Fidenza Hospital

Fidenza, Italy

Fidenza Hospital

Fidenza, Italy
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Osti L.,Hesperia Hospital | Buda M.,University of Ferrara | Del Buono A.,Fidenza Hospital | Osti R.,University of Ferrara | And 3 more authors.
British Medical Bulletin | Year: 2017

Introduction Excessive apoptosis has been hypothesized as possible cause of tendinopathy and tear in the tendons of the rotator cuff (RC). Different mechanisms and molecules play a key role in cell regulation. Biological interventions can affect the process of apoptosis to control the tendinopathy process, and may be useful to design new treatments. Source of data We identified basic science, in vitro and in vivo preclinical and clinical studies listed in the Pubmed Google Scholar, CINAHL, Cochrane Central and Embase Biomedical databases in English, Spanish, Italian and French concerning the effects of apoptosis on RC tendons. Areas of agreement The homeostasis between the apoptotic and inflammatory processes is dynamic and controlled by pro- and anti-apoptotic mechanisms and signals, with variable balance in different areas of the RC tendons in human specimens. Areas of controversy Apoptosis can be identified along the whole tendon, not only in the area of the lesion. Therefore, it is not necessary to undertake wide debridement of the torn edges of the tendon when undertaking a repair. Growing points The identification of the various factors that control apoptosis and its mechanisms can help to design new treatments and exert positive effects in the recovery from tendon tears. Areas timely for developing research Further studies are needed to produce clear guidelines to determine how to balance the apoptosis process to reduce the failed healing response found in non-traumatic RC tears. © The Author 2017. Published by Oxford University Press.


Maffulli N.,University of Salerno | Maffulli N.,Mile End Hospital | Del Buono A.,Fidenza Hospital | Oliva F.,University of Rome Tor Vergata
Muscles, Ligaments and Tendons Journal | Year: 2017

Background: Patellar tendon chronic ruptures are more debated to manage that acute injuries as the patella tends to retract proximally (after 2 weeks), and surrounding soft tissues may make the repair more complicate. Purpose: We propose a novel technique in which the patellar tendon is reconstructed using ipsilateral hamstring tendons. This surgical procedure implies to drill a single tunnel through the patella and another through the tibia to reduce the risk of bony breakage. In addition, the tendon is secured to the bone, at the tunnel exit points, by periostium sutures without requiring any additional surgery for hardware removal. Methods: We assessed 19 patients (16 men and 3 women) who underwent PT reconstruction at an average of 5.8 years (range, 4 to 7.8 years, SD: 3.5) from the index surgery. The mean age at surgery was 46 ± 9.2 years (range, 38-59 years). Results: All patients had a complete tear of the patellar tendon. Conclusions: The main indication for this procedure is the reconstruction of the PT in patients with chronic rupture (>6 weeks) in which the tendon gap is greater than 2 centimeters and the scar tissues and degenerated tendon ends do not allow to juxtapose the tendon stumps to each other. Level of evidence: Level IV. © 2017, CIC Edizioni Internazionali s.r.l. All rights reserved.


Spyropoulos A.C.,Hamilton Health Sciences | Anderson Jr. F.A.,University of Massachusetts Medical School | FitzGerald G.,University of Massachusetts Medical School | Decousus H.,Jean Monnet University | And 14 more authors.
Chest | Year: 2011

