RESUMEN
INTRODUCTION: Desmoid tumors are benign tumors, yet can lead to significant morbidity due to aggressive local expansions. Treatment starts with a wait-and-see policy, however, more aggressive treatments like broad margin resection surgery might be necessary in case of tumor progression. PATIENTS AND METHODS: We report the case of a 26-year-old female with a symptomatic desmoid tumor in the left rectus muscle. The initial wait-and-see policy led to an increase in tumor size and progression of symptoms. Computed tomography (CT) angiography revealed a dominant arterial blood supply via a branch of the inferior epigastric artery. We then performed a super selective embolization of the dominant arterial blood supply, to avoid the need for broad margin resection. RESULTS: At three months follow-up, the patient was asymptomatic and magnetic resonance imaging (MRI) showed no residual tumor. At nine months follow-up, MRI scan reconfirmed the successful outcome. CONCLUSIONS: Embolization of a primary supplying vessel of a desmoid tumor is a viable treatment option. However, scientific evidence remains limited and further research is mandatory for inclusion in evidence based treatment algorithms.
Asunto(s)
Embolización Terapéutica/métodos , Fibromatosis Agresiva/diagnóstico por imagen , Fibromatosis Agresiva/terapia , Recto del Abdomen/diagnóstico por imagen , Adulto , Angiografía por Tomografía Computarizada/métodos , Progresión de la Enfermedad , Femenino , Fibromatosis Agresiva/patología , Estudios de Seguimiento , Humanos , Angiografía por Resonancia Magnética/métodos , Esclerosis Múltiple/complicaciones , Esclerosis Múltiple/diagnóstico , Enfermedades Raras , Recto del Abdomen/patología , Recto del Abdomen/cirugía , Medición de Riesgo , Índice de Severidad de la Enfermedad , Resultado del TratamientoRESUMEN
The renal proximal tubule (PT) is the major target of cadmium (Cd2+) toxicity where Cd2+ causes stress and apoptosis. Autophagy is induced by cell stress, e.g., endoplasmic reticulum (ER) stress, and may contribute to cell survival or death. The role of autophagy in Cd2+-induced nephrotoxicity remains unsettled due to contradictory results and lack of evidence for autophagic machinery damage by Cd2+. Cd2+-induced autophagy in rat kidney PT cell line NRK-52E and its role in cell death was investigated. Increased LC3-II and decreased p62 as autophagy markers indicate rapid induction of autophagic flux by Cd2+ (5-10 µM) after 1 h, accompanied by ER stress (increased p-PERK, p-eIF2α, CHOP). Cd2+ exposure exceeding 3 h results in p62/LC3-II accumulation, but diminished effect of lysosomal inhibitors (bafilomycin A1, pepstatin A +E-64d) on p62/LC3-II levels, indicating decreased autophagic flux and cargo degradation. At 24 h exposure, Cd2+ (5-25 µM) activates intrinsic apoptotic pathways (Bax/Bcl-2, PARP-1), which is not evident earlier (≤6 h) although cell viability by MTT assay is decreased. Autophagy inducer rapamycin (100 nM) does not overcome autophagy inhibition or Cd2+-induced cell viability loss. The autophagosome-lysosome fusion inhibitor liensinine (5 µM) increases CHOP and Bax/Bcl-2-dependent apoptosis by low Cd2+ stress, but not by high Cd2+. Lysosomal instability by Cd2+ (5 µM; 6 h) is indicated by increases in cellular sphingomyelin and membrane fluidity and decreases in cathepsins and LAMP1. The data suggest dual and temporal impact of Cd2+ on autophagy: Low Cd2+ stress rapidly activates autophagy counteracting damage but Cd2+ stress accrual disrupts autophagic flux and lysosomal stability, possibly resulting in lysosomal cell death.
Asunto(s)
Autofagia/efectos de los fármacos , Cadmio/toxicidad , Lisosomas/efectos de los fármacos , Animales , Apoptosis/efectos de los fármacos , Apoptosis/fisiología , Cadmio/administración & dosificación , Línea Celular , Relación Dosis-Respuesta a Droga , Estrés del Retículo Endoplásmico/efectos de los fármacos , Isoquinolinas/farmacología , Túbulos Renales Proximales/citología , Proteínas de Membrana de los Lisosomas/metabolismo , Lisosomas/metabolismo , Lisosomas/patología , Proteínas Asociadas a Microtúbulos/metabolismo , Fenoles/farmacología , Ratas , Sirolimus/farmacología , Respuesta de Proteína Desplegada/efectos de los fármacosRESUMEN
AIMS: The aim of this systematic review is to gain insight into the published experience on percutaneous closure of a post-infarction ventricular septal rupture (VSR). METHOD: Relevant literature was obtained by MeSH-term searches in the online search-engine PubMed. Articles published in the last 10 years were included. Further filtering was done by using search limits and individual article selection based on the aims of this systematic review. CONCLUSION: Percutaneous closure is a potential technique in a select group of patients. The presence of cardiogenic shock and closure in the acute phase after VSR diagnosis are important risk factors of mortality. Device implantation is in general successful with few procedure-related complications. Reduction of the shunt fraction has been reported frequently. This technique is a less invasive alternative to surgical treatment and should be applied on a case-by-case basis.