BackgroundOur objective was to evaluate the efficacy (clinical and biomarker) and safety of intravenous bapineuzumab in patients with mild to moderate Alzheimer’s disease (AD).MethodsTwo of four phase 3, multicenter, randomized, double-blind, placebo-controlled, 18-month trials were conducted globally: one in apolipoprotein E ε4 carriers and another in noncarriers. Patients received bapineuzumab 0.5 mg/kg (both trials) or 1.0 mg/kg (noncarrier trial) or placebo every 13 weeks. Coprimary endpoints were change from baseline to week 78 on the 11-item Alzheimer’s Disease Assessment Scale–Cognitive subscale and the Disability Assessment for Dementia.ResultsA total of 683 and 329 patients completed the current carrier and noncarrier trials, respectively, which were terminated prematurely owing to lack of efficacy in the two other phase 3 trials of bapineuzumab in AD. The current trials showed no significant difference between bapineuzumab and placebo for the coprimary endpoints and no effect of bapineuzumab on amyloid load or cerebrospinal fluid phosphorylated tau. (Both measures were stable over time in the placebo group.) Amyloid-related imaging abnormalities with edema or effusion were confirmed as the most notable adverse event.ConclusionsThese phase 3 global trials confirmed lack of efficacy of bapineuzumab at tested doses on clinical endpoints in patients with mild to moderate AD. Some differences in the biomarker results were seen compared with the other phase 3 bapineuzumab trials. No unexpected adverse events were observed.Trial registrationNoncarriers (3000) ClinicalTrials.gov identifier NCT00667810; registered 24 Apr 2008.Carriers (3001) ClinicalTrials.gov identifier NCT00676143; registered 2 May 2008.Electronic supplementary materialThe online version of this article (doi:10.1186/s13195-016-0189-7) contains supplementary material, which is available to authorized users.

An evaluation of iron metabolism has been carried out in 23 untreated patients with Hodgkin's disease and 6 patients with other lymphomata. The reduction in red cell life span is related to the stage of the disease. There is an almost universal impairment of iron release from the reticuloendothelial system with a consequent sideropenia and failure of iron delivery to the bone marrow for erythropoiesis. This defect is found in all stages of the disease and is not related to systemic symptoms.

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