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1.
Public Health Nurs ; 36(5): 591-602, 2019 09.
Artigo em Inglês | MEDLINE | ID: mdl-31168851

RESUMO

BACKGROUND: Although the Chronic Disease Self-Management Program (CDSMP) improves chronic disease outcomes, little is known about CDSMP participation in populations less than 65 years of age. We explore study and CDSMP participation rates by demographic characteristics with younger (40-64 years old), lower-to-middle wage workers with chronic disease in a randomized clinical trial (RCT) conducted in North Carolina. METHODS: Descriptive statistics and regression models were used to examine associations between demographic, chronic disease burden, and employment variables, and time-dependent study enrollment and intervention participation outcomes that ranged from initiating consent (n = 1,067) to CDSMP completion (n = 41). RESULTS: Overall, participation among non-Whites was disproportionately higher (43%-59%) than that of Whites (42%-57%) relative to the age-matched racial composition of North Carolina (31% non-White and 69% White). Among participants randomized to the CDSMP, racial and ethnic minorities had the highest rates of participation. There were no significant demographic, chronic disease burden, or employment predictors among the participation outcomes examined, although this may have been due to the limited number of CDSMP workshop participation observations. CONCLUSIONS: Extending the CDSMP to lower-to-middle wage workers may be particularly effective in reaching racial and ethnic minority populations, who complete the program to a greater extent than their White, non-Hispanic counterparts.


Assuntos
Doença Crônica/terapia , Autogestão , Adulto , Coleta de Dados , Etnicidade/estatística & dados numéricos , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Grupos Minoritários/estatística & dados numéricos , North Carolina , Pobreza , Salários e Benefícios , Resultado do Tratamento , População Branca
2.
PLoS One ; 7(2): e29531, 2012.
Artigo em Inglês | MEDLINE | ID: mdl-22363403

RESUMO

CONTEXT: Non alcoholic fatty liver disease (NAFLD) is the hepatic manifestation of the metabolic syndrome. NAFLD represents a spectrum of liver disease ranging from reversible hepatic steatosis, to non alcoholic steato-hepatitis (NASH) and cirrhosis. The potential role of glucocorticoids (GC) in the pathogenesis of NAFLD is highlighted in patients with GC excess, Cushing's syndrome, who develop central adiposity, insulin resistance and in 20% of cases, NAFLD. Although in most cases of NAFLD, circulating cortisol levels are normal, hepatic cortisol availability is controlled by enzymes that regenerate cortisol (F) from inactive cortisone (E) (11ß-hydroxysteroid dehydrogenase type 1, 11ß-HSD1), or inactivate cortisol through A-ring metabolism (5α- and 5ß-reductase, 5αR and 5ßR). OBJECTIVE AND METHODS: In vitro studies defined 11ß-HSD1 expression in normal and NASH liver samples. We then characterised hepatic cortisol metabolism in 16 patients with histologically proven NAFLD compared to 32 obese controls using gas chromatographic analysis of 24 hour urine collection and plasma cortisol generation profile following oral cortisone. RESULTS: In patients with steatosis 5αR activity was increased, with a decrease in hepatic 11ß-HSD1 activity. Total cortisol metabolites were increased in this group consistent with increased GC production rate. In contrast, in patients with NASH, 11ß-HSD1 activity was increased both in comparison to patients with steatosis, and controls. Endorsing these findings, 11ß-HSD1 mRNA and immunostaining was markedly increased in NASH patients in peri septal hepatocytes and within CD68 positive macrophages within inflamed cirrhotic septa. CONCLUSION: Patients with hepatic steatosis have increased clearance and decreased hepatic regeneration of cortisol and we propose that this may represent a protective mechanism to decrease local GC availability to preserve hepatic metabolic phenotype. With progression to NASH, increased 11ß-HSD1 activity and consequent cortisol regeneration may serve to limit hepatic inflammation.


Assuntos
Fígado Gorduroso/metabolismo , Hidrocortisona/metabolismo , Fígado/metabolismo , 11-beta-Hidroxiesteroide Desidrogenase Tipo 1/genética , 11-beta-Hidroxiesteroide Desidrogenase Tipo 1/metabolismo , Adulto , Estudos de Casos e Controles , Progressão da Doença , Fígado Gorduroso/complicações , Fígado Gorduroso/enzimologia , Fígado Gorduroso/urina , Regulação Enzimológica da Expressão Gênica , Humanos , Hidrocortisona/urina , Fígado/enzimologia , Fígado/patologia , Pessoa de Meia-Idade , Modelos Biológicos , Hepatopatia Gordurosa não Alcoólica , Obesidade/complicações , Obesidade/urina , RNA Mensageiro/genética , RNA Mensageiro/metabolismo , Reação em Cadeia da Polimerase em Tempo Real
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