BackgroundThe pathophysiology of insulin resistance-induced hypertension and hyperlipidemia might entail differences in dementia risk in cases with hypertension and hyperlipidemia without prior diabetes mellitus (DM). This study investigated whether incident hypertension, incident hyperlipidemia, or both, increased the dementia risk in patients with and without DM.MethodsA nationwide retrospective cohort study was conducted. The study sample was obtained from the National Health Insurance Research Database. We enrolled 10,316 patients with a new diagnosis of DM between 2000 and 2002 in the DM cohort. For the same period, we randomly selected 41,264 patients without DM in the non-DM cohort (matched by age and sex at a 1:4 ratio with the DM cohort). Both cohorts were then separately divided into four groups on the basis of incident hypertension or incident hyperlipidemia status.ResultsIn total, 51,580 patients aged between 20 and 99 years were enrolled. The dementia risk was higher in the DM cohort than in the non-DM cohort (adjusted hazard ratio (HR) = 1.47, 95% confidence interval (CI) = 1.30–1.67, p < 0.001). In the DM cohort, the dementia risk in patients with both hypertension and hyperlipidemia did not significantly increase compared with that in those without hypertension and hyperlipidemia (p = 0.529). Similar results were observed in those with either hypertension (p = 0.341) or hyperlipidemia (p = 0.189). In the non-DM cohort, patients with both hypertension and hyperlipidemia had a higher dementia risk (adjusted HR = 1.33, 95% CI = 1.09–1.63, p = 0.006). The results remained largely unchanged in patients with only hypertension (adjusted HR = 1.22, 95% CI = 1.05–1.40, p = 0.008). However, the dementia risk did not increase significantly in patients with only hyperlipidemia (p = 0.187).ConclusionsThe development of hypertension, hyperlipidemia, or both, following a diagnosis of incident diabetes is secondary to diabetes onset and likely mediated through insulin resistance associated with diabetes, which does not further accentuate dementia risk. DM itself (i.e., the systemic influence of hyperglycemia) might be the main driver of increased dementia risk.
Background and Purpose-The close relationship between stroke and chronic kidney disease (CKD) has been well-documented. However, few studies have focused on silent brain infarction (SBI) in CKD. We investigated the prevalence of SBI in different stages of CKD. Methods-We included 1312 participants aged 30 to 93 years who came from either a random sample of residents or from a group of physically examined subjects in the same community. Basic information, clinical evaluations, laboratory tests, and MRI images were assessed. Subjects were divided into groups 1, 2, 3a, and 3b, corresponding to the estimated glomerular filtration rate (eGFR) levels of Ն90.0, 60.0 to 89.9, 45.0 to 59.9, and 30.0 to 44.9 mL/min/1.73 m 2 . Results-The crude prevalence was 4.7%: 2.6% (20 of 759 subjects) in group 1; 6.3% (32 of 506) in group 2; 12.9% (4 of 31) in group 3a; and 37.5% (6 of 16) in group 3b (PϽ0.001). Additionally, SBI also correlated with age, male sex, hypertension, diabetes, moderate carotid plaque, higher blood pressures, obesity, and levels of triglyceride, high-density lipoprotein cholesterol, high-sensitivity C-reactive protein, and uric acid (all PϽ0.05).
BackgroundThe microsatellite polymorphism of heme oxygenase (HO)-1 gene promoter has been shown to be associated with the susceptibility to ischemic event, including coronary artery disease (CAD), myocardial infarction, and peripheral vascular disease. We aimed to examine whether the length of (GT)n repeats in HO-1 gene promoter is associated with ischemic stroke in people with CAD risk factors, especially low level of HDL.MethodsA total of 183 consecutive firstever ischemic stroke inpatients and 164 non-stroke patients were screened for the length of (GT)n repeats in HO-1 promoter. The long (L) and short (S) genotype are defined as the averaged repeat number >26 and ≦26, respectively.ResultsStroke patients tended to have more proportions of hypertension, diabetics and genotype L, than those of genotype S. Patients with genotype L of HO-1 gene promoter have higher stroke risk in comparison with genotype S especially in dyslipidemia individuals. The significant differences on stroke risk in multivariate odds ratios were found especially in people with low HDL-C levels.ConclusionsSubjects carrying longer (GT)n repeats in HO-1 gene promoter may have greater susceptibility to develop cerebral ischemic only in the presence of low HDL-C, suggesting the protective effects in HO-1 genotype S in the process of ischemic stroke, particularly in subjects with poor HDL-C status.
BackgroundThe relationship of alteration of metabolic syndrome (MetS) with dementia remains unclear. The purpose of study was to evaluate the association between dynamic change in MetS status around a 5‐year period and dementia.Methods and ResultsThe cohort study was conducted from the Taiwanese Survey on Prevalence of Hypertension, Hyperglycemia, and Hyperlipidemia in 2002, with follow‐up in 2007. The sample was subsequently linked to the National Health Insurance Research Database. Participants were divided into 3 groups: persistent MetS (MetS both in 2002 and 2007); nonpersistent MetS (MetS either in 2002 or 2007); and non‐MetS (MetS neither in 2002 nor 2007). Furthermore, the individuals with nonpersistent MetS were categorized as improved MetS (MetS in 2002 but not in 2007) and worsened MetS (MetS not in 2002 but in 2007). Each participant was tracked until the end of 2011 to identify the development of dementia. In total, 3458 participants aged 40 to 80 years were included. Up to 10 years and 31 741 person‐years of follow‐up, 76 patients developed dementia. Only a relationship was found between the nonpersistent MetS and dementia (adjusted hazard ratio=1.93; 95% confidence interval =1.17–3.19; P=0.010). Moreover, a significantly higher dementia risk was observed in patients with worsened MetS (adjusted hazard ratio=2.22; 95% confidence interval=1.32–3.72; P=0.003), but not those with persistent (P=0.752) or improved (P=0.829) MetS. Similar results were detected in participants aged ≥65 years.ConclusionsPatients with worsened MetS had an increased dementia risk during the 10‐year follow‐up period in a population‐based sample.
Background Ghrelin has a protective effect on endothelial cells. Endothelial cell dysfunction is associated with cardiovascular disease (CVD) and CVD remains the leading cause of morbidity in hemodialysis (HD) patients. Acylated ghrelin (A-Ghr) is the functional form of ghrelin, so we hypothesized that A-Ghr is associated with the occurrence of CVD in HD patients. Methods We conducted a prospective cohort study in 412 HD patients. The cohort was sub-grouped into low and high A-Ghr groups according to the median A-Ghr level of 4.88 pg/mL. The association between the low/high A-Ghr groups and the incidence of CVD were analyzed. Results The HD patients in a low A-Ghr group had a greater risk of incidental CVD than those in a high A-Ghr ghrelin. This association remained significant after the adjustment for possible confounding factors, including age, gender, HD duration, BMI, diabetes, albumin, nPCR and Charlson's comorbidity index score. Conclusion It appears that a low serum A-Ghr level is associated with the development of CVD in HD patients.
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