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1.
Ann Thorac Surg ; 103(2): 416-421, 2017 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-27825692

RESUMO

BACKGROUND: The 5-year survival of patients with low socioeconomic status (SES) and esophageal cancer is significantly lower than that in patients with high SES. It is poorly understood what causes these worse outcomes. We hypothesized that a qualitative approach could elucidate the underlying causes of these differences. METHODS: Patients with a diagnosis of esophageal cancer were recruited through flyers in regional cancer centers as well as through Facebook advertisements in cancer support groups and newspapers; they participated in a 1-hour semistructured interview or completed an online survey. Patients were stratified into low- and high-SES groups and were surveyed about their health history and access to cancer care. Data were coded into common themes based on participant responses. RESULTS: Eighty patients completed the interviews or surveys, with 38 in the high-SES group and 42 in the low-SES group. There were no clinically significant differences between the groups in comorbidities and cancer staging. Patients with low SES were offered operative treatment at significantly lower rates (19 of 42 [44.7%] versus 29 of 38 [76.3%]; p = 0.0048), had a decreased rate of second opinions (10 of 42 [23.8%] versus 25 of 38 [65.8%]; p = 0.00016), and were more likely to lose their jobs (14 of 42 [33.3%] versus 1 of 38 [2.6%]; p = 0.00044) than their high-SES counterparts. Thematic analysis found that communication difficulties, lack of understanding of treatment, and financial troubles were consistently reported more prominently in the lower-SES groups. Having a facilitator (eg, social worker) improved care by helping patients navigate complex treatments and financial concerns. CONCLUSIONS: Financial and communication barriers exist, which may lead to disparities in cancer outcomes for patients with low SES. There is a critical need for medical advocates to assist patients with limited resources.


Assuntos
Neoplasias Esofágicas/terapia , Acessibilidade aos Serviços de Saúde , Estadiamento de Neoplasias , Inquéritos e Questionários , Populações Vulneráveis , Neoplasias Esofágicas/diagnóstico , Neoplasias Esofágicas/economia , Feminino , Humanos , Masculino , Michigan , Pessoa de Meia-Idade , Fatores Socioeconômicos
2.
Ann Clin Transl Neurol ; 1(10): 799-812, 2014 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-25493271

RESUMO

OBJECTIVE: This study focused on altered mitochondrial dynamics as a potential mechanism for diabetic peripheral neuropathy (DPN). We employed both an in vitro sensory neuron model and an in situ analysis of human intraepidermal nerve fibers (IENFs) from cutaneous biopsies to measure alterations in the size distribution of mitochondria as a result of hyperglycemia and diabetes, respectively. METHODS: Neurite- and nerve-specific mitochondrial signals within cultured rodent sensory neurons and human IENFs were measured by employing a three-dimensional visualization and quantification technique. Skin biopsies from distal thigh (DT) and distal leg (DL) were analyzed from three groups of patients; patients with diabetes and no DPN, patients with diabetes and confirmed DPN, and healthy controls. RESULTS: This analysis demonstrated an increase in mitochondria distributed within the neurites of cultured sensory neurons exposed to hyperglycemic conditions. Similar changes were observed within IENFs of the DT in DPN patients compared to controls. This change was represented by a significant shift in the size frequency distribution of mitochondria toward larger mitochondria volumes within DT nerves of DPN patients. There was a length-dependent difference in mitochondria within IENFs. Distal leg IENFs from control patients had a significant shift toward larger volumes of mitochondrial signal compared to DT IENFs. INTERPRETATION: The results of this study support the hypothesis that altered mitochondrial dynamics may contribute to DPN pathogenesis. Future studies will examine the potential mechanisms that are responsible for mitochondrial changes within IENFs and its effect on DPN pathogenesis.

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