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1.
Braz. j. med. biol. res ; 45(12): 1301-1307, Dec. 2012. ilus, tab
Artigo em Inglês | LILACS | ID: lil-659661

RESUMO

Protein-energy malnutrition (PEM) is a treatable disease with high prevalence among hospitalized patients. It can cause significant increases in the duration of hospitalization and costs. PEM is especially important for health systems since malnourished patients present higher morbidity and mortality. The objective of the present study was to assess the evolution of nutritional status (NS) and the effect of malnutrition on clinical outcome of patients at a public university hospital of high complexity in Brazil. Patients hospitalized in internal medicine (n = 54), oncology (n = 43), and infectious diseases (n = 12) wards were included. NS was evaluated using subjective global assessment up to 48 h after admission, and thereafter at intervals of 4-6 days. On admission, patients (n = 109) were classified as well-nourished (n = 73), moderately malnourished or at risk of malnutrition (n = 28), and severely malnourished (n = 8). During hospitalization, malnutrition developed or worsened in 11 patients. Malnutrition was included in the clinical diagnosis of only 5/36 records (13.9% of the cases, P = 0.000). Nutritional therapy was administered to only 22/36 of the malnourished patients; however, unexpectedly, 6/73 well-nourished patients also received commercial enteral diets. Complications were diagnosed in 28/36 malnourished and 9/73 well-nourished patients (P = 0.000). Death occurred in 12/36 malnourished and 3/73 well-nourished patients (P = 0.001). A total of 24/36 malnourished patients were discharged regardless of NS. In summary, malnutrition remains a real problem, often unrecognized, unappreciated, and only sporadically treated, even though its effects can be detrimental to the clinical course and prognosis of patients. The amount of public and private funds unnecessarily dispersed because of hospital malnutrition is significant.


Assuntos
Adulto , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Apoio Nutricional/métodos , Desnutrição Proteico-Calórica/terapia , Brasil , Hospitais Universitários , Tempo de Internação , Estado Nutricional , Prognóstico , Estudos Prospectivos , Desnutrição Proteico-Calórica/mortalidade , Índice de Gravidade de Doença
2.
Braz. j. med. biol. res ; 44(10): 992-999, Oct. 2011.
Artigo em Inglês | LILACS | ID: lil-600690

RESUMO

The present review evaluates the role of sleep and its alteration in triggering problems of glucose metabolism and the possible involvement of adipokines in this process. A reduction in the amount of time spent sleeping has become an endemic condition in modern society, and a search of the current literature has found important associations between sleep loss and alterations of nutritional and metabolic contexts. Studies suggest that sleep loss is associated with problems in glucose metabolism and a higher risk for the development of insulin resistance and type 2 diabetes mellitus. The mechanism involved may be associated with the decreased efficacy of regulation of the hypothalamus-pituitary-adrenal axis by negative feedback mechanisms in sleep-deprivation conditions. In addition, changes in the circadian pattern of growth hormone (GH) secretion might also contribute to the alterations in glucose regulation observed during sleep loss. On the other hand, sleep deprivation stress affects adipokines - increasing tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) and decreasing leptin and adiponectin -, thus establishing a possible association between sleep-debt, adipokines and glucose metabolism. Thus, a modified release of adipokines resulting from sleep deprivation could lead to a chronic sub-inflammatory state that could play a central role in the development of insulin resistance and type 2 diabetes mellitus. Further studies are necessary to investigate the role of sleep loss in adipokine release and its relationship with glucose metabolism.


Assuntos
Humanos , Adipocinas/metabolismo , /etiologia , Intolerância à Glucose/metabolismo , Resistência à Insulina/fisiologia , Privação do Sono/complicações , Adiponectina/metabolismo , /metabolismo , /metabolismo , Leptina/metabolismo , Privação do Sono/metabolismo , Fator de Necrose Tumoral alfa/metabolismo
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