A software tool for prediction of prosthesis failure at the carpometacarpal joint of the thumb.

Early recognition of prosthesis failure is difficult. A tool that helps to identify faulty prosthesis - a cause of early implant loosening - is needed. The aim of this study was to detect early implant loosening by applying a software program EBRA (Ein-Bild-Röntgen-Analyse). EBRA was applied to the radiographs of a series of 76 patients, with a total of 102 thumb carpometacarpal joint de la Caffinière prostheses, with an average follow-up of 14.5 months (range 0.5-24). The data were used to draw graphs of cup migration and inclination over time. Corresponding regression lines of migration and inclination in relation to time were made up to the point of loosening. The gradient of regression was calculated for all implants. The gradient of regression on the x and y axes differed significantly between stable and loose implants. Loose and stable implants showed significantly different cup migration on the x and y axes over time. EBRA proved to be a reliable tool to visualize cup migration in the trapeziometacarpal joint and to predict implant failure.

Serum tenascin-C is an indicator of inflammatory bowel disease activity.

Tenascin-C is a multifunctional matrix protein that is induced in inflammation and neoplasia. In the colonic mucosa of ulcerative colitis patients tenascin-C indicates tissue repair, and mucosal concentrations are correlated with local disease activity. We prospectively examined the relationship between serum concentrations of tenascin-C parameters of disease activity in surgically treated patients with ulcerative colitis and patients with inflammatory bowel disease (IBD). Perioperative serum concentrations were quantified by ELISA in 58 patients admitted for restorative proctocolectomy; controls were 37 patients with familial adenomatous polyposis receiving the same treatment. We also measured tenascin-C serum levels in 47 patients with ulcerative colitis and Crohn's disease who were receiving nonsurgical treatment. Preoperative serum tenascin-C levels were significantly higher in ulcerative colitis patients than in controls (17.2 +/- 14.6 microg/ml vs. 3.2 +/- 1.7 microg/ml) and were significantly correlated with clinical and histological parameters of disease activity; levels decreased significantly after restorative proctocolectomy. Serum tenascin-C levels were also correlated with the course of disease activity in conservatively treated IBD patients. Tenascin-C is thus not disease-specific. However, it does indicate the activity of IBD and may reflect the degree of tissue remodeling. The tenascin-C levels therefore offers a novel serum parameter for assessing disease activity and monitoring therapy in patients with IBD.

Duodenal adenomatosis in familial adenomatous polyposis coli. A review of the literature and results from the Heidelberg Polyposis Register.

Familial adenomatous polyposis coli (FAP) is an autosomal dominant genetic disorder caused by mutations of the APC gene on the long arm of chromosome 5. While multiple colorectal adenomas usually developing in early adolescence represent the most conspicuous phenotypic feature, the disease represents a generalized hyperproliferative disorder with various extracolonic manifestations. Duodenal cancer and desmoids are the leading causes of death in FAP patients after prophylactic colectomy. The prevalence of duodenal adenomatosis among FAP patients varies from 50% to greater than 90%, while only few patients (3-5%) develop duodenal cancer. Periampullary adenomas seem to carry a high risk of malignant transformation. The sensitivity of endoscopic procedures for early detection of severely dysplastic or malignant duodenal lesions is low, and the prognosis of duodenal cancer is poor. Thus the question arises whether it is possible to define a subgroup of high-risk patients for duodenal malignancy, and whether severe duodenal adenomatosis should lead to an aggressive prophylactic surgical approach. This contribution discusses the current literature and presents the experience of the Heidelberg Polyposis Register based on gastroduodenoscopy findings in 231 FAP patients. In 135 cases (58.4%) macroscopic duodenal adenomas were observed. The majority of patients displayed numerous lesions throughout the duodenum, while adenomas were restricted to the periampullary region in ten. Four patients suffered from duodenal cancer. Twenty-two required an endoscopic or operative intervention. Five were treated by laparotomy and duodenotomy, while ampullary excision was indicated in six cases. Eight patients underwent partial pancreaticoduodenectomy for severe duodenal adenomatosis.

Detection of tenascin-C isoforms in colorectal mucosa, ulcerative colitis, carcinomas and liver metastases.

