RESUMO
BACKGROUND: Although epilepsy is an uncommon comorbidity of Parkinson's disease (PD), the exact incidence of PD among the patients with epilepsy is not clarified yet. OBJECTIVES: We aimed to estimate the incidence of PD in patients with epilepsy and explore the association between epilepsy and PD. METHODS: Epilepsy patients enrolled in the National Health Insurance Service Health Screening Cohort (NHIS-HealS) (2002-2013) between 2003 and 2007 were set up as the experimental group. The major outcome was the occurrence of PD. Non-epilepsy patients were obtained through Propensity Score Matching of 'greedy nearest neighbor' algorithm in 1:1 ratio. The Cox Proportional Hazards model was used to calculate PD incidence and hazard ratio (HR). RESULTS: A total of 10,510 patients were finally included in the study, which contained 5255 patients in epilepsy and non-epilepsy groups, respectively. During the follow-up period, 85 patients with Parkinson's disease among 5255 patients with epilepsy and 57 patients with Parkinson's disease among 5255 patients without epilepsy occurred. The 10,000 Person-Year (PY), representing the number of PD patients per 10,000 per year, was 21.38 in the epilepsy group and 11.18 in the non-epilepsy group. When all variables were adjusted, it was found that the epilepsy group had a 2.19 times significantly higher risk of developing Parkinson's disease than the control group (The adjusted HR: 2.19 (95% CI, 1.55-3.12)). CONCLUSION: This study indicates an increased risk of PD in patients with epilepsy. However, further research is needed to prove an exact causal relationship between these two brain disorders.
Assuntos
Epilepsia , Doença de Parkinson , Humanos , Estudos de Coortes , Incidência , Doença de Parkinson/complicações , Doença de Parkinson/epidemiologia , Comorbidade , Epilepsia/epidemiologia , Epilepsia/complicações , Fatores de RiscoRESUMO
BACKGROUND: Previous studies have reported that xylose selectively inhibited the activity of sucrase. Xylose supplementation may have a beneficial effect on the postprandial glycemic response. However, no studies have investigated patients with IFG or the effectivity of a dose of D-xylose less than 10 % (w/w). METHODS: The present study determined the effect of xylose consumption on postprandial hyperglycemia in normal (n = 25) and hyperglycemic subjects (n = 50). Subjects in this double-blind crossover design study were randomly assigned to consume a sucrose drink (Control, sucrose 50 g + deionized water 100 g) or a sucrose drink additionally containing 5 g (Test 1, sucrose:xylose = 10:1), 3.33 g (Test 2, sucrose:xylose = 15:1), or 2.5 g (Test 3, sucrose:xylose = 20:1) of D-xylose separated by a one-week interval. RESULTS: Normal subjects in all test groups exhibited a significant decrease in serum glucose levels 15 min and 30 min after consuming the xylose-containing drinks compared to the control group. Significantly lower serum levels of insulin were observed at 15 min and 30 min after consuming the xylose-containing drinks compared to the control group. The test 1 group also exhibited a significantly lower insulin area under the curve than the control group. Hyperglycemic subjects (n = 50) in all test groups exhibited a significant decrease in serum glucose levels at 30 min compared to the control group. However, the test 1 group exhibited a significant increase in serum glucose levels at 120 min compared to the control group. Glucose-related markers did not significantly differ in each group. CONCLUSION: Xylose supplementation may exert a beneficial effect on postprandial glycemic responses in subjects with normal glucose levels and prediabetes. TRIAL REGISTRATION: ClinicalTrials.gov identifier: NCT02654301 . Registered 12 January 2016.