Nutritional Therapy with Vitamin K1 Is Effective in the Improvement of Vitamin K Status and Bone Turnover Markers in Patients with Severe Motor and Intellectual Disabilities.

We have previously reported that patients with severe motor and intellectual disabilities (SMID) have a high prevalence of vitamin K deficiency both in the liver and bone. Thus, vitamin K therapy for SMID patients should be considered. In the present study, we have studied the efficacy of nutritional therapy with vitamin K1 for improving their vitamin K status and bone metabolism markers in patients with SMID. During the 3-mo period, 19 patients under enteral feeding received vitamin K1 treatment, the dose of which was determined to meet each subject's energy requirement. Biomarkers of vitamin K insufficiency; protein induced by vitamin K absence or antagonist-II (PIVKA-II), undercarboxylated osteocalcin (ucOC), intact osteocalcin (intact OC) and bone turnover markers (tartrate-resistant acid phosphatase-5b: TRACP-5b and bone alkaline phosphatase: BAP) were measured at baseline and post treatment. The ucOC/OC ratio was calculated as a more sensitive index than ucOC for vitamin K status in the bone. After treatment, the median vitamin K intake increased from 66 to 183 µg/d, and serum levels of PIVKA-II and ucOC/OC ratio were significantly decreased. Decrements of serum ucOC level and ucOC/OC ratio were significantly associated with vitamin K intake, indicating that both markers well reflect the dose-dependent vitamin K effects. Serum levels of BAP and TRACP-5b were significantly increased after vitamin K1 therapy. Nutritional therapy with vitamin K1 effectively improved the markers for vitamin K status and bone turnover, and was considered to be a good candidate for treatment in SMID patients.

The association between high-sensitivity C-reactive protein at admission and progressive motor deficits in patients with penetrating artery infarctions.

BACKGROUND: A fraction of patients with penetrating artery infarction (PAI) experience progressive motor deficit deterioration (PMD). We sought to investigate the role of high-sensitivity C-reactive protein (hs-CRP) at admission in predicting PMD. METHODS: From January 2015 to September 2018, consecutive patients with PAI from three centers were prospectively enrolled in this study. PMD was defined as worsening of motor function score by ≥1 point on the National Institutes of Health Stroke Scale during the first 5 days after admission. Multivariable logistic regression analyses were performed to explore the relationship between hs-CRP and PMD in patients with PAI. We also performed receiver operating characteristic curve analysis and constructed a nomogram to assess the overall discriminative ability of hs-CRP in predicting PMD. RESULTS: We ultimately included 544 patients (mean age, 65.4 ± 11.8 years). A total of 85 (15.6%) patients were identified to have PMD. Multivariate logistic regression analysis showed that hs-CRP was independently associated with PMD (P = 0.001). The optimal cutoff value for hs-CRP as a predictor for PMD was 3.48 mg/L, with a sensitivity of 73.64% and a specificity of 82.35% (area under curve, 0.792). Moreover, the nomogram we constructed indicated that higher level of hs-CRP was an indicator of PMD (c-index = 0.780, P < 0.001). CONCLUSIONS: Our study suggested that hs-CRP might be a useful biomarker for predicting the risk of PMD in patients with PAI.

Antiphospholipid Antibodies: Cognitive and Motor Decline, Neuroimaging and Neuropathology.

