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1.
World J Urol ; 37(4): 661-666, 2019 Apr.
Artículo en Inglés | MEDLINE | ID: mdl-30810832

RESUMEN

PURPOSE: Evaluate the main etiologies and clinical characteristics of male urethral stricture disease (USD) in Brazil. METHODS: This multicentric study was performed using retrospective data collected from six Brazilian referral centers of urethral reconstruction. The database comprised data from 899 patients with USD who had undergone surgical treatment from 2008 to 2018. Age, stricture site and primary stricture etiology were identified for each patient. RESULTS: The mean age was 52.13 ± 16.9 years. The most common etiology was iatrogenic (43.4%), followed by idiopathic (21.7%), trauma (21.5%) and inflammatory (13.7%). Of the iatrogenic causes, 59% were secondary to urethral instrumentation (60% by urethral catheterization and 40% by transurethral procedures), 24.8% by other procedures (prostatectomy, radiotherapy, postectomy) and 16.2% by failed hypospadia repairs. Pelvic fracture urethral distraction injuries were responsible for most of the trauma-related strictures (62.7%). When stratified by age, the most common stricture etiology was trauma in the 0-39 years old group (42.8%), idiopathic in the 40-59 years old group (32.4%) and iatrogenic in patients over 60 years old (68%). In regard to the stricture site, 80% presented with an anterior urethral stricture and 20% with a posterior stenosis. In the anterior stenosis group, the most common stricture site was bulbar (39.5%). CONCLUSION: In Brazil, as in many developed countries, the most common cause of urethral stricture diseases is iatrogenic, especially urethral catheterization. These findings emphasize the need of a careful urethral manipulation and a better training of healthcare professionals. Trauma is still responsible for a great proportion of strictures and inflammatory etiologies are now less frequently observed.


Asunto(s)
Países en Desarrollo , Enfermedad Iatrogénica/epidemiología , Complicaciones Posoperatorias/epidemiología , Estrechez Uretral/epidemiología , Adolescente , Adulto , Distribución por Edad , Anciano , Anciano de 80 o más Años , Brasil/epidemiología , Niño , Preescolar , Fracturas Óseas/complicaciones , Humanos , Hipospadias/cirugía , Liquen Escleroso y Atrófico/complicaciones , Liquen Escleroso y Atrófico/epidemiología , Masculino , Persona de Mediana Edad , Huesos Pélvicos/lesiones , Complicaciones Posoperatorias/etiología , Estudios Retrospectivos , Estrechez Uretral/etiología , Uretritis/complicaciones , Uretritis/epidemiología , Cateterismo Urinario/efectos adversos , Procedimientos Quirúrgicos Urológicos Masculinos/efectos adversos , Adulto Joven
2.
PLoS One ; 11(7): e0158908, 2016.
Artículo en Inglés | MEDLINE | ID: mdl-27454431

RESUMEN

Emerging evidence has highlighted the pivotal role of microvasculature injury in the development and progression of renal fibrosis. Angiopoietin-1 (Ang-1) is a secreted vascular growth factor that binds to the endothelial-specific Tie2 receptor. Ang-1/Tie2 signaling is critical for regulating blood vessel development and modulating vascular response after injury, but is dispensable in mature, quiescent vessels. Although dysregulation of vascular endothelial growth factor (VEGF) signaling has been well studied in renal pathologies, much less is known about the role of the Ang-1/Tie2 pathway in renal interstitial fibrosis. Previous studies have shown contradicting effects of overexpressing Ang-1 systemically on renal tubulointerstitial fibrosis when different engineered forms of Ang-1 are used. Here, we investigated the impact of site-directed expression of native Ang-1 on the renal fibrogenic process and peritubular capillary network by exploiting a conditional transgenic mouse system [Pax8-rtTA/(TetO)7 Ang-1] that allows increased tubular Ang-1 production in adult mice. Using a murine unilateral ureteral obstruction (UUO) fibrosis model, we demonstrate that targeted Ang-1 overexpression attenuates myofibroblast activation and interstitial collagen I accumulation, inhibits the upregulation of transforming growth factor ß1 and subsequent phosphorylation of Smad 2/3, dampens renal inflammation, and stimulates the growth of peritubular capillaries in the obstructed kidney. Our results suggest that Ang-1 is a potential therapeutic agent for targeting microvasculature injury in renal fibrosis without compromising the physiologically normal vasculature in humans.


Asunto(s)
Angiopoyetina 1/genética , Expresión Génica , Enfermedades Renales/genética , Enfermedades Renales/patología , Túbulos Renales/metabolismo , Túbulos Renales/patología , Actinas/genética , Actinas/metabolismo , Animales , Biomarcadores , Colágeno Tipo I/genética , Colágeno Tipo I/metabolismo , Modelos Animales de Enfermedad , Fibrosis , Regulación de la Expresión Génica , Enfermedades Renales/metabolismo , Ratones , Ratones Transgénicos , Microcirculación , Neovascularización Patológica/genética , Transducción de Señal , Factor de Crecimiento Transformador beta1/genética , Factor de Crecimiento Transformador beta1/metabolismo
3.
Case Rep Urol ; 2015: 748495, 2015.
Artículo en Inglés | MEDLINE | ID: mdl-26525589

RESUMEN

Leydig cell tumors represent 3% of testicular masses and usually occur in prepubertal boys and men between 30 and 60 years of age. Leydig cell tumors are benign in children but can be malignant in 10% of adults. This case report describes a 41-year-old patient who was diagnosed with a Leydig cell tumor that originated in his right testicle that subsequently metastasized to his liver, lungs, and retroperitoneum. We discuss the patient's presentation and review the radiographic findings, surgical treatment, surgical pathology, chemotherapeutic treatment, and published literature on this rare pathology.

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