Connective tissue growth factor expression is increased in collagenous colitis and coeliac disease
Medical Clinic I Gastroenterology, Infectious Diseases, Rheumatology, Charité-Campus Benjamin Franklin, Berlin, Germany. Histopathology
(Impact Factor: 3.45).
09/2010; 57(3):427-35. DOI: 10.1111/j.1365-2559.2010.03652.x
Subepithelial collagen deposition is a classical feature of collagenous colitis (CC), but is also seen in untreated coeliac disease. The end-stage mediator of excess cellular collagen production is connective tissue growth factor (CTGF). The aim of this study was to investigate CTGF expression by in situ hybridization (ISH) and polymerase chain reaction (PCR) in CC and coeliac disease as well as lymphocytic colitis (LC), Crohn's colitis and ulcerative colitis (UC).
For coeliac disease we analysed fresh frozen material by quantitative reverse transcription-polymerase chain reaction (RT-PCR) and archival material for ISH. PCR transcripts in coeliac disease were moderately elevated and labelled cells were significantly increased in the subepithelial zone. For CC, LC and UC we investigated archival material because of the rarity of the first two conditions. There was a marked increase in CTGF expression in the subepithelial zone in CC, localizing to cells with the morphology of smooth muscle cells, which was not seen in LC.
The colocalization of CTGF transcripts with areas of excessive collagen deposition in coeliac disease and CC suggest that it might be the end-stage mediator of local fibrosis in these conditions.
Available from: Ebubekir Senates
- "It has been shown that CTFG induces the production of extracellular matrix by stimulating transcription of type 1 collagen . Also recent reports have shown higher CTFG expression in cases with increased connective tissue in lungs, bowel, kidney and liver       . Also another recent study has found increased expression of CTFG correlating with severity of fibrosis independent of inflammation in patients with chronic hepatitis C . "
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ABSTRACT: In this study, we aimed to investigate the relationship between the histological fibrosis stage of nonalcoholic fatty liver disease (NAFLD) and serum connective tissue growth factor (CTGF) to determine the usefulness of this relationship in clinical practice.
Serum samples were collected from 51 patients with biopsy-proven NAFLD and 28 healthy controls, and serum levels of CTGF were assayed by ELISA.
Levels of CTGF were significantly higher in patients with NAFLD compared with controls (P=0.001). The serum CTGF levels were significantly increased, that correlated with histological fibrosis stage, in patients with NAFLD [in patients with no fibrosis (stage 0) 308.2 ± 142.9, with mild fibrosis (stage 1-2) 519.9 ± 375.2 and with advanced fibrosis (stage 3-4) 1353.2 ± 610 ng/l, P < 0.001]. Also serum level of CTGF was found as an independent predictor of histological fibrosis stage in patients with NAFLD (β = 0.662, t=5.6, P <0.001). The area under the ROC curve was estimated 0.931 to separate patients with severe fibrosis from patients with other fibrotic stages.
Serum levels of CTGF may be a clinical utility for distinguishing NAFLD patients with and without advanced fibrosis.
Available from: Anastasios Koulaouzidis
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ABSTRACT: Microscopic colitis (MC) is considered an "umbrella term", comprising two subtypes, i.e., collagenous colitis (CC) and lymphocytic colitis (LC). They are classically associated with normal or unremarkable colonoscopy. In the last few years, reports have been published revealing findings that are thought to be characteristic or pathognomonic of MC, especially CC. A systematic electronic and manual search of PubMed and EMBASE (to December 2010), for publications on distinct endoscopic findings in MC, resulted in 42 relevant reports for inclusion in this review. Eighty eight patients with collagenous colitis were presented. Only one publication describing a distinct endoscopic pattern in LC was found. Typical findings in CC are alteration of the vascular mucosal pattern, mucosal nodularity, a sequence of change from mucosal defects to mucosal cicatricial lesions, and perhaps (although of doubtful relevance) mucosal pseudomembranes. A causal connection of mucosal defects with the use of lansoprazole seems to exist. Adoption of the proposed lesion description herein is recommended in order to improve homogeneity of future reports.
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ABSTRACT: Lymphocytic colitis (LC) and collagenous colitis (CC), 2 histologic forms of microscopic colitis, were recognized as rare disease entities 4 decades ago. An increasing body of evidence accumulated in the past 40 years reveals increasing incidence and prevalence rates, a wide spectrum of clinical presentations, and several histologic variants. Although several recent randomized clinical trials confirmed the efficacy of oral budesonide in treating LC and CC, disease relapse after a short-duration treatment is common. Despite their common clinical presentations and well-defined histologic diagnostic criteria, there are only few studies on the immunologic abnormalities in colonic tissue. The aim of this review is to (1) familiarize the pathologists in general practice with histomorphology of LC and CC, including the rare histologic variants and the clinical implication associated with these 2 diagnoses, (2) summarize the data from recent randomized clinical trials of oral budesonide, and (3) review immunological studies on colonic tissue. Overall, immunologic abnormalities of colonic tissue seem to explain for the histomorphologic features and the clinical symptomatology of LC and CC. Advances in the understanding of the underlying immunologic abnormalities in the colonic tissue may help develop novel and effective therapies for these 2 diseases.
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