RESUMO
We describe a case of an infected popliteal artery stent with septic emboli presenting 6 years after peripheral vascular intervention for intermittent claudication. Management included resection of the stent and popliteal artery and revascularization by femoral-popliteal bypass with autogenous vein. This case demonstrates that peripheral stent infections can develop years after intervention. We performed an English-language PubMed literature review of arterial peripheral vascular stent infections on using the search term, "Non-coronary stent or stent graft infection from 1966 to present." Written informed consent was obtained for publication.
Assuntos
Angioplastia/efeitos adversos , Angioplastia/instrumentação , Remoção de Dispositivo , Artéria Femoral/cirurgia , Doença Arterial Periférica/terapia , Artéria Poplítea/cirurgia , Infecções Relacionadas à Prótese/cirurgia , Veia Safena/transplante , Stents Metálicos Autoexpansíveis/efeitos adversos , Idoso , Ligas , Angiografia por Tomografia Computadorizada , Feminino , Humanos , Doença Arterial Periférica/diagnóstico por imagem , Artéria Poplítea/diagnóstico por imagem , Artéria Poplítea/microbiologia , Desenho de Prótese , Infecções Relacionadas à Prótese/diagnóstico , Infecções Relacionadas à Prótese/microbiologia , Resultado do Tratamento , Ultrassonografia Doppler DuplaRESUMO
Mice with T-cell-specific loss of the tumor suppressor gene PTEN early in T-cell ontogeny develop thymic lymphomas that invariably harbor a reciprocal translocation involving the T-cell receptor α/δ locus and c-myc, t(14;15). In addition to its known function as a lipid phosphatase opposing PI3K signaling, PTEN has also been described as playing a prominent role in promoting genomic stability. As a result, it has been uncertain which one(s) of these 2 separable features were required to block the development of lymphoma. Here, using a conditional model in which T cells selectively express 1 phosphatase-dead PTEN mutant (C124S) and maintain 1 null allele, we show that PTEN phosphatase activity is required for preventing the emergence of a malignant T-cell population harboring t(14;15), thus constituting a critical function of PTEN in preventing lymphomagenesis.