Background: Acutely ill hospitalized medical patients are at risk for VTE. We assessed the incidence of VTE in the observational International Medical Prevention Registry on Venous Thromboembolism (IMPROVE) study and derived VTE risk assessment scores at admission and associative VTE scores during hospitalization. Methods: Data from 15,156 medical patients were analyzed to determine the cumulative incidence of clinically observed VTE over 3 months after admission. Multiple regression analysis identified factors associated with VTE risk. Results: Of the 184 patients who developed symptomatic VTE, 76 had pulmonary embolism, and 67 had lower-extremity DVT. Cumulative VTE incidence was 1.0%; 45% of events occurred after discharge. Factors independently associated with VTE were previous VTE, known thrombophilia, cancer, age > 60 years, lower-limb paralysis, immobilization ≥ 7 days, and admission to an ICU or coronary care unit (first four were available at admission). Points were assigned to each factor identified to give a total risk score for each patient. At admission, 67% of patients had a score ≥ 1. During hospitalization, 31% had a score ≥ 2; for a score of 2 or 3, observed VTE risk was 1.5% vs 5.7% for a score ≥ 4. Observed and predicted rates were similar for both models (C statistic, 0.65 and 0.69, respectively). During hospitalization, a score ≥ 2 was associated with higher overall and VTE-related mortality. Conclusions: Weighted VTE risk scores derived from four clinical risk factors at hospital admission can predict VTE risk in acutely ill hospitalized medical patients. Scores derived from seven clinical factors during hospitalization may help us to further understand symptomatic VTE risk. These scores require external validation. © 2011 American College of Chest Physicians.


Decousus H.,French Institute of Health and Medical Research | Tapson V.F.,Duke University | Bergmann J.-F.,University Paris Diderot | Chong B.H.,University of New South Wales | And 14 more authors.
Chest | Year: 2011

Background: Acutely ill, hospitalized medical patients are at risk of VTE. Despite guidelines for VTE prevention, prophylaxis use in these patients is still poor, possibly because of fear of bleeding risk. We used data from the International Medical Prevention Registry on Venous Thromboembolism (IMPROVE) to assess in-hospital bleeding incidence and to identify risk factors at admission associated with in-hospital bleeding risk in acutely ill medical patients. Methods: IMPROVE is a multinational, observational study that enrolled 15,156 medical patients. The in-hospital bleeding incidence was estimated by Kaplan-Meier analysis. A multiple regression model analysis was performed to identify risk factors at admission associated with bleeding. Results: The cumulative incidence of major and nonmajor in-hospital bleeding within 14 days of admission was 3.2%. Active gastroduodenal ulcer (OR, 4.15; 95% CI, 2.21-7.77), prior bleeding (OR, 3.64; 95% CI, 2.21-5.99), and low platelet count (OR, 3.37; 95% CI, 1.84-6.18) were the strongest independent risk factors at admission for bleeding. Other bleeding risk factors were increased age, hepatic or renal failure, ICU stay, central venous catheter, rheumatic disease, cancer, and male sex. Using these bleeding risk factors, a risk score was developed to estimate bleeding risk. Conclusions: We assessed the incidence of major and clinically relevant bleeding in a large population of hospitalized medical patients and identified risk factors at admission associated with in-hospital bleeding. This information may assist physicians in deciding whether to use mechanical or pharmacologic VTE prophylaxis. © 2011 American College of Chest Physicians.


PubMed | Mario Negri Sud Foundation, University of Chieti Pescara, Fidenza Hospital, Santonio Abate Hospital and 19 more.
Type: Comparative Study | Journal: Brain : a journal of neurology | Year: 2015

