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1.
World J Urol ; 37(4): 661-666, 2019 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-30810832

RESUMO

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.


Assuntos
Países em Desenvolvimento , Doença Iatrogênica/epidemiologia , Complicações Pós-Operatórias/epidemiologia , Estreitamento Uretral/epidemiologia , Adolescente , Adulto , Distribuição por Idade , Idoso , Idoso de 80 Anos ou mais , Brasil/epidemiologia , Criança , Pré-Escolar , Fraturas Ósseas/complicações , Humanos , Hipospadia/cirurgia , Líquen Escleroso e Atrófico/complicações , Líquen Escleroso e Atrófico/epidemiologia , Masculino , Pessoa de Meia-Idade , Ossos Pélvicos/lesões , Complicações Pós-Operatórias/etiologia , Estudos Retrospectivos , Estreitamento Uretral/etiologia , Uretrite/complicações , Uretrite/epidemiologia , Cateterismo Urinário/efeitos adversos , Procedimentos Cirúrgicos Urológicos Masculinos/efeitos adversos , Adulto Jovem
2.
PLoS One ; 11(7): e0158908, 2016.
Artigo em Inglês | MEDLINE | ID: mdl-27454431

RESUMO

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.


Assuntos
Angiopoietina-1/genética , Expressão Gênica , Nefropatias/genética , Nefropatias/patologia , Túbulos Renais/metabolismo , Túbulos Renais/patologia , Actinas/genética , Actinas/metabolismo , Animais , Biomarcadores , Colágeno Tipo I/genética , Colágeno Tipo I/metabolismo , Modelos Animais de Doenças , Fibrose , Regulação da Expressão Gênica , Nefropatias/metabolismo , Camundongos , Camundongos Transgênicos , Microcirculação , Neovascularização Patológica/genética , Transdução de Sinais , Fator de Crescimento Transformador beta1/genética , Fator de Crescimento Transformador beta1/metabolismo
3.
Case Rep Urol ; 2015: 748495, 2015.
Artigo em Inglês | MEDLINE | ID: mdl-26525589

RESUMO

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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