Assuntos
Bacteriemia/terapia , Resistência a Vancomicina , Idoso , Antibacterianos/uso terapêutico , Bacteriemia/microbiologia , Enterococcus , Infecções por Bactérias Gram-Positivas/terapia , Humanos , Higiene , Masculino , Salas Cirúrgicas/organização & administração , Isolamento de Pacientes , Assistência PerioperatóriaRESUMO
The major multidrug-resistant pathogens (MRE) in human medicine are methicillin-resistant Staphylococcus aureus (MRSA), vancomycin-resistant enterococci (VRE) and multidrug-resistant Gram-negative rod bacteria (MRGN). MRE are a very heterogeneous group with respect to epidemiology and therapeutic or hospital hygiene consequences. After MRSA played an important role among MREs at the beginning of the twenty-first century, VRE and MRGN have come to the fore in recent years. During work in the operating room and on the intensive care unit, there are many possibilities for transmission of MRE between the patient environment and the patient, especially via the hands, e.â¯g. during intubation or catheterization in vessels, tissues or the urinary tract. For this reason, hand and surface hygiene is of particular relevance in the prevention of nosocomial colonization or infection, in particular with MRE.
Assuntos
Farmacorresistência Bacteriana , Higiene , Controle de Infecções/normas , Unidades de Terapia Intensiva/normas , Salas Cirúrgicas/normas , Antibacterianos/uso terapêutico , Infecção Hospitalar/prevenção & controle , Hospitais/normas , Humanos , Staphylococcus aureus Resistente à Meticilina , Enterococos Resistentes à VancomicinaRESUMO
Antibiotic stewardship (ABS) comprises a bundle of different interventions to improve anti-infective treatment in a hospital setting. An important component of ABS interventions is the interdisciplinary approach to infection management. Besides improving infrastructural aspects on a hospital level, including surveillance of the use of anti-infective agents and nosocomial infections, collation and interpretation of statistics on resistance and formulation of local treatment guidelines, ABS teams go to the wards and advise treating physicians on antibiotic therapy. Frequent approaches for optimization are selection of substances, administration route, dosing of medication and duration of treatment. An important overall objective of ABS is the reduction of resistance induction in order to preserve the therapeutic efficiency of antibiotics. A number of studies have shown that this goal can be achieved in different clinical settings without negatively affecting patient outcome. The strategies of ABS can also be applied with no problems to critically ill patients on the intensive care unit.
Assuntos
Anti-Infecciosos/administração & dosagem , Gestão de Antimicrobianos , Antibacterianos/administração & dosagem , Infecção Hospitalar/tratamento farmacológicoRESUMO
The introduction of drug-eluting stents (DES) to interventional cardiology has been a breakthrough in the treatment of in-stent restenosis. However, the downside of reduced restenosis is a significantly prolonged and practically incalculable time to reendothelialization of thrombogenic stent-surfaces with an increased risk for coronary thrombosis. As the use of DES in non-coronary arteries (e.g. carotid, renal, infrainguinal and even cerebral arteries) is increasing, new vascular beds might be put at risk of ischemia. The practice of stopping antiplatelet drugs in a perioperative setting is highly problematic and contemporary guidelines released by scientific societies from different medical specialties have recently addressed this problem. While many case reports have reported alarming incidents of stent thrombosis, prospective clinical data are scarcely available to guide anticoagulation during the perioperative phase. This review summarizes information on the vascular biology of DES and associated adverse events based on a systematic search of the available literature in public data bases. An emphasis is put on the growing use of DES in non-coronary vessels and the associated danger of putting new vascular beds at risk of thrombotic complications.
Assuntos
Doença da Artéria Coronariana/terapia , Stents Farmacológicos , Procedimentos Endovasculares/instrumentação , Intervenção Coronária Percutânea/instrumentação , Doença Arterial Periférica/terapia , Anticoagulantes/administração & dosagem , Reestenose Coronária/etiologia , Reestenose Coronária/prevenção & controle , Esquema de Medicação , Procedimentos Endovasculares/efeitos adversos , Humanos , Intervenção Coronária Percutânea/efeitos adversos , Inibidores da Agregação Plaquetária/administração & dosagem , Guias de Prática Clínica como Assunto , Desenho de Prótese , Medição de Risco , Fatores de Risco , Trombose/etiologia , Trombose/prevenção & controle , Fatores de Tempo , Resultado do TratamentoRESUMO
Gardner fibroma represents a rare and recently described soft tissue tumor entity in children and young adults. It consists of haphazardly arranged coarse and hyalinized collagen fibers combined with loosely arranged bland spindle and fibroblastic cells. The case of a 13-year-old male patient with Gardner fibroma and osteoma and multicentric desmoid type fibromatosis in his mother is presented with detection of a (heterozygotic) germline mutation of the APC gene leading to a de novo stop codon (deletion of base pairs 5033-5036). FISH analysis revealed a structural loss of heterozygosity (LOH) in the APC gene on chromosomal locus 5q21 in one out of five analysed desmoids of the mother, no LOH of APC gene in the Gardner fibroma. Gardner fibroma in children and young adults may serve as an indicator lesion for familial adenomatous polyposis (FAP), Gardner syndrome, a familial desmoid type fibromatosis without other manifestations of APC or a new APC gene mutation. For the clinician, this diagnosis should be commented upon accordingly by the surgical pathologist. As the result of a detected APC gene mutation, continuous follow-up for the development of colorectal tumors and desmoid type fibromatosis as well as a familial screening for FAP is recommended.
Assuntos
Fibromatose Agressiva/genética , Fibromatose Agressiva/patologia , Síndrome de Gardner/genética , Síndrome de Gardner/patologia , Genes APC , Mutação em Linhagem Germinativa/genética , Perda de Heterozigosidade , Osteoma/genética , Osteoma/patologia , Neoplasias de Tecidos Moles/genética , Neoplasias de Tecidos Moles/patologia , Adolescente , Adulto , Biomarcadores Tumorais/genética , Neoplasias da Mama/genética , Neoplasias da Mama/patologia , Deleção Cromossômica , Cromossomos Humanos Par 5/genética , Códon de Terminação/genética , Análise Mutacional de DNA , Feminino , Seguimentos , Triagem de Portadores Genéticos , Humanos , Hibridização in Situ Fluorescente , Masculino , Recidiva Local de Neoplasia/genética , Recidiva Local de Neoplasia/patologia , Adulto JovemRESUMO
Myxoid/round cell liposarcoma are characterized by typical chromosomal translocations. This genetic alteration might result in specific gene-expression profiles in this tumor entity. To identify over-expressed genes in myxoid/round cell liposarcoma DNA microarray analysis was performed on four tumors and four samples of adult fat tissue. Genes ret, cdk4, cyclin D2 and c-myc showed over-expression by means of microarray analysis and Northern blotting. Immunohistochemistry demonstrated cytoplasmic localization of associated proteins in 36 different tumors. The localization of ret was seen in endothelial cells of plexiform vasculature in addition to its accumulation in tumor cells (25% of cases). The results show an over-expression of cdk4, cyclin D2, c-myc and ret on both the transcriptional and protein level in myxoid/round cell liposarcoma. For cyclin D2 and ret this finding has not been reported in this tumor type. The increase of ret on transcriptional level might be explained by its expression in endothelium in intratumoral plexiform blood vessels. For the molecular pathogenesis of myxoid/round cell liposarcoma our findings imply the involvement of these four genes in the deregulation of the cell cycle, especially as cdk4 and cyclin D2 are target genes of c-myc.