Volta U.,University of Bologna |
Villanacci V.,Spedali Civili
Cellular and Molecular Immunology | Year: 2011
Until a few years ago, celiac disease (CD) was thought to be a rare food intolerance that was confined to childhood and characterized by severe malabsorption and flat intestinal mucosa. Currently, CD is regarded as an autoimmune disorder that is common in the general population (affecting 1 in 100 individuals), with possible onset at any age and with many possible presentations. The identification of CD is challenging because it can begin not only with diarrhea and weight loss but also with atypical gastrointestinal (constipation and recurrent abdominal pain) and extra-intestinal symptoms (anemia, raised transaminases, osteoporosis, recurrent miscarriages, aphthous stomatitis and associated autoimmune disorders), or it could be completely symptomless. Over the last 20 years, the diagnostic accuracy of serology for CD has progressively increased with the development of highly reliable tests, such as the detection of IgA tissue transglutaminase and antiendomysial and IgG antideamidated gliadin peptide antibodies. The routine use of antibody markers has allowed researchers to discover a very high number of borderline cases, characterized by positive serology and mild intestinal lesions or normal small intestine architecture, which can be classified as potential CD. Therefore, it is evident that the old celiac disease with flat mucosa is only a part of the spectrum of CD. It is possible that serology could identify CD in its early stages, before the appearance of severe intestinal damage. In cases with a positive serology but with mild or absent intestinal lesions, the detection of HLA-DQ2 and HLA-DQ8 can help reinforce or exclude the diagnosis of gluten sensitivity. © 2011 CSI and USTC. All rights reserved.
Clini E.,University of Modena and Reggio Emilia |
Crisafulli E.,Ospedale Villa Pineta |
Radaeli A.,Spedali Civili |
Malerba M.,University of Brescia
Internal and Emergency Medicine | Year: 2013
Chronic Obstructive Pulmonary Disease (COPD) has been recently recognized as a condition involving more than the lungs. The presence of common factors in COPD and in other chronic extra-pulmonary diseases, as well as the co-existence of these conditions in the same adult individual, supports the hypothesis of a shared pathogenetic pathway. We will here review the interplay between coexisting COPD and the metabolic syndrome (MS), based on the most updated knowledge. We will discuss this clinical condition from the definition, to the pathophysiology and to the clinical implications. Basically, MS is more likely to be present in a COPD patients, and increased levels of circulatory pro-inflammatory proteins from both the lung and adipose tissue coincide in these patients. The relative impact of the coexisting COPD and MS may depend on several factors: the presence of physical inactivity and of systemic inflammation related to a smoking habit, sedentary lifestyle, airway inflammation and obstruction, adipose tissue and inflammatory marker activation. More studies will be required to elucidate the association between COPD and MS and to formulate individualized management approaches for this specific disease phenotype. © 2011 SIMI.
Cioffi G.,Villa Bianca Hospital |
Tarantini L.,Ospedale Civile S. Martino |
Faggiano P.,Spedali Civili
IJC Metabolic and Endocrine | Year: 2014
Hypothesis: Type 2 diabetes mellitus (T2DM) and chronic heart failure (CHF) are associated with renal dysfunction. We tested the hypothesis that the degree of renal dysfunction influences the negative impact on the outcome of T2DM in patients with CHF and reduced left ventricular ejection fraction (LVEF). Methods: From November 1, 2009 to December 31, 2012, the "Trieste Registry of CV Diseases" enrolled 19,589 patients. Those with diagnosis of CHF and reduced LVEF were analyzed. The primary end-point was all-cause mortality. Results: 554 patients were selected (73±10years old, 32% females), 192 had T2DM (35%). During follow-up (23±11months), all-cause death occurred in 57 patients (30%) who had T2DM and in 58 (16%, p<0.001) who had not; T2DM was associated with an increased risk of death (adjusted HR 2.55 [95% CI 1.02-6.36], p=0.04). The prognostic impact of T2DM was lost when patients were selected according to renal function: adjusted HR 1.44 [0.21-9.93], p=0.71, in patients with normal renal function, defined as estimated glomerular filtration rate (eGFR) >60, and adjusted HR 3.37 [0.96-11.80], p=0.08 in patients with renal dysfunction (eGFR<60ml/min*1.73m2). T2DM predicted all-cause mortality only in the subgroup with eGFR between 90 and 30ml/min*1.73m2 (adjusted HR 2.52 [1.01-6.30], p=0.04). Conclusions: In patients with CHF and reduced LVEF the prognostic impact of T2DM depends on the degree of renal dysfunction. Its contribution in all-cause mortality risk prediction is limited to mild-moderate renal dysfunction subgroup, while prognostic power is lost in normal renal function and in severe renal dysfunction patients. © 2014 The Authors.