The comparative effectiveness of fingolimod versus interferon beta/glatiramer acetate was assessed in a multicentre, observational, prospectively acquired cohort study including 613 patients with relapsing multiple sclerosis discontinuing natalizumab in the Italian iMedWeb registry. First, after natalizumab suspension, the relapse risk during the untreated wash-out period and during the course of switch therapies was estimated through Poisson regression analyses in separated models. During the wash-out period an increased risk of relapses was found in patients with a higher number of relapses before natalizumab treatment (incidence rate ratio = 1.31, P = 0.0014) and in patients discontinuing natalizumab due to lack of efficacy (incidence rate ratio = 2.33, P = 0.0288), patients choice (incidence rate ratio = 2.18, P = 0.0064) and adverse events (incidence rate ratio = 2.09, P = 0.0084). The strongest independent factors influencing the relapse risk after the start of switch therapies were a wash-out duration longer than 3 months (incidence rate ratio = 1.78, P < 0.0001), the number of relapses experienced during and before natalizumab treatment (incidence rate ratio = 1.61, P < 0.0001; incidence rate ratio = 1.13, P = 0.0118, respectively) and the presence of comorbidities (incidence rate ratio = 1.4, P = 0.0097). Switching to fingolimod was associated with a 64% reduction of the adjusted-risk for relapse in comparison with switching to interferon beta/glatiramer acetate (incidence rate ratio = 0.36, P < 0.0001). Secondly, patients who switched to fingolimod or to interferon beta/glatiramer acetate were propensity score-matched on a 1-to-1 basis at the switching date. In the propensity score-matched sample a Poisson model showed a significant lower incidence of relapses in patients treated with fingolimod in comparison with those treated with interferon beta/glatiramer acetate (incidence rate ratio = 0.52, P = 0.0003) during a 12-month follow-up. The cumulative probability of a first relapse after the treatment switch was significantly lower in patients receiving fingolimod than in those receiving interferon beta/glatiramer acetate (P = 0.028). The robustness of this result was also confirmed by sensitivity analyses in subgroups with different wash-out durations (less or more than 3 months). Time to 3-month confirmed disability progression was not significantly different between the two groups (Hazard ratio = 0.58; P = 0.1931). Our results indicate a superiority of fingolimod in comparison to interferon beta/glatiramer acetate in controlling disease reactivation after natalizumab discontinuation in the real life setting.


Corradi D.,University of Parma | Callegari S.,Fidenza Hospital | Gelsomino S.,Careggi Hospital | Lorusso R.,Community Hospital | Macchi E.,University of Parma
International Journal of Cardiology | Year: 2013

Experimental and clinical evidence suggests that the natural history of atrial fibrillation is characterised by increased structural remodelling, which may play a pivotal role in maintaining the arrhythmia and clinically favours progression from paroxysmal to persistent atrial fibrillation. In this setting, anti-arrhythmic therapy gradually becomes inefficient, and this limitation has led to the introduction of new non-pharmacological interventions such as surgical or catheter ablation. At the same time, interest in the functional morphology and electrophysiological properties of the atria and their related anatomical structures has greatly increased. This article is the first of a two-part review whose main purpose is to describe the anatomical and functional details of some of the principal anatomical locations that are commonly targeted by ablative procedures to treat this supraventricular arrhythmia. In particular, this manuscript has dealt with the atrial structures (atrial myocardium and coronary sinus). General information on ablation procedures has also been provided. © 2013 Elsevier Ireland Ltd. All rights reserved.


Corradi D.,University of Parma | Callegari S.,Fidenza Hospital | Gelsomino S.,Careggi Hospital | Lorusso R.,Community Hospital | Macchi E.,University of Parma
International Journal of Cardiology | Year: 2013

The inadequate long-term efficacy of anti-arrhythmic therapy has been one of the main reasons for the development of non-pharmacological interventions for patients with atrial fibrillation such as catheter and surgical ablation. This has greatly increased interest in the functional morphology and electrophysiological properties of the atria and related anatomical structures. This article is the second of a two-part review that aims to provide anatomical and functional details concerning some of the principal anatomical sites commonly targeted by ablative procedures for treating atrial fibrillation, and covers pulmonary veins, ganglionated plexi, caval veins, and the ligament of Marshall. It also provides some general information about site-specific ablation procedures. © 2013 Elsevier Ireland Ltd. All rights reserved.


Benecchi L.,Fidenza Hospital | Pieri A.M.,Fidenza Hospital | Destro Pastizzaro C.,Fidenza Hospital | Potenzoni M.,Fidenza Hospital
Journal of Urology | Year: 2011

