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Background Recent systematic reviews and meta-analyses suggest that medication reconciliation (MR) is effective in decreasing the risk of medication discrepancies. Nevertheless, the association between MR and subsequent improved healthcare outcomes is not well established. Objectives This systematic review of reviews set out to identify published systematic reviews on the impact of MR programs on health outcomes and to describe key components of the intervention, the health outcomes assessed and any associations between MR and health outcomes. Methods PubMed, EMBASE, Cochrane Library, Cumulative Index to Nursing and Allied Health Literature (CINAHL) and SCOPUS were searched from inception to May 2019. Systematic reviews of all study designs, populations, intervention providers and settings that measured patient-related outcomes or healthcare utilization were considered. Methodological quality was assessed using A Measurement Tool to Assess Systematic Reviews 2 (AMSTAR 2). Two investigators performed study selection, quality assessment and data collection independently. Results Five systematic reviews met the inclusion criteria: 2 were rated as low quality and 3 as critically low quality. Reviews included primary studies in different settings (hospitals, the community and residential aged care facilities) that reported the impact of MR on mortality, length of stay, Emergency Department (ED) visits, readmissions, physician visits and healthcare utilization. Only one review reported results on mortality. However, healthcare utilization, which usually included ED visits and readmissions, was communicated in all reviews. Meta-analyses were conducted in all reviews except one. Medication reconciliation was not consistently found to be associated with improvements in health outcomes. Conclusions Few systematic reviews support the value of MR in achieving good patient-related outcomes and healthcare utilization improvements. The quality of the systematic reviews was low and the primary studies included commonly involved additional activities related to MR. There was no clear evidence in favor of intervention in mortality, length of stay, ED visits, unplanned readmissions, physician visits and healthcare utilization.

9 Figuras, Polyphenols are a group of chemical substances found in plants, with immunomodulatory, antiproliferative, and anti-inflammatory properties that might be useful in the prophylaxis and treatment of graft-versus-host disease (GVHD). Polyphenolic extract (PE) obtained from extra virgin olive oil (EVOO) decreased the activation and proliferation of activated T cells. In addition, a decreased production of proinflammatory cytokines was observed upon exposure to PE. Western blot assays showed a marked inhibition of Akt phosphorylation and nuclear translocation of NF-κB in activated T cells. In a murine model of acute GVHD, we observed that mice that received a diet supplemented in PE (600 ppm) presented a higher survival rate and lower risk of developing GVHD when compared with the group that received a control diet. Histopathologic examination showed a significantly lower gut involvement in mice receiving PE, with a decrease in proinflammatory cytokines (IL-2, IL-17, and TNF-α) in serum and the reestablishment of butyrate concentration in the gut. In conclusion, PE obtained from EVOO exerted a potent immunomodulatory effect, reducing the activation and proliferation of activated T cells and the production of proinflammatory cytokines. In a murine model of acute GVHD, a PE-supplemented diet reduced the incidence and severity of the disease and increased survival after transplantation.

The hallmark of rheumatoid arthritis (RA) pathology is characterized by both hyperproliferation of synovial fibroblasts (SFs) and massive infiltration of inflammatory immune cells. This study was conducted to evaluate the efficacy of hydroxytyrosol (HTy) and hydroxytyrosol-acetate (HTy-Ac) in regulating IL-1β-induced production of metalloproteases (MMPs) and proinflammatory cytokines in human synovial cell line. Treatment with HTy or HTy-Ac significantly inhibited IL-1β-induced MMPs, tumour necrosis factor (TNF)-α and IL-6 production. IL-1β-up regulation COX-2 and mPGE-1 was downregulated by HTy and HTy-Ac. IL-1β-induced MAPKs phosphorylation and NF-κB activation were inhibited by HTy and HTy-Ac. These results suggest that these EVOO phenols reduce the production of proinflammatory mediators in SW982 cells; these protective effects could be related to the inhibition of MAPKs and NF-κB signalling pathways. Thus, HTy and HTy-Ac might be promising targets for the prevention and management of diseases associated with overactivation of synovial fibroblasts, like RA.

Current epidemiological and experimental studies support a beneficial role of dietary polyphenols in several gastrointestinal diseases, including inflammatory bowel disease. The aim of this study was to gain a better understanding of the effects of a naturally occurring polyphenol, ellagic acid, present in some fruits such as pomegranate, raspberries and nuts among others, in an experimental murine model of Crohn's disease by intra-colonic administration of TNBS in rats. Analysis of the lesions were carried out by macroscopic and histological technics. Inflammation response was assessed by histology and myeloperoxidase activity. iNOS and COX-2 are upregulated by MAPKs and NF-κB nuclear transcription factor in intestinal epithelial cells thus, we determined the expression of iNOS, COX-2 and the involvement of the p38, JNK, ERK1/2 MAPKs and NF-κB signalling in the protective effect of EA by western blotting. Oral administration of EA (10–20 mg/kg) diminished the severity and extension of the intestinal injuries induced by TNBS although there was no observed a significant dose–response. In addition, EA increased mucus production in goblet cells in colon mucosa, decreased neutrophil infiltration and pro-inflammatory proteins COX-2 and iNOS overexpression. Also EA was capable of reducing the activation of p38, JNK and ERK1/2 MAPKs, preventing the inhibitory protein IκB-degradation and inducing an inhibition of the nuclear translocation level of p65 in colonic mucosa. In conclusion, EA reduces the damage in a rat model of Crohn's disease, alleviates the oxidative events and returns pro-inflammatory proteins expression to basal levels probably through MAPKs and NF-κB signalling pathways. Junta de Andalucía y Ministerio de Ciencia e Innovación de España AGL 2008-02475

7 páginas, 5 figuras, 1 tabla., In the search of new therapeutic targets improving the quality of life of elderly, melatonin, “the chemical expression of darkness”, seems to play a remarkable role in aging process possibly due to its antioxidant, immunoenhancer and anti-aging properties. The present study was designed to elucidate effects of aging in melatonin extrapineal synthesis and investigate evident age-related alterations in the action mechanisms involved. The presence of the two key enzymes involved in melatonin synthesis, arylalkylamine-N-acetyltransferase (AA-NAT) and hydroxyindole-O-methyltransferase (HIOMT) was analyzed in thymus, spleen, liver, kidney and heart of 3- and 12 month-old rats using real time PCR as well as its functionality by enzymatic activity assays. In addition, extrapineal melatonin content was measured by a competitive enzyme immunoassay (ELISA). The results of this study reveal that all rat tissues studied including thymus, and for the first time, spleen, liver, kidney and heart have the necessary machinery to synthesize melatonin. Moreover, we report an age-related decline in rat extrapineal melatonin synthesis with a consequent HIOMT functionality decrease in spleen, liver and heart during physiological aging. On the contrary, NAT enzymatic activity maintains unchanged without evident alterations with advancing age. Moreover, diminished melatonin concentrations were measured in these tissues cited above during aging except in the thymus, where, surprisingly, melatonin content, NAT/HIOMT expression, and enzymatic functionality assays revealed no significant alterations with age. As a conclusion, we report evident age-related changes in melatonin synthesis in some rat peripheral organs. We suggest that thymus may develop compensatory mechanisms to counteract the loss of immune activity and consequently, the loss of this potent antioxidant, during physiological aging., This work was supported by grants of the Andalucía (P06-CTS-1604) and Spanish (PI 060091; RD06/00130001) governments. MSH gratefully acknowledges support from a Postgraduate National Program of FPU fellowship and financial sponsorship from the Spanish MEC.