RESUMEN
OBJECTIVE: Gastrointestinal (GI) cancer patients often experience severe malnutrition during cancer therapies due to gastrointestinal dysfunctions including poor digestion and absorption as well as tumor-associated anorexia. In this study, we performed a randomized clinical trial to determine the efficacy of oral nutrition supplement (ONS) enriched with omega-3 fatty acids on nutritional status, quality of life (QOL), and pro-inflammatory indices. METHODS: Patients diagnosed with GI cancers were recruited and screened for eligibility. A total of 58 patients were randomly allocated to either the control group (n=27) or the experimental group (n=31). The intervention group received 200 ml ONS twice a day while the control group received routine care. Anthropometrics, Patient-Generated Subjective Global Assessment (PG-SGA) score, QOL score and nutrient intake data were collected at baseline, week 4 and week 8. Blood was drawn for biochemical assessments. Nine patients from each group dropped out of the study Forty patients (18 control patients and 22 intervention patients) completed the study. RESULTS: This study showed that ONS intervention improved PG-SGA scores in the intervention group (p<0.01). Scores of physical functioning score and role functioning were declined only in the control group and the difference between week 8 and baseline for role functioning was significant (p<0.001). Fatigue score was steadily decreased in the experiment group, and the differences between week 8 and baseline was significant between two groups (p<0.02). However, no statistically significant improvement in biochemical markers of nutritional status and pro-inflammatory cytokine concentrations were found. These results suggests that ONS intervention for 8 weeks improves PG-SGA scores and QOL scores in patients undergoing cancer therapy.
Asunto(s)
Suplementos Dietéticos , Ácidos Grasos Omega-3/administración & dosificación , Neoplasias Gastrointestinales/terapia , Desnutrición/prevención & control , Estado Nutricional , Anciano , Fatiga/etiología , Fatiga/prevención & control , Femenino , Estado Funcional , Neoplasias Gastrointestinales/complicaciones , Neoplasias Gastrointestinales/fisiopatología , Humanos , Masculino , Desnutrición/etiología , Persona de Mediana Edad , Evaluación Nutricional , Calidad de Vida , Resultado del TratamientoRESUMEN
Vitamin A is essential to mucosal immunity and cell differentiation. The fact that lack of it might involve chronic inflammation and increased risk of cancer has been reported. Little is known about the mechanism of vitamin A deficiency in the development of colitis and its influence on development of colorectal cancer. To determine the influence of vitamin A deficiency on colitis and colorectal cancer development, an experimental study using a colitis mouse model was performed. Dextran sulfate sodium (DSS) colitis was induced in vitamin A-deficient and vitamin A-supplemented mice. Further, colorectal carcinoma was induced by a combination of azoxymethane preinjection and DSS colitis. Results were compared between the two groups mainly by immunohistochemical analysis. Colitis was more severe and recovery from colitis was slower in vitamin A-deficient mice than in vitamin A-supplemented mice. Compared with vitamin A-supplemented mice, vitamin A-deficient mice had decreases in colonic subepithelial myofibroblasts and the ratio of mucosal IgA(+)/IgG(+) cells, increases in CD11c(+) dendritic cells, and a higher rate of development of colorectal carcinoma with colitis following azoxymethane. Vitamin A lipid droplets in subepithelial myofibroblasts were decreased in vitamin A-deficient mice, suggesting alterations in colonic crypt niche function. Thus, vitamin A inhibited colitis and the development of colorectal cancer.
Asunto(s)
Colitis/inducido químicamente , Colitis/tratamiento farmacológico , Neoplasias del Colon/inducido químicamente , Neoplasias del Colon/tratamiento farmacológico , Vitamina A/uso terapéutico , Enfermedad Aguda , Animales , Carcinogénesis/patología , Células Dendríticas/metabolismo , Sulfato de Dextran , Modelos Animales de Enfermedad , Femenino , Homeostasis/efectos de los fármacos , Inmunohistoquímica , Mucosa Intestinal/efectos de los fármacos , Mucosa Intestinal/metabolismo , Mucosa Intestinal/patología , Gotas Lipídicas/efectos de los fármacos , Gotas Lipídicas/metabolismo , Ratones Endogámicos BALB C , Miofibroblastos/efectos de los fármacos , Miofibroblastos/metabolismo , Miofibroblastos/patología , Vitamina A/farmacologíaRESUMEN
BACKGROUND. Silent peptic ulcer has been considered to be associated with nonsteroidal anti-inflammatory drug (NSAID). The recent studies have reported no relationship between them. AIM. We attempted to investigate an association between asymptomatic peptic ulcer and NSAID in Korean adults. METHODS. The subjects were enrolled from participants visiting Myongji Hospital for health examination program of the Korean National Health Insurance Corporation. The questionnaires were designed to investigate individual medical information and gastroduodenal symptoms. RESULTS. From May 2005 to March 2009, 5459 participants were enrolled and 299 participants were excluded. Of 5160 participants, 3144 (60.9%) participants were asymptomatic and 424 (8.2%) participants had peptic ulcer. Among 3144 asymptomatic participants, NSAID-taking participants had the odds ratio of 1.4 [95% confidence interval (CI): 0.7-2.6, p = 0.339] for the risk of peptic ulcer. Among 424 peptic ulcer patients, 247 (58.3%) were asymptomatic. They had lower prevalence of NSAID use (4.9% vs. 14.7%). The asymptomatic gastric ulcer patients had smaller size and more frequent healing stage than the symptomatic gastric ulcer patients. In multivariable analysis of 424 peptic ulcer patients, NSAID patients had the odds ratio of 0.249 (95%CI: 0.115-0.536, p < 0.05) for asymptomatic peptic ulcer. In subgroup analysis of 284 gastric ulcer patients, NSAID-taking patients had the odds ratio of 0.263 (95% CI: 0.105-0.657, p = 0.004) for asymptomatic peptic ulcer. CONCLUSION. NSAID has an inverse association with asymptomatic patients with gastric peptic ulcer, but has no association with gastroduodenal symptoms in duodenal ulcer patients. These suggest that NSAID may be associated with gastroduodenal symptoms rather than masking symptoms, at least in gastric ulcer patients.