Αρχειοθήκη ιστολογίου

Τετάρτη 6 Δεκεμβρίου 2017

Nichtinvasives Harnblasenkarzinom

Zusammenfassung

Hintergrund

Das nichtinvasive Harnblasenkarzinom ist ein häufiger Tumor mit einer komplexen Diagnostik und Therapie.

Ziel

Der aktuelle Stand in Diagnostik und Therapie wird dargelegt und insbesondere das risikoadaptierte Patientenmanagement erläutert.

Material und Methode

Grundlage ist eine selektive Literaturrecherche in der Datenbank PubMed zu Ätiologie, Diagnostik, Therapie und risikoadaptiertem Patientenmanagement des nichtinvasiven Harnblasenkarzinoms.

Ergebnisse

Das nichtinvasive Harnblasenkarzinom äußert sich in aller Regel mit einer schmerzlosen Makrohämaturie. Lediglich eine Zystoskopie kann eine sichere Diagnose ermöglichen, während es keine sichere urinmarkerbasierte Methode gibt. Am Anfang der Therapie steht in aller Regel eine transurethrale Resektion des Blasentumors, die einerseits eine histopathologisch verifizierte Diagnose liefert und andererseits die Grundlage für die Therapie sowie in einigen Fällen bereits die alleinige Therapie ist. Die Histopathologie ist für die weitere Therapiestrategie entscheidend und ermöglicht mit wenigen klinischen und zystoskopischen Parametern eine entsprechende Risikoeinteilung. Bei niedrigem Risiko genügt eine transurethrale Resektion mit einer einmaligen frühpostoperativen Instillationstherapie mit einem Chemotherapeutikum. Bei mittlerem Risiko folgen der Resektion mehrere ambulante Instillationstherapien mit einem Chemotherapeutikum oder Bacille Calmette-Guerin (BCG). Bei hohem Risiko erfolgt nach der ersten Resektion eine zweite sowie eine Instillationstherapie mit BCG; es wird aber auch eine Zystektomie erwogen. In allen Fällen sind Schemata einer strukturierten Nachsorge etabliert und wichtig.

Schlussfolgerung

Auch wenn eine hohe Rezidivrate und bei einer Hochrisikokonstellation eine wesentliche Progressionsrate das nichtinvasive Harnblasenkarzinom kennzeichnen, so kann unter Ausschöpfung der aktuellen Möglichkeiten insgesamt eine relativ gute Prognose bezüglich des rezidivfreien und eine sehr gute bezüglich. des tumorspezifischen Überlebens erreicht werden.



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Choice of desflurane or propofol for the maintenance of general anesthesia does not affect the risk of periprocedural myocardial damage in patients undergoing transfemoral transcatheter aortic valve implantation

Abstract

Purpose

This study aimed to reveal whether the occurrence of periprocedural myocardial damage (PMD) decreases in patients who received volatile anesthetics to maintain general anesthesia compared with those who received propofol during transcatheter aortic valve implantation (TAVI).

Methods

We included one hundred and forty adult patients who underwent transfemoral TAVI under general anesthesia from January 2015 to March 2017 in this single-center retrospective review. We compared the rate of patients who developed PMD between those who received desflurane (Group D, n = 72) and propofol (Group P, n = 68) for anesthetic maintenance. PMD was represented by the peak levels of creatine kinase myocardial band (CK-MB) and troponin I within 72 h following the procedure and defined as an increase >5 times in CK-MB or >15 times in troponin I compared with the institutional upper reference limits. Further analysis was performed to identify the independent predictors of PMD.

Results

There was no significant difference in the rate of PMD between groups (Group D 72.2% to Group P 70.6%, P = 0.85) or levels of CK-MB (Group D 7.85 [1.3–72.7] ng/mL to Group P 8.45 [1.8–49.7] ng/mL; P = 0.59) and troponin I (Group D 1.061 [0.050–10.8] ng/mL to Group P 1.214 [0.036–29.0] ng/mL; P = 0.97). The risk of PMD was higher in patients with more intraprocedural blood loss (odds ratio 1.49 per 100 mL, P = 0.048) and lower in those with an implanted permanent pacemaker (odds ratio 0.17; P = 0.02).

