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1.
J Am Coll Surg ; 230(4): 535-541, 2020 04.
Artigo em Inglês | MEDLINE | ID: mdl-32032724

RESUMO

BACKGROUND: Nipple-sparing mastectomy (NSM) is an alternative to skin-sparing mastectomy in appropriately selected patients. The aim of this study was to review our experience with NSM and to evaluate for oncologic safety. STUDY DESIGN: Patients who underwent NSM at our institution from September 2008 through August 2017 were identified after IRB approval. Data included patient age, tobacco use, tumor size, hormone receptor status, lymph node status, radiation and chemotherapy use, incision type, and reconstruction type. Statistical analyses were performed using ANOVA and chi-square tests. RESULTS: There were 322 patients who underwent 588 NSM (83% bilateral, 17% unilateral), including 399 (68%) for malignancy (Stage 0 [27%], I [44%], II [25%] and III [4%]). The overall rate of wound complication was 18.9%. Tobacco use increased complication (37.5% vs 16.3%, p < 0.001), as did adjuvant radiation therapy (31.4% vs 17.4%, p = 0.014). Patients with lymph node involvement and larger tumor size had a higher rate of complication (31.3% vs 17.2%, p = 0.016). Patients undergoing circumareolar incisions had a higher rate of complication than those undergoing lateral radial, inframammary fold, or curvilinear incisions (43.5% vs 17.4% vs 17.4% vs 14.3%, respectively, p = 0.018). Six (1%) local chest wall recurrences occurred during the follow-up period, none of which involved the nipple-areolar complex. Four patients (1%) suffered a distant recurrence. CONCLUSIONS: Most NSM performed at our institution are in patients with malignancy. The oncologic safety is confirmed by the low locoregional recurrence rate. Tobacco use and adjuvant radiation therapy remain the most significant risk factors for complication, highlighting the need for careful patient selection and patient counseling regarding modifiable risk factors and expected outcomes.


Assuntos
Neoplasias da Mama/cirurgia , Mastectomia Subcutânea/métodos , Adulto , Idoso , Estudos de Coortes , Feminino , Humanos , Mastectomia Subcutânea/efeitos adversos , Pessoa de Meia-Idade , Mamilos , Tratamentos com Preservação do Órgão , Estudos Retrospectivos , Resultado do Tratamento , Adulto Jovem
2.
J Interferon Cytokine Res ; 33(7): 376-83, 2013 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-23600861

RESUMO

This study examined inflammatory cell and cytokine production in brain tissue from a lipopolysaccharide (LPS)-treated rat model that mimics many of the neuropathologic changes associated with neurodegenerative diseases We also monitored the appearance of a glial cell line-derived neurotrophic factor (GDNF) and circulating nitric oxide (NO) levels, as well as an immune system-associated cells in a selected area of the brain, the olfactory lobe. The studies were based on the hypothesis that LPS treatment stimulates temporal changes within the brain and that these responses include immune cell recruitment, increased tissue levels of immune modulating cytokines and NO, as well as greater glial cell activation resulting in increased production of GDNF. As previously reported by other investigators, our animal model of systemic LPS treatment leads to an increase in the concentrations of circulating cytokines, including TNF-α, IL-Iß, and IL-6, with a maximum response 6 h post LPS administration. Concomitant with cytokine elevations, circulating NO levels were elevated for several hours post LPS administration. The brain content of the GDNF was also elevated over a similar time frame. Lymphocytes, neutrophils, macrophages, plasma cells, and cytokines were all seen in various areas of LPS-treated brains, often around blood vessels associated with the meninges, with these localizations possibly indicating involvement of both the blood-brain and blood-cerebral spinal fluid barriers in these inflammatory episodes. Our results suggest an involvement of both the peripheral and the central nervous system immune components in response to inflammation and inflammatory episodes. This leads us to propose that inflammation initiates an immune response by activating both microglia and astrocytes and that the presence of continuing and increasing proinflammatory mechanisms results in a situation, where cellular protective mechanisms are overcome and the more susceptible cells enter into cell death pathways, initiating a train of events that is a major part of neurodegeneration.


Assuntos
Fator Neurotrófico Derivado de Linhagem de Célula Glial/metabolismo , Inflamação/imunologia , Leucócitos/imunologia , Doenças Neurodegenerativas/imunologia , Bulbo Olfatório/metabolismo , Animais , Barreira Hematoencefálica/imunologia , Movimento Celular/imunologia , Células Cultivadas , Citocinas/metabolismo , Modelos Animais de Doenças , Fator Neurotrófico Derivado de Linhagem de Célula Glial/genética , Humanos , Mediadores da Inflamação/metabolismo , Lipopolissacarídeos/imunologia , Masculino , Óxido Nítrico/metabolismo , Bulbo Olfatório/imunologia , Ratos , Ratos Sprague-Dawley
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