This review identifies the emerging evidence to support policy for the management of people with multimorbidity and common comorbidities in primary care and community settings. There are remaining uncertainties about the effectiveness of interventions for people with multimorbidity in general due to the relatively small number of RCTs conducted in this area to date, with mixed findings overall. It is possible that the findings may change with the inclusion of large ongoing well-organised trials in future updates. The results suggest an improvement in health outcomes if interventions can be targeted at risk factors such as depression, or specific functional difficulties in people with multimorbidity.
BackgroundMultimorbidity affects up to one quarter of primary care populations. It is associated with reduced quality of life, an increased risk of mental health difficulties and increased healthcare utilisation. Functional decline is defined as developing difficulties with activities of daily living and is independently associated with poorer health outcomes. The aim of this systematic review was to examine the association between multimorbidity and functional decline and to what extent multimorbidity predicts future functional decline.MethodsA systematic literature search (1990-2014) and narrative analysis was conducted. Inclusion criteria: Population; Community-dwelling adults (≥18 years), Risk; Multimorbidity defined as the presence of ≥2 chronic medical conditions in an individual, Primary outcome; Physical functional decline measured using a validated instrument, Study design; cross-sectional or cohort studies. The following databases were included: PubMed, EMBASE, CINAHL, the Cochrane Library and the International Research Community on Multimorbidity (IRCMo) publication list. Methodological quality assessment of included studies was conducted with a suitable risk of bias tool.ResultsA total of 37 studies were eligible for inclusion (28 cross-sectional studies and 9 cohort studies). The majority of cross-sectional studies (n = 24/28) demonstrated a consistent association between multimorbidity and functional decline. Twelve of these studies reported that increasing numbers of chronic condition counts were associated with worsening functional decline. Nine cohort studies included 14,133 study participants with follow-up periods ranging from one to six years. The majority (n = 5) found that multimorbidity predicted functional decline. Of the five studies that reported the impact of increasing numbers of conditions, all reported greater functional decline with increasing numbers of conditions. One study examined disease severity and found that this also predicted greater functional decline. Overall, cohort studies were of good methodological quality but were mixed in terms of participants, multimorbidity definitions, follow-up duration, and outcome measures.ConclusionsThe available evidence indicates that multimorbidity predicts future functional decline, with greater decline in patients with higher numbers of conditions and greater disease severity. This review highlights the importance of considering physical functioning when designing interventions and systems of care for patients with multimorbidity, particularly for patients with higher numbers of conditions and greater disease severity.Electronic supplementary materialThe online version of this article (doi:10.1186/s12955-015-0355-9) contains supplementary material, which is available to authorized users.
Background-Pulmonary arterial hypertension (PAH) is a hyperproliferative vascular disorder observed predominantly in women. Estrogen is a potent mitogen in human pulmonary artery smooth muscle cells and contributes to PAH in vivo; however, the mechanisms attributed to this causation remain obscure. Curiously, heightened expression of the estrogenmetabolizing enzyme cytochrome P450 1B1 (CYP1B1) is reported in idiopathic PAH and murine models of PAH. Methods and Results-Here, we investigated the putative pathogenic role of CYP1B1 in PAH. Quantitative reverse transcriptionpolymerase chain reaction, immunoblotting, and in situ analysis revealed that pulmonary CYP1B1 is increased in hypoxic PAH, hypoxicϩSU5416 PAH, and human PAH and is highly expressed within the pulmonary vascular wall. PAH was assessed in mice via measurement of right ventricular hypertrophy, pulmonary vascular remodeling, and right ventricular systolic pressure. Hypoxic PAH was attenuated in CYP1B1 Ϫ/Ϫ mice, and the potent CYP1B1 inhibitor 2,3Ј,4,5Ј-tetramethoxystilbene (TMS; 3 mg ⅐ kg Ϫ1 ⅐ d
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