RESUMEN
RATIONALE: Sodium polystyrene sulfonate is commonly administered to treat hyperkalemia. Severe pneumonia due to aspiration of this drug is rare and no survival case has thus far been reported. PATIENT CONCERNS: A 45-year-old man was hospitalized for acute decompensated heart failure and acute kidney injury with hyperkalemia. He aspirated sodium polystyrene sulfonate while consuming the drug. Severe acute respiratory distress syndrome (ARDS) developed rapidly, and he was transferred to the intensive care unit (ICU). DIAGNOSES: Chest radiography results after aspiration showed new consolidation in the left upper lung. He underwent emergency bronchoscopy, which revealed a considerable amount of yellow mud-like material in the trachea and bronchi. Chest radiography results after the bronchoscopic removal of the foreign material revealed rapid resolution of the left upper lung consolidation. INTERVENTIONS: In the ICU, mechanical ventilation with low tidal volume and high positive end-expiratory pressure was administered and extracorporeal membrane oxygenation (ECMO) was set up for treating severe ARDS. We arranged an emergency bronchoscopy for diagnosis and removal of polystyrene sulfonate. OUTCOMES: ECMO was discontinued after 10 days and the patient was discharged after approximately 2 weeks. LESSONS: Aspiration of sodium polystyrene sulfonate is not common but can be lethal. Clinicians should be cautious and appropriately inform patients of the aspiration risk while administering this drug. Mechanical ventilation and bronchoscopy were effective treatments for severe ARDS caused by aspiration of this drug.
Asunto(s)
Poliestirenos/efectos adversos , Aspiración Respiratoria/complicaciones , Síndrome de Dificultad Respiratoria/inducido químicamente , Síndrome de Dificultad Respiratoria/terapia , Broncoscopía/métodos , Oxigenación por Membrana Extracorpórea/métodos , Humanos , Masculino , Persona de Mediana Edad , Respiración Artificial/métodos , Índice de Severidad de la EnfermedadRESUMEN
New magnetic-based core-shell particles (MBCSPs) were developed to target skin cancer cells while delivering chemotherapeutic drugs in a controlled fashion. MBCSPs consist of a thermo-responsive shell of poly(N-isopropylacrylamide-acrylamide-allylamine) and a core of poly(lactic-co-glycolic acid) (PLGA) embedded with magnetite nanoparticles. To target melanoma cancer cells, MBCSPs were conjugated with Gly-Arg-Gly-Asp-Ser (GRGDS) peptides that specifically bind to the α(5)ß(3) receptors of melanoma cells. MBCSPs consist of unique multifunctional and controlled drug delivery characteristics. Specially, they can provide dual drug release mechanisms (a sustained release of drugs through degradation of PLGA core and a controlled release in response to changes in temperature via thermo-responsive polymer shell), and dual targeting mechanisms (magnetic localization and receptor-mediated targeting). Results from in vitro studies indicate that GRGDS-conjugated MBCSPs have an average diameter of 296 nm and exhibit no cytotoxicity towards human dermal fibroblasts up to 500 µg ml(-1). Further, a sustained release of curcumin from the core and a temperature-dependent release of doxorubicin from the shell of MBCSPs were observed. The particles also produced a dark contrast signal in magnetic resonance imaging. Finally, the particles were accumulated at the tumor site in a B16F10 melanoma orthotopic mouse model, especially in the presence of a magnet. Results indicate great potential of MBCSPs as a platform technology to target, treat and monitor melanoma for targeted drug delivery to reduce side effects of chemotherapeutic reagents.
Asunto(s)
Resinas Acrílicas/química , Sistemas de Liberación de Medicamentos/métodos , Ácido Láctico/química , Melanoma/tratamiento farmacológico , Nanopartículas/química , Ácido Poliglicólico/química , Neoplasias Cutáneas/tratamiento farmacológico , Animales , Muerte Celular/efectos de los fármacos , Fibroblastos/efectos de los fármacos , Fibroblastos/patología , Humanos , Hidrodinámica , Imagen por Resonancia Magnética , Magnetismo , Melanoma/patología , Ratones , Nanopartículas/toxicidad , Tamaño de la Partícula , Fantasmas de Imagen , Copolímero de Ácido Poliláctico-Ácido Poliglicólico , Neoplasias Cutáneas/patología , Propiedades de Superficie/efectos de los fármacosRESUMEN
Despite significant advances in the understanding of tissue responses to biomaterials, most implants are still plagued by inflammatory responses which can lead to fibrotic encapsulation. This is of dire consequence in tissue engineering, where seeded cells and bioactive components are separated from the native tissue, limiting the regenerative potential of the design. Additionally, these interactions prevent desired tissue integration and angiogenesis, preventing functionality of the design. Recent evidence supports that mesenchymal stem cells (MSC) and hematopoietic stem cells (HSC) can have beneficial effects which alter the inflammatory responses and improve healing. The purpose of this study was to examine whether stem cells could be targeted to the site of biomaterial implantation and whether increasing local stem cell responses could improve the tissue response to PLGA scaffold implants. Through incorporation of SDF-1alpha through factor adsorption and mini-osmotic pump delivery, the host-derived stem cell response can be improved resulting in 3X increase in stem cell populations at the interface for up to 2 weeks. These interactions were found to significantly alter the acute mast cell responses, reducing the number of mast cells and degranulated mast cells near the scaffold implants. This led to subsequent downstream reduction in the inflammatory cell responses, and through altered mast cell activation and stem cell participation, increased angiogenesis and decreased fibrotic responses to the scaffold implants. These results support that enhanced recruitment of autologous stem cells can improve the tissue responses to biomaterial implants through modifying/bypassing inflammatory cell responses and jumpstarting stem cell participation in healing at the implant interface.