BACKGROUND: Few data are available on associations of antiphospholipid (aPL) antibodies with cognitive and motor decline in aging, and cerebrovascular disease on in vivo neuroimaging and postmortem neuropathology. METHODS: This longitudinal, clinical-pathologic study (aPL antibodies, brain infarcts, and cognitive and motor decline in aging), was derived from 2 ongoing community-based cohort studies. A panel of 3 aPL antibodies was assayed in serum from 956 older individuals (mean age = 81.1 years; 72% women). Serum was also tested in a subset for markers of inflammation (C-reactive protein [CRP]) and blood-brain barrier breakdown (matrix metalloproteinases, MMPs). Annual clinical evaluations documented cognitive (17 neuropsychological tests) and motor function including parkinsonism. Cerebrovascular disease data were derived from in vivo neuroimaging and postmortem neuropathologic evaluations (699 individuals). We examined associations of aPL with cognitive and motor decline, other serum markers, neuroimaging, and neuropathology. RESULTS: Of 956 individuals, 197 (20.6%) had aPL positivity, defined as positivity on any of the assays, at the time of first measurement. During a mean follow-up of 6.6 years (SD 4), overall aPL positivity was not associated with change in global cognition (estimate = -0.005, SE 0.011; p = 0.622) or parkinsonian signs (estimate = -0.003, SE 0.017; p = 0.860). aPL were not associated with serum CRP or MMPs (both p > 0.268). aPL were not associated with in vivo brain magnetic resonance imaging white matter hyperintensities or infarcts (both p > 0.376). Among those autopsied, aPL were not associated with pathologically confirmed brain infarcts, or cerebral atherosclerosis or arteriolosclerosis (all p≥ 0.447). CONCLUSIONS: In older individuals followed longitudinally, aPL do not relate to cognitive or motor decline, inflammation, or cerebrovascular disease on in vivo neuroimaging or postmortem neuropathology.

Ceruloplasmin in Parkinson's disease and the nonmotor symptoms.

OBJECTIVES: To investigate the relationship between ceruloplasmin (CP) and Parkinson's disease (PD), and the correlation between CP level and the time difference between nonmotor symptoms and motor symptoms and the diagnosis were also mentioned. MATERIALS AND METHODS: Sixty-six patients diagnosed with PD for the first time were included in the study. They were divided into CP reduction group (31 cases) and CP normal group (35 cases) according to their CP level. The estimated time difference between nonmotor symptoms and motor symptoms and the diagnosis were recorded respectively. The magnetic sensitive nigra phase value was measured by susceptibility weighted imaging (SWI). RESULTS: Ceruloplasmin level was middling correlated with age (r = .561, p < .001). There was strong negative correlation between CP level and UPDRS scores (r = -.727, p < .001). The CP level was significantly correlated with the magnetic sensitive nigra phase value (r = .891, p < .001). CP level showed moderate correlation with the time difference from nonmotor symptoms to motor symptoms (r = .559, p < .001), besides, the time difference between nonmotor symptoms and the diagnosis (r = .525, p < .001) and CP level was also moderately related. CONCLUSIONS: Ceruloplasmin interference in iron metabolism was closely related with PD development. And there were slight corrections between CP level and the time difference from nonmotor symptoms to motor symptoms or the diagnosis.

Neonatal Magnesium Levels Between 24 and 48 Hours of Life and Outcomes for Epilepsy and Motor Impairment in Premature Infants.

OBJECTIVE: Elevated rates of epilepsy and motor impairments including cerebral palsy are observed in children who were born prematurely. Maternal antenatal magnesium supplementation has been associated with decreased rates of cerebral palsy in infants born prematurely. Our objective was to determine whether the neonatal serum magnesium level between 24 and 48 hours after birth is associated with better long-term neurodevelopmental outcomes (epilepsy, motor impairment) in premature infants. METHODS: We performed a retrospective cohort analysis in infants born less than 37-weeks gestation over a ten-year period. Prenatal, perinatal, and postnatal clinical and demographic information was collected. Crude and adjusted odds ratios were estimated under generalized linear models with generalized estimating equations to examine the association of the neonatal serum magnesium level between 24 and 48 hours after birth with the risk of epilepsy and/or motor impairment (spasticity; hypotonia; cerebral palsy). RESULTS: The final cohort included 5461 infants born less than 37-weeks gestation from 2002 to 2011. The adjusted relative risk ratio for the combined outcomes of epilepsy and/or motor impairment, controlling for gestational age, current age, maternal magnesium supplementation, maternal steroid administration, five-minute Apgar score, neonatal infection, need for vasopressor use, and birth weight and with serum magnesium level as the main independent variable, was 0.85 (P = 0.24). Stratified analyses by gestational age less than 32 or greater than 32 weeks were not significantly associated with adverse neurodevelopmental outcome (risk ratio = 0.79 and 1.2, P = 0.12 and 0.49, respectively). A multivariate analysis for the risk of motor impairment alone had a risk ratio of 0.94 (P = 0.72). CONCLUSION: This study demostrates that the neonatal magnesium level between 24 and 48 hours of life in premature infants is not significantly associated with the risk for developing epilepsy or motor impairment.