The glycoprotein tenascin-C is up-regulated in inflammatory and neoplastic diseases. Most available data on tissue tenascin-C content do not distinguish its various isoforms. We have quantified tissue tenascin-C signals in colorectal mucosa, ulcerative colitis, colorectal carcinomas and liver metastases using 5 monoclonal antibodies (MAbs) with different binding sites. Tenascin-C of tissue extracts was analyzed by a standardized Western blot technique and densitometry. As a reference MAb, K8 displayed tenascin-C tissue concentrations of 4.1 +/- 2.3 microgram/mg total protein in normal mucosa, 13.8 +/- 4.7 microgram/mg in ulcerative colitis, 28.8 +/- 14.5 microgram/mg in colorectal carcinomas and 25.6 +/- 8.9 microgram/mg in liver metastases. The optical density values per microgram protein tissue extract of the 5 MAbs reflect the levels of the corresponding tenascin-C epitopes. Various signal intensities indicate a distinct diagnostic usefulness of the MAbs in detecting colorectal carcinomas. The binding characteristics of MAb J1/tn2 point to an under-representation of the TNfnD domain in metastasizing colorectal carcinomas, while MAb 19H12 showed an increased binding rate on the TNfnA1,2,4 region. Our comparative study of tenascin-C in inflammatory and neoplastic diseases of the colon mucosa substantiates the occurrence of large differences in the diagnostic value of tenascin-C MAbs. The detected alterations of tenascin-C in metastasizing colorectal carcinomas might indicate a prognostic value of specific tenascin-C isoforms.

Mucosal tenascin C content in inflammatory and neoplastic diseases of the large bowel.

PURPOSE: Tenascin C is a glycoprotein of the extracellular matrix. It is upregulated during embryologic development, wound healing, and under conditions of normal and neoplastic growth. Most available data on tenascin C expression in tissues is based on immunohistologic studies. The present study was designed to quantify tissue concentrations in patients with inflammatory and neoplastic diseases of the large bowel. METHODS: Fifty patients with ulcerative colitis, 19 patients suffering from familiar adenomatous polyposis without malignant transformation, and 69 patients with colorectal carcinoma were investigated. Tenascin C concentrations in tissue extracts were determined by semiquantitative Western blotting. RESULTS: The tenascin C tissue concentration of normal mucosa was 2.6 +/- 3.4 microg/mg (n = 55), 2.9 +/- 2.1 microg/mg in colorectal adenomas (n = 19), 7.5 +/- 4.7 microg/mg in ulcerative colitis (n = 50), and 18 +/- 15 microg/mg in colorectal carcinomas (n = 69; mean +/- standard deviation). In ulcerative colitis, the mucosal tenascin C content correlated with histopathologic disease activity. No differences were found between subgroups of adenomas or carcinomas. CONCLUSIONS: Tenascin C tissue concentrations were not altered in adenomas, slightly elevated in ulcerative colitis, and substantially increased in colorectal carcinomas. Although less useful as a diagnostic parameter, tenascin C tissue levels serve as an instrument for assessing the activity of stromal remodeling in large-bowel diseases generally. Specifically, they may reflect disease activity in ulcerative colitis.

[Long-term results after restorative proctocolectomy and ileoanal pouch in children with familial adenomatous polyps]. / Langzeitergebnisse nach restaurativer Proktokolektomie und ileoanaler Pouchanlage (IAP) bei Kindern mit FAP.

Restorative proctocolectomy and ileal pouch-anal anastomosis (IPAA) is considered the therapy of choice for the prophylactic treatment of FAP in adults, while straight ileoanal endorectal pull-throughs were often favored in children. However, our experience with five children undergoing an ileoanal J-pouch procedure under the age of 15 years (7-15) due to early onset of a severe symptomatic FAP phenotype suggests results which are superior to those after direct ileoanal anastomosis. Even after a primary straight ileoanal pull-through with local complications and a high defecation rate, secondary IPAA should be considered.

[Heidelberg polyposis register. Experiences with ileoanal pouch in familial adenomatous polyposis coli (FAP): the ileoanal anastomosis problem zone]. / Heidelberger Polyposisregister. Erfahrungen mit der ileoanalen Pouchanlage bei familiärer adenomatöser Polyposis coli (FAP): Problemzone ileoanale Anastomose.

