Decreased kidney function relates to progression of cerebral microbleeds in lacunar stroke patients.

BACKGROUND: It is hypothesized that impaired kidney function and cerebral microbleeds represent microvascular damage in different organs. Several cross-sectional studies found impaired kidney function to be associated with the presence of cerebral microbleeds. AIM: To further confirm the association between both small vessel diseases, we aimed to determine whether kidney function is related to progression of cerebral microbleeds in a longitudinal study design. METHODS: In 89 lacunar stroke patients, baseline brain magnetic resonance imaging (including gradient-echo images), baseline estimated glomerular filtration rate (eGFR), blood pressure measurements, and follow-up brain magnetic resonance imaging after two years were available. Presence of cerebral microbleeds on baseline and follow-up magnetic resonance imaging was scored visually. Cerebral microbleeds progression was defined as the presence of any new microbleed on follow-up magnetic resonance imaging. The association between cerebral microbleeds progression (dependent variable) and eGFR (independent variable) was assessed by logistic regression analysis. RESULTS: Cerebral microbleeds progression was present in 17 patients (19.1%). Lower eGFR was associated with cerebral microbleeds progression (OR 1.55 per 10 ml/min/1.73 m(2) decrease, 95% CI 1.05-2.30, with correction for sex and age). After additional correction for baseline presence of cerebral microbleeds or correction for cardiovascular risk factors, including blood pressure, this result remained significant. CONCLUSIONS: In this longitudinal study, we found an independent association between lower eGFR and cerebral microbleeds progression. Cerebral microbleeds and impaired kidney function are both seen as manifestations of microvascular organ damage and our findings further strengthen the association between both small vessel pathologies and also the assumption that small vessel disease could be considered a multisystem disorder.

Plasma tPA-Activity and Progression of Cerebral White Matter Hyperintensities in Lacunar Stroke Patients.

INTRODUCTION: Tissue plasminogen activator (tPA)-activity and plasminogen activator inhibitor type 1 (PAI-1) antigen are considered to be haemostasis-related markers of endothelial activation and relate to presence of cerebral white matter hyperintensities (WMH) as was earlier shown in a cross-sectional study. We investigated whether tPA-activity and PAI-1 levels are associated with WMH progression in a longitudinal study. METHODS: In 127 first-ever lacunar stroke patients in whom baseline brain MRI and plasma levels of tPA-activity and PAI-1-antigen were available, we obtained a 2-year follow-up MRI. We assessed WMH progression by a visual WMH change scale. We determined the relationship between levels of tPA-activity and PAI-1 and WMH progression, by logistic regression analysis. RESULTS: Plasma tPA-activity was associated with periventricular WMH progression (OR 2.36, 95% CI 1.01-5.49, with correction for age and sex and baseline presence of WMH), but not with deep or any (periventricular and/or deep) WMH progression. PAI-1 levels were lower in patients with WMH progression, but these results were not significant. CONCLUSION: We found a relationship between plasma tPA-activity and progression of periventricular WMH. More research is needed to determine whether there is a (direct) role of tPA in the development and progression of WMH.

Vitamin B12 and progression of white matter lesions. A 2-year follow-up study in first-ever lacunar stroke patients.

In cross-sectional studies periventricular white matter lesions (WML) were related to low plasma levels of vitamin B12. Whether low vitamin B12 levels are also related to progression of WML is still unknown. We studied baseline vitamin B12 levels and its association with progression of WML over 2 years of follow-up in first-ever lacunar stroke patients. In 107 first-ever lacunar stroke patients in whom baseline brain MRI and vitamin B12 status were available, we obtained a follow-up brain MRI after 2 years. We assessed progression of periventricular WML (pWML) and deep WML (dWML) using a visual WML change scale. We studied the relationship between baseline levels of plasma vitamin B12 and progression of WML after 2 years of follow-up by binary logistic regression analyses. Vitamin B12 deficiency was more frequent in patients with progression of pWML compared to those without progression (41.9% and 19.7% respectively, p = 0.02). Corrected for sex and age, progression of pWML was associated with lower baseline levels of vitamin B12 (OR 1.42 per 50 unit decrease, 95% CI 1.00-1.92). Vitamin B12 levels were not associated with progression of dWML. In conclusion progression of pWML after 2 years of follow-up relates to low levels of vitamin B12 at baseline in first-ever lacunar stroke patients. Whether this population could benefit from vitamin B12 supplementation is unknown and requires further investigation.

Failure of vancomycin treatment for meningitis caused by vancomycin-susceptible Enterococcus faecium.

This case report describes a nosocomial vancomycin-sensitive Enterococcus faecium meningitis with poor response to vancomycin. E. faecium infections continue to represent a therapeutic challenge in Europe, even in countries where vancomycin resistance is still rare. In the case of vancomycin-sensitive E. faecium meningitis, intravenous chloramphenicol should be considered as a treatment option.