancer screening. Guidelines for optimal bowel preparation of CE have been suggested. The main challenges in CE are the development of new devices with the ability to provide therapy, air inflation for better visualization of the small bowel, biopsy sampling systems attached to the capsule, and the possibility of guiding and moving the capsule by an external motion controller. We review the current status and future directions of CE, and address all aspects of clinical practice, including the role of CE and long-term clinical outcomes.
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Amyloidosis is characterized by the abnormal deposition of extracellular amyloid fibrils. Cases involving amyloid light-chain amyloidosis in the small intestine have been reported infrequently in Korea. Here, we report a case of localized light chain protein amyloidosis in the small intestine. Esophagogastroduodenoscopy, push enteroscopy, and capsule endoscopy revealed submucosal tumor-like lesions, multiple shallow ulcers, and several erosions in the distal duodenum and jejunum. An endoscopic biopsy established the diagnosis of amyloidosis. In through an immunohistochemical analysis, the presence of lambda light chain protein was detected. The patient had no evidence of an underlying clonal plasma cell disorder or additional organ involvement. Therefore, we concluded that the patient had localized amyloidosis of the small intestine.
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Ethanol administration causes intestinal epithelial cell damage by increasing intestinal permeability and the translocation of endotoxins from intestinal bacterial flora. Heat shock proteins (HSPs) are associated with recovery and protection from cell damage. The aim of the current study was to investigate differences in the expression of HSPs in the small intestine and the biochemical changes attributable to ethanol-induced intestinal damage.
Ethanol (20%) was injected intraperitoneally (2.75 g/kg, 5.5 g/kg, 8.25 g/kg) in ICR mice and the same volume of saline was administered to controls. After 1 hour, the proximal, middle, and distal segments were taken from the small intestine and the degree of damage was analyzed. In each segment, the expression of HSPs was analyzed by western blotting. The expression of inflammatory mediators including interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α), cyclooxygenase-2 (COX-2), and antioxidant enzyme such as glutathione-S-transferase were compared using real-time polymerase chain reaction assays.
In the control group, HSP70 increased in all segments of small intestine. Additionally, increases in the expression of HSP40 and HSP90 in the distal regions and an increase in HSP32 in the middle regions were observed. After ethanol treatment, greater histological damage was observed in the distal small intestine and significant decreases in HSPs were observed generally. Increased expression of IL-1β, TNF-α, and COX-2 was observed in small intestinal tissues exposed to ethanol-induced damage. However, there was no significant difference in the expression of an antioxidant enzyme.
Significant differences in the expression of HSPs in different intestinal regions were observed. These differences may have been attributable to the distribution of intestinal bacteria.
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