1,750 research outputs found
New evidences for C-reactive protein (CRP) deposits in the arterial intima as a cardiovascular risk factor
Fabrizio Montecucco, François MachDivision of Cardiology, Foundation for Medical Research, University Hospital, Geneva, SwitzerlandAbstract: Inflammatory processes are orchestrated by several soluble molecules, which interact with cell populations involved. Cytokines, chemokines, acute-phase reactants, and hormones are crucial in the evolution of several inflammatory disorders, such as atherosclerosis. Several evidences suggest that C-reactive protein (CRP) started to be considered as a cardiovascular risk factor, since CRP directly induces atheroslerosis development. The recent demonstration of CRP production not only by the liver, but also within atherosclerotic plaques by activated vascular cells, also suggests a possible dual role, as both a systemic and tissue agent. Although more studies are needed, some therapeutic approaches to reduce CRP levels have been performed with encouraging results. However, given the strong limitations represented by its low specificity and still accordingly with the American Heart Association, there is no need for high sensitivity CRP screening of the entire adult population as a public-health measure. The measure of serum CRP might be useful only for patients who are considered at intermediate risk.Keywords: atherosclerosis, inflammation, plaque, cardiovascular risk, C-reactive protei
Inflammation and pericarditis: Are neutrophils actors behind the scenes?
The morbidity of acute pericarditis is increasing over time impacting on patient quality of life. Recent clinical trials focused especially on clinical aspects, with a modest interest in pathophysiological mechanisms. This narrative review, based on papers in English language obtained via PubMed up to April 2018, aims at focusing on the role of the innate immunity in pericarditis and discussing future potential therapeutic strategies impacting on disease pathophysiology. In developed countries, most cases of pericarditis are referred to as idiopathic, although etiological causes have been described, with autoreactive/lymphocytic, malignant, and infectious ones as the most frequent causes. Apart the known impairment of the adaptive immunity, recently a large body evidence indicated the central role of the innate immune system in the pathogenesis of recurrent pericarditis, starting from similarities with autoinflammatory diseases. Accordingly, the "inflammasome" has been shown to behave as an important player in pericarditis development. Similarly, the beneficial effect of colchicine in recurrent pericarditis confirms that neutrophils are important effectors as colchicine, which can block neutrophil chemotaxis, interferes with neutrophil adhesion and recruitment to injured tissues and abrogate superoxide production. Anyway, the role of the adaptive immune system in pericarditis cannot be reduced to a black or white issue as mechanisms often overlap. Therefore, we believe that more efficient therapeutic strategies have to be investigated by targeting neutrophil-derived mediators (such as metalloproteinases) and disentangling the strict interplay between neutrophils and platelets. In this view, some progress has been done by using the recombinant human interleukin-1 receptor antagonist anakinra
Big data and data sharing: Opportunities for the urgent challenges in cardiovascular disease
The past half-century has witnessed unbelievable progress in cardiovascular (CV) medicine, determining a swirling reduction in mortality. Despite this progress, the decline in incidence and mortality leveled off in recent years. Age-adjusted CV mortality remained flat independently of race and ethnicity, with only few exceptions. In other words, disparity in CV health is still observed across sex, race and ethnicity. The rise of obesity, diabetes and other risk factors has been widely used to explain this trend in CV mortality
Steroid-induced hyperglycemia: An underdiagnosed problem or clinical inertia? A narrative review
Corticosteroids are widely diffused drugs. An important side effect is the impairment of glycemic control both in patients with known diabetes and in normoglycemic ones potentially leading to steroid-induced diabetes mellitus (SIDM). In this review based on papers released on PubMed, MEDLINE, and EMBASE from January 2015 to October 2017, we summarized and discussed main updates about the definition, the diagnosis, and the pathophysiology of steroid-induced hyperglycemia (SIH), with a look to new therapies. Main alterations responsible for the diabetogenic effect of corticosteroids are a negative impact on insulin sensitivity along with a derangement on insulin secretion, explaining the typical post-prandial hyperglycemia linked to the promotion of gluconeogenesis. An early and precise diagnosis of SIH and/or SIDM is necessary, but current criteria do not seem sensible enough. As an afterthought, the treatment should be reasoned and tailored according to proposed glycemic thresholds and patient comorbidities, choosing between antidiabetic oral drugs and insulin, the latter being preferable among hospitalized patients. SIDM and SIH are frequent problems, but often underdiagnosed due to old diagnostic criteria. Dedicated guidelines universally shared are mandatory in order to harmonize the treatment of these conditions, thus overtaking single therapeutic strategies mostly arising from literature
How to manage the abundant COVID‐19 submissions to a peer‐reviewed Scientific Journal
In January 2020, both authors became Editors of the peer-reviewed European Journal of Clinical Investigation (EJCI). After one year, we feel it is time for a first balance of our activities. The COVID-19 pandemic deeply impacted not only on the editorial work, but also in all our professional and private lives. As Medical Doctors, every day we were involved in patients' care during this pandemic. As new Scientific Editors, we not only received a huge amount of COVID-19-related submissions (N=195), but also non-COVID-19 submissions increased tremendously (N=1101)
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