Targeted biopsy protocols guided by either chromoendoscopy or CEM led to higher detection rates of IEN and are thus mandatory for surveillance colonoscopies in patients with long-standing UC. Random biopsy protocols should be replaced by chromoendoscopy-guided protocols.
EndoClot expanded the therapeutic options in the management of GI bleeding. It was applicable as a monotherapy or in combination with other techniques from oozing bleeding type or lower. It was most effective in diffuse or extensive bleeding activity or when access to the bleeding vessel was difficult. EndoClot can be applied as a bridge to surgery when classical methods of hemostasis have failed.
CEM improves rapid diagnosis of acute intestinal GvHD with high accuracy while performing endoscopy. Platelet transfusions and unnecessary biopsy acquisition can be avoided once acute intestinal GvHD has been diagnosed in vivo.
Elevated cytokines, especially TNF-alpha, have been implicated in the pathogenesis of necrotising enterocolitis (NEC). We have previously shown that TNF-alpha drives the production of matrix degrading enzymes, the matrix metalloproteinases (MMPs), in the gut wall. In this study we have therefore investigated the role of MMPs in the pathogenesis of NEC in neonates. Nine newborn infant nonnecrotic resected bowels with confirmed NEC were studied and 8 newborn infants with neonatal bowel obstructions were used as controls. Immunostaining was used to identify the numbers of monocytes, macrophages, neutrophils, and T cells in the tissue. We used quantitative, competitive RT-PCR to analyze the number of TNF-alpha, IFN-gamma, MMP, and TIMP mRNA transcripts and western blotting to analyze MMP and TIMP protein production. Double labeling (immunostaining and in situ hybridization) was used to identify the phenotype of MMP mRNA expressing cells. We found increased numbers of monocytes, macrophages, and neutrophils in NEC tissue compared with controls. The number of T cells was unexpectedly low in NEC as was the number of IFN-gamma transcripts in comparison with the control samples. Increased numbers of transcripts for TNF-alpha were detected in NEC tissue, as was mRNA expression and protein production for stromelysin-1 and TIMP-1 but not collagenase, gelatinases, or TIMP-2. The cellular source of stromelysin-1 in NEC was alpha-smooth muscle actin positive cells. These results suggest that stromelysin-1, which has the ability to degrade the mucosal extra-cellular matrix, may be responsible for the extensive tissue injury in infants with NEC.
Classic Whipple disease (CWD) is a systemic infection caused by Tropheryma whipplei. Different diagnostic tools have been developed over the last decades: periodic acid-Schiff (PAS) staining, T whipplei-specific polymerase chain reaction (PCR), and T whipplei-specific immunohistochemistry (IHC). Despite all these advances, CWD is still difficult to diagnose because of a variety of clinical symptoms and possibly a long time span between first unspecific symptoms and the full-blown clinical picture of the disease.Herein, we report an observational cohort study summarizing epidemiologic data, clinical manifestations, and diagnostic parameters of 191 patients with CWD collected at our institution. Gastrointestinal manifestations are the most characteristic symptoms of CWD affecting 76% of the cohort. Although the small bowel was macroscopically conspicuous in only 27% of cases, 173 (91%) patients presented with characteristic histological changes in small bowel biopsies (in 2 patients, these changes were only seen within the ileum). However, 18 patients displayed normal small bowel histology without typical PAS staining. In 9 of these patients, alternative test were positive from their duodenal specimens (ie, T whipplei-specific PCR and/or IHC). Thus, in 182 patients (95%) a diagnostic hint toward CWD was obtained from small bowel biopsies. Only 9 patients (5%) were diagnosed solely based on positive T whipplei-specific PCR and/or IHC of extraintestinal fluids (eg, cerebrospinal fluid, synovial fluid) or extraintestinal tissue (eg, lymph node, synovial tissue), respectively.Thus, despite efforts to diagnose CWD from alternative specimens, gastroscopy with duodenal biopsy and subsequent histological and molecular–biological examination is the most reliable diagnostic tool for CWD.
The assessment of duodenal histology by CEM in patients with celiac disease is sensitive and specific in determining increased numbers of IELs and villous atrophy, but insufficient in respect of crypt hyperplasia. For routine use of CEM in patients with celiac disease, the technique would need to be improved.
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