Cardiovascular calcification in end-stage renal disease.

Cardiovascular diseases are common in patients with end-stage renal disease (ESRD) and cardiovascular morbidity and mortality among dialysis patients are substantially higher than in the general population. The reasons for this high incidence are multiple. They include traditional factors such as hypertension, diabetes, dyslipidaemia, sodium overload, and elevated homocysteine levels as well as disturbances of mineral metabolism, specifically abnormalities in phosphorus and calcium homeostasis. This review will describe the specific cardiovascular complications related to calcifications in ESRD, the implications of the abnormalities of mineral metabolism in its pathogenesis and the current imaging techniques available for the detection of cardiovascular calcifications. Excess of calcium load contributes to the development of cardiac calcifications; therefore, alternative strategies to diminish exogenous calcium load should be considered in patients with ESRD.     

Reactive microglia in the developing brain

Summary Reactive microglia in the developing brain after stab wound was studied by morphological, cytochemical, and autoradiographic methods. Morphologically, early reactive cells are of the M cell type (Matthews 1974). They show an activated nucleus, cytoplasm rich in ribosomes with wide Golgi complex and variable numbers of lipid inclusions. Big clear vacuoles are found in many of these cells. Microtubules not associated with centrioles and filaments may or may not be present. Junctional complexes of the zonula or puncta adherentia types are occasionally found. Strong NADPH dehydrogenase, weak NADH dehydrogenase, strong ATPase, and strong acid phosphatase, in addition to nonspecific esterase activites were demonstrated in many reactive cells. Intravenous infusion of labelled bone marrow cells from a donor showed labelled macrophages and labelled perivascular cells at the site of injury. Intracerebral injection of a small dose of tritiated thymidine at the time of injury resulted in the appearance of labelled macrophages in the following days. These data suggest that many of the reactive cells have an exogenous, more probably monocytic, origin; but a certain amount of endogenous cells also act as macrophages in brain injuries.     

Cost‐utility analysis of idelalisib in combination with rituximab in relapsed or refractory chronic lymphocytic leukaemia

Objective

To evaluate the incremental cost‐utility ratio (ICUR) of idelalisib in combination with rituximab (IR) versus rituximab monotherapy (R) in the treatment of patients with relapsed or refractory (R/R) chronic lymphocytic leukaemia (CLL), from the Spanish National Health System (NHS) perspective.

Methods

A partitioned survival Markov model for a lifetime horizon (30 years) was developed to estimate costs (€, 2016) and quality‐adjusted life years (QALY) with IR and R. Initial cohort included patients with CLL receiving a second or subsequent line (2L) of treatment with IR or R. Survival data were based on CLL clinical trial. Drug, administration, monitoring, adverse events and clinical management of CLL costs were included in the model. Costs and outcomes were discounted using a 3% annually. Deterministic and probabilistic sensitivity analyses (PSA) were performed.

Results

Compared to R, 2L IR treatment resulted in QALY gain of 3.147 (4.965 versus 1.818). Total costs were €118 254 for IR versus €23 874 for R. ICUR was €29 990/QALY gained with IR versus R. In the PSA, IR was cost‐effective in 78% of iterations using a threshold of €45 000/QALY.

Conclusion

IR can be considered a cost‐effective treatment compared to R, in the treatment of R/R CLL patients for the Spanish NHS.