Lown-3 polyunsaturated fatty acid (PUFA) status may be associated with neuro-degenerative disorders, in particular Alzheimer's disease, which has been associated with poor dietary fish orn-3 PUFA intake, and low docosahexaenoic acid (DHA) status. The present case–control study used an established biomarker ofn-3 PUFA intake (serum cholesteryl ester-fatty acid composition) to determinen-3 PUFA status in patients with Alzheimer's disease, who were free-living in the community. All cases fulfilled the National Institute of Neurological and Communicative Disorders and Stroke and Alzheimer's Disease and Related Disorders Association criteria for Alzheimer's disease. Detailed neuropsychological testing and neuroimaging established the diagnosis in all cases. The subjects (119 females and twenty-nine males) aged 76·5 (SD 6·6) YEARS HAD A CLINICAL DEMENTIA RATING (CDR) OF 1 (sd 0·62) and a mini mental state examination (MMSE) score of 19·5 (sd 4·8). The control subjects (thirty-six females and nine males) aged 70 (sd 6·0) years were not cognitively impaired (defined as MMSE score <24): they had a mean MMSE score of 28·9 (sd 1·1). Serum cholesteryl ester-eicosapentaenoic acid and DHA levels were significantly lower (P<0·05 andP<0·001 respectively) in all MMSE score quartiles of patients with Alzheimer's disease compared with control values. Serum cholesteryl ester-DHA levels were progressively reduced with severity of clinical dementia. DHA levels did not differ in patients with Alzheimer's disease across age quartiles: all were consistently lower than in control subjects. Step-wise multiple regression analysis showed that cholesteryl ester-DHA and total saturated fatty acid levels were the important determinants of MMSE score and CDR. It remains to be determined whether low DHA status in Alzheimer's disease is a casual factor in the pathogenesis and progression of Alzheimer's disease.
Oxidized low-density lipoprotein (oxLDL)/beta(2)-glycoprotein I (beta2GPI) complexes have been implicated in atherogenesis. oxLDL/beta2GPI complexes were measured in 339 patients with suspected acute coronary syndromes. Approximately 68% had angiographically documented coronary artery disease (CAD) and significantly higher mean + or - SD levels of oxLDL/beta2GPI (3.75 + or - 6.31 U/mL) than patients with normal coronary arteries (2.21 + or - 3.03 U/mL; P = .0026). Patients with severe CAD had significantly higher mean + or - SD levels of oxLDL/beta2GPI (8.71 + or - 12.87 U/mL) compared with the overall mean of 3.25 U/mL (P < .05) and a significantly higher rate (28.9%) of adverse events than the overall rate of 11.2% (P < .05). Patients with adverse events had higher mean + or - SD levels of oxLDL/beta2GPI (4.05 + or - 5.38 U/mL) than patients without adverse events (3.15 + or - 5.53; P = .029). The relative risk for adverse events in higher oxLDL/beta2GPI quartiles was 3.1 (95% confidence interval, 1.0-9.1; P = .06) for quartile 3 and 3.5 (95% confidence interval, 1.2-10.4; P = .02) for quartile 4. Our results support the concept that oxLDL/beta2GPI complexes are associated with severity of CAD and a 3.5-fold increased risk for adverse outcomes.
Antiphospholipid antibodies (aPLs) have been implicated in atherogenesis. We studied 344 patients with acute coronary syndromes; approximately 40% were aPL+ in 1 or more tests and 60% aPL-. In 215 patients, coronary artery disease (CAD) was angiographically documented, with 43.7% positive for aPL vs 34.9% of patients without CAD positive for aPLs. Anti-beta(2)-glycoprotein I (beta2GPI; 54%) and anti-oxidized low-density lipoprotein (oxLDL)/beta2GPI (48%) were most frequent, accounting for 87% of all aPL+ CAD cases. aPLs correlated with severity of CAD (P = .012). Adverse events occurred in 16.7% of patients with CAD, more frequently in patients who were aPL+ (P = .0006; relative risk, 2.9; 95% confidence interval, 1.5-5.6). Patients who were aPL+ with severe CAD had more adverse events than patients who were aPL- with severe CAD (P = .005) and aPL+ patients undergoing revascularization procedures (P = .001). Vascular events occurred in 21.7% of aPL+ patients compared with 7.1% of aPL- patients (P = .005). Anti-beta2GPI and anti-oxLDL/beta2GPI were associated with CAD severity and adverse outcomes.
Beta2-glycoprotein I (beta2GPI) is a plasma protein suspected to have a role in inhibition of thrombosis. This suspicion is reinforced by the observation that beta2GPI is the major target for autoantibodies in the antiphospholipid syndrome. However, little is known about its circulating levels in common thrombotic diseases or inflammation. We measured beta2GPI levels in 344 healthy controls, 58 normal pregnancies, 102 patients with non-haemorrhagic stroke, 121 patients with acute coronary syndrome and 200 patients with elevated C-reactive protein (CRP). In healthy individuals, we found a strong positive correlation between age and beta2GPI concentration (r = 0.274, P < 0.001) and that beta2GPI levels fall significantly after the eighth week of pregnancy (P = 0.002). We also found significantly reduced levels of beta2GPI in patients with stroke and in elderly patients with myocardial syndrome (P = 0.013 and 0.043). However, in neither group did beta2GPI levels change in the following six months, suggesting that the reduced levels were not a transient post-event phenomenon. In patients with inflammation, beta2GPI levels showed a significant negative correlation with CRP (r = -0.284, P < 0.001) and positively correlated with albumin and transferrin (r = 0.372 and 0.453, respectively with P < 0.001 for both). Furthermore, the largest reduction in beta2GPI levels occurred in patients with the highest CRP values (P < 0.001).
BNP levels were significantly elevated on postnatal day one in preterm infants without a PDA, but then decreased by day five and continued to stay low after that. Gestational age did not have an effect on BNP levels.
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