Agabiti-Rosei E.,Spedali Civili |
Grassi G.,Clinica Medica
Current Medical Research and Opinion | Year: 2013
Objectives: This article discusses the results of clinical and experimental studies that examine the association of hyperuricemia and gout with cardiovascular (CV) disease. Methods: Key papers for inclusion were identified by a PubMed search, and articles were selected for their relevance to the topic, according to the authors' judgment. Results and conclusions: Significant progress has been made in confirming an association, possibly causal, between hyperuricemia and CV outcomes. Xantine-oxidase (XO) inhibitors appear to be the most promising agents for prevention and treatment of CV consequences associated with hyperuricemia. Several small and medium sized studies have examined the effect of these agents on CV function in a variety of patient populations. Improvements in measures of endothelial function, oxidative stress, cardiac function, hemodynamics, and certain inflammatory indices have been demonstrated. Compounds for XO inhibition with more specific clinical effects and fewer side effects than allopurinol may be promising options to further explore the therapeutic potential in patients with CV disease. It is too early to make clinical recommendations with regard to the benefits of using XO inhibitor allopurinol or the novel febuxostat in patients with asymptomatic increased UA levels and high CV risk because only a small number of studies have shown that they may be beneficial in terms of CV outcomes. More studies are therefore needed to determine the potential of these drugs for reducing the risk of developing CV disease. © 2013 Informa UK Ltd.
Oliva F.,Cardiologia 2 Heart Failure and Heart Transplant Program |
Oliva F.,Outcome Coordinating Center |
Mortara A.,Policlinico di Monza |
Cacciatore G.,San Giovanni Addolorata Hospital |
And 7 more authors.
European Journal of Heart Failure | Year: 2012
Aims Registries and surveys improve knowledge of the 'real world'. This paper Aims to describe baseline clinical profiles, management strategies, and the in-hospital outcome of patients admitted to hospital for an acute heart failure (AHF) episode.Methods and resultsIN-HF Outcome is a nationwide, prospective, multicentre, observational study conducted in 61 Cardiology Centres in Italy. Up to December 2009, 5610 patients had been enrolled, 1855 (33) with AHF and 3755 (67) with chronic heart failure (CHF). Baseline and in-hospital outcome data of AHF patients are presented. Mean age was 72 ± 12 years, and 39.8 were female. Hospital admission was due to new-onset heart failure (HF) in 43 of cases. Co-morbid conditions were observed more frequently in the worsening HF group, while those with de novo HF showed a higher heart rate, blood pressure, and more preserved left ventricular ejection fraction (LVEF). Electrical devices were previously implanted in 13.3 of the entire group. Inotropes were administered in 19.4 of the patients. The median duration of hospital stay was 10 days (interquartile range 7-15). All-cause in-hospital death was 6.4, similar in worsening and de novo HF. Older age, hypotension, cardiogenic shock, pulmonary oedema, symptoms of hypoperfusion, hyponatraemia, and elevated creatinine were independent predictors of all-cause death.ConclusionOur registry confirms that in-hospital mortality in AHF is still high, with a long length of stay. Pharmacological treatment seems to be practically unchanged in the last decades, and the adherence to HF guidelines concerning implantable cardioverter defibrillators/cardiac resynchronization therapy is still very low. Some AHF phenotypes are characterized by worst prognosis and need specific research projects. © 2012 The Author.