Restorative proctocolectomy and ileal pouch-anal anastomosis (IPAA) is the therapy of choice for the prophylactic treatment of FAP. Despite maximal radicality, we frequently observed remaining rectal mucosa and in some cases even adenomas at the pouch-anal anastomosis. Therefore, we changed our postoperative care by adding a yearly proctoscopy to regular pouchoscopies.

[Mutation localization as a guide for surgical approach in familial adenomatous polyposis?]. / Mutationslokalisation als Wegweiser zur operativen Taktik bei FAP?

Restorative proctocolectomy and ileal pouch-anal anastomosis (IPAA) is considered the operative therapy of choice for the prophylactic treatment of FAP. Recently, Vasen and coworkers [5] after correlating the incidence of metachronous rectal cancer with the site of the causative APC mutation suggested subtotal colectomy and IRA to be the primary treatment in patients with mutations proximal to codon 1250, whereas IPAA should be performed in those with mutations beyond this codon. Mutation analysis in our patients after IRA, however, shows the majority of APC mutations to be located proximal to codon 1250 even in those patients with severe rectal polyposis and metachronous rectal cancer, thus not supporting the therapeutic recommendations of Vasen and coworkers.

CD95 (APO-1/Fas)-mediated apoptosis in colon epithelial cells: a possible role in ulcerative colitis.

BACKGROUND & AIMS: Ligation of CD95 (APO-1/Fas) by antibody or CD95 ligand (CD95L) induces apoptosis and, in some cell lines, growth. Normal colonic epithelial cells constitutively express CD95. The function of CD95 on colonocytes is unknown. The aim of this study was to elucidate the role of epithelial CD95 in the normal colon and in ulcerative colitis. METHODS: Intact colonic crypts were isolated, and the effects of CD95 ligation in vitro were studied. CD95L-expressing cells and apoptotic cells were detected in situ by RNA hybridization, immunohistochemistry, and DNA nick end labeling. RESULTS: On CD95 ligation, isolated colonic crypt cells underwent apoptosis within 4 hours. No growth-promoting effect was observed. In normal colon, CD95L expression was restricted to few mononuclear cells randomly scattered within the lamina propria. Therefore, the CD95-CD95L system is very unlikely to operate in the regeneration of the colonic epithelium. However, in ulcerative colitis, the number of interstitial CD95L+ cells and the frequency of apoptosis in both lamina propria and epithelium were increased considerably. Further, a focal association of subepithelial CD95L+ mononuclear cells and epithelial apoptosis was observed. CONCLUSIONS: In ulcerative colitis, soluble CD95L-mediated epithelial apoptosis may lead to a breakdown of the epithelial barrier function facilitating the invasion of pathogenic microorganisms.

Tenascin-C tissue concentration in inflammatory and neoplastic diseases of the colon mucosa.

BACKGROUND: Tenascin-C is a gycoprotein of the extracellular matrix with predominantly antiadhesive qualities. In the colon mucosa tenascin-C has been found to be induced in inflammatory and neoplastic diseases by immunohistology. This study aimed at quantitating mucosal tenascin-C induction. MATERIALS AND METHODS: Mucosal tenascin-C concentration was determined by Western blotting quantified by densitometry in fresh frozen specimens of the colon from patients with ulcerative colitis, familial polyposis, and colorectal carcinomas. RESULTS: The tenascin-C concentration in normal mucosa was 2.6 micrograms/mg protein (SD +/- 3.4 micrograms/mg). Colorectal adenomas displayed an equal tissue concentration of 2.8 micrograms/mg protein (SD +/- 2.0 micrograms/mg). In ulcerative colitis statistically significant elevated tissue content of 7.5 micrograms/mg protein (SD +/- 4.7 micrograms/mg) was found. Colorectal carcinomas had a tissue tenascin-C level of 18.0 micrograms/mg protein (SD +/- 14.6 micrograms/mg), which was significantly different from the other groups. CONCLUSIONS: Tenascin-C concentration is elevated in inflammatory and neoplastic diseases of the colorectal mucosa. The distinct increase in the tenascin-C content in colorectal carcinomas in contrast to normal levels in colorectal adenomas reflects an association of tenascin-C induction with malignant disease.