Intravenous immunoglobulin increases plasma viscosity without parallel rise in blood pressure.

WHAT IS KNOWN AND OBJECTIVE: Intravenous immunoglobulin (IVIg) is a commonly used therapy for autoimmune disease, but may cause chronic hypertension and thrombosis. We determined whether: (i) IVIg systematically affects blood pressure in the short term; (ii) acute changes in plasma viscosity because of IVIg correlate with blood pressure effects; (iii) effects of IVIg on acute blood pressure are related to baseline blood pressure or hypertension status and (iv) IVIg influences plasma markers of inflammation, anticardiolipin antibodies and homocysteine as additional putative prothrombotic risk factors. METHODS: Twenty adults with autoimmune neurological disease who received a course of IVIg were evaluated immediately before and after each infusion, on every day of the course. Blood pressure, pulse and the following haematological parameters were determined: plasma viscosity, erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), haematocrit, fibrinogen, interleukin-6 (IL-6), homocysteine and anticardiolipin positivity. RESULTS: Intravenous immunoglobulin caused both acute and cumulative rises in plasma viscosity across a treatment course, but no concordant changes in blood pressure. There was also no correlation between individual blood pressure changes and viscosity, baseline blood pressure or hypertension status. Levels of IL-6 rose across the course of therapy, but the acute-phase reactants CRP and fibrinogen did not. One patient developed anticardiolipin antibodies during therapy. WHAT IS NEW AND CONCLUSION: Individual courses of IVIg do not systematically raise blood pressure. Where IVIg is found to cause hypertension, this does not appear to be due to a direct effect of IVIg on plasma viscosity.

Hypertension increases the probability of Alzheimer's disease and of mild cognitive impairment in an Arab community in northern Israel.

BACKGROUND: We aimed to determine whether vascular risk factors are associated with Alzheimer's disease (AD) and mild cognitive impairment (MCI) in an elderly Arab population. METHODS: An Arabic-speaking team performed a door-to-door survey of consecutive residents aged > or =65 years. We estimated the odds of AD or MCI versus normal controls as a function of age, gender, education and presence of vascular factors by multinomial logistic regression with interactions. RESULTS: Out of 767 subjects (54% men), 444 were cognitively normal, 234 had MCI and 89 had AD. AD was significantly associated with hypertension (p = 0.01; OR = 2.08; 95% CI: 1.18-3.65), age (p < 0.0001; OR = 1.19; 95% CI: 1.14-1.24), female gender (p = 0.0016; OR = 3.06; 95% CI: 1.53-6.15) and education (p = 0.0002; OR = 0.75; 95% CI: 0.65-0.88). MCI was significantly associated with hypertension (p = 0.0042; OR = 1.69; 95% CI: 1.25-2.44), age (p < 0.0001; OR = 1.06; 95% CI: 1.03-1.09) and education (p < 0.0001; OR = 0.76; 95% CI: 0.71-0.83), but not with gender. CONCLUSIONS: Hypertension, older age and low education significantly increase the probability of AD and MCI. The effect of hypertension on the odds of AD versus controls is over and above the effects of age, gender and education. For MCI versus controls there is no gender effect, and the effect of hypertension is over and above the effects of age and education.

Aspirin responsiveness in acute brain ischaemia: association with stroke severity and clinical outcome.

PURPOSE: Platelets play a critical role in the pathogenesis of acute brain ischaemia. We studied the association between the degree of inhibition of platelet function by aspirin (ASA) and the severity and outcome of acute brain ischaemia. METHODS: Platelet responsiveness to ASA was assessed in patients with acute brain ischaemia, treated with ASA since hospital admission. The degree of ASA responsiveness was assessed by optical aggregometry and categorized into patients with good response, partial response and complete unresponsiveness to ASA (good responders, partial responders and non-responders, respectively). An additional evaluation of responsiveness to ASA was performed by Impact-R (cone and platelet analyzer). Patients underwent serial clinical assessment during hospitalization, at discharge and during follow-up. RESULTS: Among 105 patients (mean age 63 +/- 12 years; 66% men), impaired ASA responsiveness at baseline as assessed by aggregometry was associated with increased stroke severity at baseline, unfavourable clinical course, and poor functional outcome during follow-up (p < 0.05 for all). Age-adjusted odds ratios in non-responders compared to good responders were 9.8 for severe stroke on admission (95% CI 2.8-34.9), 3.1 for lack of early clinical improvement (95% CI 1.1-8.8) and 8.6 for poor functional outcome during follow-up (95% CI 2.4-30.4). Less robust trends were observed with the Impact-R. CONCLUSIONS: Impaired responsiveness to ASA in acute brain ischaemia is common and is associated with worse neurological deficits at stroke onset, early clinical deterioration and poorer functional outcome. The clinical significance of these findings requires further evaluation in larger longitudinal studies.