Purpose Prostate specific antigen acceleration can be calculated as the slope of log prostate specific antigen vs time, where log is the natural logarithm. We determined the best interval in which prostate specific antigen acceleration can be calculated with the best result in terms of specificity and sensitivity for prostate cancer diagnosis. Materials and Methods Entered in the study were 741 men who underwent transrectal ultrasound guided prostate biopsy with 12 or more cores and at least 3 prior consecutive prostate specific antigen measurements in at least 365 days. Prostate specific antigen acceleration was calculated as the slope of log prostate specific antigen vs time using a minimum of 3 prostate specific antigen measurements. Acceleration was evaluated at different intervals, including within 1 year (365 days), 2 years (730 days), 3 years (1,095 days), 4 years (1,460 days), 5 years (1,825 days) and 6 years (2,190 days) before the last measurement. Results A total of 255 cancers (34.4%) were found. On ROC analysis the AUC of prostate specific antigen acceleration (0.728, 95% CI 0.694-0.760) was better than that of prostate specific antigen, prostate specific antigen velocity and prostate specific antigen doubling time. The highest AUC of prostate specific antigen kinetics was for prostate specific antigen acceleration calculated within 3 to 4 years (731 to 1,460 days) before the last measurement. Conclusions Three or more prostate specific antigen measurements within 3 to 4 years (731 to 1,460 days) before the last measurement enabled more accurate calculation of prostate specific antigen acceleration than measurement within 1 to 2 years (0 to 730 days). © 2011 American Urological Association Education and Research, Inc.


Corradi D.,University of Parma | Maestri R.,University of Parma | MacChi E.,University of Parma | Callegari S.,Fidenza Hospital
Journal of Cardiovascular Electrophysiology | Year: 2011

Functional Anatomy of the Atria. The fact that some atrial and ventricular disorders (e.g., atrial fibrillation and heart failure) have a structural basis and cause atrial myocardial remodeling has led to increasing attention being paid to the atrial chambers. Furthermore, the rapid development of mapping and ablative procedures as a means of diagnosing and treating supraventricular arrhythmias has generated considerable interest in atrial gross anatomy, histology and ultrastructure. The aim of this article is to provide a comprehensive overview of the structure of the left and right atria (at macroscopic, histological and ultrastructural level) in relation to their function. In addition to analyzing normal atria, we also discuss functional anatomy in the case of atrial fibrillation and heart failure. © 2010 Wiley Periodicals, Inc.


Ianni M.,University of Bologna | Porcellini E.,University of Bologna | Carbone I.,University of Bologna | Potenzoni M.,Fidenza Hospital | And 4 more authors.
Prostate Cancer and Prostatic Diseases | Year: 2013

Background:Prostate cancer (PCa) displays a strong familiarity component and genetic factors; genes regulating inflammation may have a pivotal role in the disease. Epigenetic changes control chromosomal integrity, gene functions and ultimately carcinogenesis. The enzyme glycine-N-methyltransferase (GNMT) contributes to S-adenosylmethionine level regulation and, by affecting DNA methylation, influences gene expression. The genotype and allele distribution of single-nucleotide polymorphisms (SNPs) in the promoter regions of vascular endothelial growth factor (VEGF), interleukin (IL)-10, IL-1β, alpha-1-antichymotrypsin (ACT) and GNMT genes, the level of global DNA methylation and the influence of GNMT SNP upon DNA methylation in a PCa case-control study have been investigated.Methods:SNPs of VEGF (rs699947), ACT (rs1884082), IL-1β (rs16944), IL-10 (rs1800896) and GNMT (rs9462856) genes were assessed by PCR or by real-time PCR methods. DNA methylation was assessed by an ELISA assay.Results:Frequencies of the VEGF AA genotype, the IL-10 A allele and GNMT T allele were higher in PCa. The concomitant presence of the AA genotype of VEGF, the A allele of IL-10 and T allele of GNMT increased the risk of PCa. Total DNA methylation was decreased in PCa; control GNMT T carriers (T+) showed the highest level of DNA methylation.Conclusions:SNPs in VEGF, IL-10 and GNMT genes might have a synergistic role in the development of PCa. The GNMT T allele may influence PCa risk by affecting DNA methylation and prostate gene expression. Our observations might help implement the screening of unaffected subjects with an increased susceptibility to develop PCa. © 2013 Macmillan Publishers Limited. All rights reserved.

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