Conclusions

Desflurane does not appear to be more cardioprotective than propofol when used for anesthetic maintenance in patients undergoing transfemoral TAVI.



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Allergens produce serine proteases-dependent distinct release of metabolite DAMPs in human bronchial epithelial cells

Abstract

Background

The respiratory epithelium is a major site for disease interaction with inhaled allergens. Additional to IgE-dependent effects, allergens contain proteases that may stimulate human bronchial epithelial cells (HBECs) through protease-activated receptors, causing the release of mediators important in driving Th2 mediated immune responses.

Objective

We aimed to investigate if different allergens induce metabolite DAMPs such as ATP and uric acid (UA) release in HBECs.

Methods

HBECs (BEAS-2B cell line) was exposed to different allergen extracts; house dust mite (HDM), Alternaria alternata, Artemisia vulgaris and Betula pendula and UA, ATP, IL-8 and IL-33 release were measured. Allergen extracts were heat-inactivated or pre-incubated with serine (AEBSF) or cysteine (E64) protease inhibitor to study involvement of protease activity in ATP, UA and IL-8 release. HDM-induced release of UA was studied in a mouse model of allergic inflammation.

Results

All allergens caused dose-dependent rapid release of ATP and IL-8, but only HDM induced UA release from HBECs. HDM also caused release of UA in vivo in our mouse model of allergic inflammation. ATP release by all four allergen extracts was significantly reduced by heat-inactivation and by serine protease inhibitors. Similarly, the HDM induced UA release was also abrogated by heat-inactivation of HDM extract and dependent on serine proteases. Furthermore, allergen-induced IL-8 mRNA expression was inhibited by serine protease inhibitors.

Conclusions and Clinical Relevance

ATP was released by all four allergens in HBECs supporting the role of ATP involvement in asthma pathology. However, HDM stands out by its capacity to cause UA release, which is of interest in view of the proposed role of UA in early initiation of allergic asthma. Although serine proteases may be involved in the activity of all the studied allergens, further work is warranted to explain differences between HDM and the other three allergens regarding effects on UA release.

This article is protected by copyright. All rights reserved.



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Topical ofloxacin use in G6PD deficiency - safe or unsafe?

Abstract

we have recently treated a paediatric patient with known glucose-6-phosphate dehydrogenase (G6PD) deficiency and wished to communicate to the clinical ENT community the controversies around the use of fluoroquinolone (FQ) antibiotic drops in this patient cohort.

This article is protected by copyright. All rights reserved.



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Correction to John D. Norton “How to build an infinite lottery machine”



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The economy of nature: the structure of evolution in Linnaeus, Darwin, and the modern synthesis

Abstract

We argue that the economy of nature constitutes an invocation of structure in the biological sciences, one largely missed by philosophers of biology despite the turn in recent years toward structural explanations throughout the philosophy of science. We trace a portion of the history of this concept, beginning with the theologically and economically grounded work of Linnaeus, moving through Darwin's adaptation of the economy of nature and its reconstitution in genetic terms during the first decades of the Modern Synthesis. What this historical case study reveals, we argue, is a window into the shifting landscape of the explanatory and ontic uses of structural concepts. In Linnaeus, the economy of nature has both ontic and explanatory import; in Darwin the ontic and explanatory aspects start to come apart (with the explanatory aspect being foregrounded); and finally, in the Modern Synthesis, the economy of nature is replaced by the conceptual toolkit of population genetics, the structural elements of which are nearly entirely explanatory. Having traced a historical trajectory of structural concepts that moves from an ontic formulation to an increasingly explanatory one, we conclude by outlining some insights for structural realism.



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