17 research outputs found

    Trimming of a Broken Migrated Biliary Metal Stent with the Nd:YAG Laser

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    Biliary metal stents are a permanent solution for bile duct stenosis. Complications can arise when the stent migrates, breaks or is overgrown by tumour. The following case demonstrates how a Nd:YAG laser can be used to solve these problems. A 93-year-old man presented with jaundice and fever. Two years earlier a 6-cm metal stent had been implanted into a postinflammatory stenosis of the common bile duct after recurrent cholangitis and repetitive plastic stenting. Duodenoscopy showed that the stent was broken. It had migrated about 3 cm into the duodenum, leading to kinking of the stent and breaking of the wires. The stent was also occluded. It was necessary to purge the common bile duct and to introduce a second stent. However, the only way to reach the papilla was through the broken wires. Placing a second stent this way was impossible. Thus we trimmed the stent with a Nd:YAG laser. The piece that had migrated into the duodenum was retrieved. Now the papilla could be reached. The rest of the metal stent was purged with NaCl 0.9%. A second metal stent was placed. Since an Nd:YAG laser is part of the equipment of most endoscopy units, it can be used to trim a broken or migrated biliary metal stent

    Folgeerkrankungen nach gastrointestinalen Operationen

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    Gastrointestinal surgery may not only lead to early postoperative complications but also chronic consequences. These have therapeutic implications for affected patients. The kind and extent of surgical intervention determines the spectrum of postsurgical phenomena which may occur. These chronic consequences are due to changes in gastrointestinal anatomy, the synchronization of digestive processes, or the ability to digest and absorb food. In case of transplantation surgery, adverse effects of immunosuppression have to be considered. Sometimes, chronic consequences of surgical procedures are difficult to recognize. The knowledge of typical problems associated with gastrointestinal surgery is necessary to enable early and timely diagnosis and treatment. Some negative effects can be avoided by early therapeutic interventions. This article summarizes typical chronic consequences of gastrointestinal surgery. Operative Eingriffe am Verdauungstrakt können nicht nur durch frĂŒhe Komplikationen, sondern auch durch das Auftreten von Folgeerkrankungen fĂŒr den Patienten therapeutisch relevante Konsequenzen haben. Das Spektrum zu bedenkender Folgeerscheinungen ist dabei abhĂ€ngig von der Art und dem Ausmaß der durchgefĂŒhrten Operation. Sie können auf VerĂ€nderungen der Anatomie, des zeitlichen Zusammenspiels der Organe des Intestinaltrakts oder der FĂ€higkeit zur Digestion und Absorption beruhen. Im Falle von Transplantationen kommen Komplikationen der Immunsuppression hinzu. Chronische Konsequenzen operativer Eingriffe sind gelegentlich schwer zu diagnostizieren. Kenntnisse ĂŒber die typischen Folgeerkrankungen sind von Bedeutung, um eine frĂŒhzeitige Diagnosestellung und Therapieeinleitung zu ermöglichen. Manche negativen Folgen lassen sich durch rechtzeitige therapeutische Maßnahmen verhindern. Dieser Beitrag beleuchtet wichtige Folgeerkrankungen der gastrointestinalen Chirurgie

    Cholangitis mit Ausbildung eines subphrenischen Leberabszesses nach komplizierter Cholezystektomie auf dem Boden verschlossener Plastikstents

