Laryngoskopische Befunde nach einem Tubusbrand bei der Laserchirurgie

Introduction: A greek patient underwent laser surgery of his larynx because of laryngeal cancer. During this operation a C02-laser induced tube fire occurred that damaged the mucosa of his pharynx, larynx and trachea. Some days after this accident he was refered to the ENT department of Hamburg University Clinics. Regular laryngoscopic investigations were done by phoniatricians. In between a laryngectomy had to be done in Greek because the patient still suffered from severe pain and from dysphagia.Conclusion: Laser-ignited endotracheal tube fires are rare but still they are a potentional danger of all patients that are treated by endolaryngeal laser surgery. This case report shall focus this problem. Careful behaviour of the surgeon and a good clinical education should be the best ways to avoid this kind of complication.Falldarstellung: Ein griechischer Patient wurde in einem norddeutschen Krankenhaus durch einen routinierten HNO-Chirurgen laserchirurgisch an einem Larynxkarzinom operiert. Dabei kam es zu einem Tubusbrand, der zu ausgedehnten Verbrennungen im Bereich von Oro- / Hypopharynx, Larynx und oberer Trachea führte. Wenige Tage nach der Operation erfolgte die Aufnahme des Patienten in der HNO-Klinik des Universitätsklinikums Hamburg-Eppendorf zur Verlaufskontrolle, wo regelmäßige konsiliarische laryngoskopische Kontrolluntersuchungen durch Phoniater erfolgten. In der Zwischenzeit musste bei dem Patienten aufgrund von therapierefraktären Schmerzen und dysphagischen Beschwerden in seinem Heimatland eine Laryngektomie durchgeführt werden.Schlussfolgerung: Intraoperative Tubusbrände im Rahmen von laserchirurgischen Eingriffen sind zwar selten, stellen aber eine potentielle Bedrohung von narkotisierten Patienten dar. Diese Falldarstellung soll dazu beitragen, aufzuzeigen, dass die Komplikation eines Tubusbrandes durch sorgsames Verhalten des Operateurs verhindert werden kann. Auch Lasertuben stellen in diesem Zusammenhang keine absolute Sicherheit für den Patienten dar, auch wenn sie das Risiko eines Tubusbrandes reduzieren

BZLF1 governs CpG-methylated chromatin of Epstein-Barr virus reversing epigenetic repression.

Epigenetic mechanisms are essential for the regulation of all genes in mammalian cells but transcriptional repression including DNA methylation are also major epigenetic mechanisms of defense inactivating potentially harmful pathogens. Epstein-Barr Virus (EBV), however, has evolved to take advantage of CpG methylated DNA to regulate its own biphasic life cycle. We show here that latent EBV DNA has an extreme composition of methylated CpG dinucleotides with a bimodal distribution of unmethylated or fully methylated DNA at active latent genes or completely repressed lytic promoters, respectively. We find this scenario confirmed in primary EBV-infected memory B cells in vivo. Extensive CpG methylation of EBV's DNA argues for a very restricted gene expression during latency. Above-average nucleosomal occupancy, repressive histone marks, and Polycomb-mediated epigenetic silencing further shield early lytic promoters from activation during latency. The very tight repression of viral lytic genes must be overcome when latent EBV enters its lytic phase and supports de novo virus synthesis in infected cells. The EBV-encoded and AP-1 related transcription factor BZLF1 overturns latency and initiates virus synthesis in latently infected cells. Paradoxically, BZLF1 preferentially binds to CpG-methylated motifs in key viral promoters for their activation. Upon BZLF1 binding, we find nucleosomes removed, Polycomb repression lost, and RNA polymerase II recruited to the activated early promoters promoting efficient lytic viral gene expression. Surprisingly, DNA methylation is maintained throughout this phase of viral reactivation and is no hindrance to active transcription of extensively CpG methylated viral genes as thought previously. Thus, we identify BZLF1 as a pioneer factor that reverses epigenetic silencing of viral DNA to allow escape from latency and report on a new paradigm of gene regulation