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    A 62-year-old lady presented with fever and abdominal pain. History revealed cholecystectomy two years ago due to cholecystolithiasis, complicated by perforation of the common bile duct, leading to hepaticojejunostomy, jejunocholedochostomy, endoscopic retrograde insertion of two plastic stents and percutaneous drainage of bilioma. The patient was lost to follow-up until she presented two years later in the emergency room. ERC was performed. Both stents were occluded. After extraction dirty bile popped out. Injection of contrast medium showed stones in the remaining common bile duct and dilatation of the intrahepatic bile ducts and the interposed jejunum. After stone extraction a subphrenic intrahepatic fluid collection became visible when injecting contrast medium in the intrahepatic bile ducts. Pus was aspirated. The abscess was drained with a nasobiliary tube. Antibiotics were given. Temperature and CRP normalized. The nasobiliary tube was removed when the biliary fluid was clear. Recovery was uneventful with complete resolution of symptoms. Eine 62-jĂ€hrige Frau stellte sich mit Fieber und rechtsseitigen Oberbauchschmerzen vor. In der Vorgeschichte war zwei Jahre zuvor wegen Steinen eine Cholezystektomie durchgefĂŒhrt worden, bei der es zu einer Perforation des Ductus choledochus am Hilus gekommen war, sodass eine Hepatikojejunostomie, eine Jejunocholedochostomie und endoskopisch Plastikstents in beide Leberlappen angelegt werden mussten. Die Patientin entzog sich den geplanten Nachkontrollen und wurde erst zwei Jahre spĂ€ter notfallmĂ€ĂŸig mit oben genannter Symptomatik wieder vorstellig. Bei der ERC zeigten sich verschlossene Plastikstents, Steine im Ductus choledochus, eine Dilatation des Gallengangssystems und des interponierten Jejunums. Weiterhin wurde eine Verbindung zwischen einem subphrenischen Verhalt und den intrahepatischen GallegĂ€ngen sichtbar, aus dem Eiter aspiriert und damit die Diagnose eines subphrenischen Abszesses gestellt wurde. Unter antibiotischer Therapie und Abszessdrainage ĂŒber eine nasobiliĂ€re Sonde bildeten sich die Beschwerden zurĂŒck und die EntzĂŒndungsparameter normalisierten sich. Der postinterventionelle Verlauf war unkompliziert. Die Patientin wurde beschwerdefrei entlassen

    The coactivator CRTC1 promotes cell proliferation and transformation via AP-1

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    Regulation of gene expression in response to mitogenic stimuli is a critical aspect underlying many forms of human cancers. The AP-1 complex mediates the transcriptional response to mitogens, and its deregulation causes developmental defects and tumors. We report that the coactivator CRTC1 cyclic AMP response element-binding protein (CREB)-regulated transcription coactivator 1 is a potent and indispensable modulator of AP-1 function. After exposure of cells to the AP-1 agonist 12-O-tetradecanoylphorbol-13-acetate (TPA), CRTC1 is recruited to AP-1 target gene promoters and associates with c-Jun and c-Fos to activate transcription. CRTC1 consistently synergizes with the proto-oncogene c-Jun to promote cellular growth, whereas AP-1–dependent proliferation is abrogated in CRTC1-deficient cells. Remarkably, we demonstrate that CRTC1-Maml2 oncoprotein, which causes mucoepidermoid carcinomas, binds and activates both c-Jun and c-Fos. Consequently, ablation of AP-1 function disrupts the cellular transformation and proliferation mediated by this oncogene. Together, these data illustrate a novel mechanism required to couple mitogenic signals to the AP-1 gene regulatory program

    TORC2 regulates germinal center repression of the TCL1 oncoprotein to promote B cell development and inhibit transformation

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    Aberrant expression of the TCL1 oncoprotein promotes malignant transformation of germinal center (GC) B cells. Repression of TCL1 in GC B cells facilitates FAS-mediated apoptosis and prevents lymphoma formation. However, the mechanism for this repression is unknown. Here we show that the CREB coactivator TORC2 directly regulates TCL1 expression independent of CREB Ser-133 phosphorylation and CBP/p300 recruitment. GC signaling through CD40 or the BCR, which activates pCREB-dependent genes, caused TORC2 phosphorylation, cytosolic emigration, and TCL1 repression. Signaling via cAMP-inducible pathways inhibited TCL1 repression and reduced apoptosis, consistent with a prosurvival role for TCL1 before GC selection and supporting an initiating role for aberrant TCL1 expression during GC lymphomagenesis. Our data indicate that a novel CREB/TORC2 regulatory mode controls the normal program of GC gene activation and repression that promotes B cell development and circumvents oncogenic progression. Our results also reconcile a paradox in which signals that activate pCREB/CBP/p300 genes concurrently repress TCL1 to initiate its silencing
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