Molinette Hospital

Sant'Ambrogio di Torino, Italy

Molinette Hospital

Sant'Ambrogio di Torino, Italy
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Ghigo A.,University of Turin | Franco I.,University of Turin | Morello F.,Molinette Hospital | Hirsch E.,University of Turin
Cardiovascular Research | Year: 2014

Myocardial damage, by different noxious causes, triggers an inflammatory reaction driving post-injury repair mechanisms and chronic remodelling processes that are largely detrimental to cardiac function. Cardiomyocytes have recently emerged as key players in orchestrating this inflammatory response. Injured cardiomyocytes release damage-associated molecular pattern molecules, such as high-mobility group box 1 (HMGB1), DNA fragments, heat shock proteins, and matricellular proteins, which instruct surrounding healthy cadiomyocytes to produce inflammatory mediators. These mediators, mainly interleukin (IL)-1β, IL-6, macrophage chemoattractant protein (MCP)-1, and tumour necrosis factor α (TNF-α), in turn activate versatile signalling networks within surviving cardiomyocytes and trigger leucocyte activation and recruitment. In this review, we will focus on recently characterized signalling pathways activated in cardiomyocytes that mediate inflammatory responses during myocardial infarction, hypertensive heart disease, and myocarditis. © The Author 2014.

Pellicano R.,Molinette Hospital | De Angelis C.,Molinette Hospital | Ribaldone D.G.,Molinette Hospital | Fagoonee S.,University of Turin | Astegiano M.,Molinette Hospital
Nutrients | Year: 2013

Celiac disease is a chronic, immune-mediated disorder, characterized by small intestinal inflammation and villous atrophy after the ingestion of gluten by genetically susceptible individuals. Several extraintestinal manifestations have been associated to celiac disease. Eosinophilic esophagitis is a primary disorder of the esophagus characterized by upper gastrointestinal symptoms, absence of gastroesophageal reflux disease and more than 15 eosinophils per high-power field in biopsy specimens. Both celiac disease and eosinophilic esophagitis are caused by aberrant, but distinct, immune responses to ingested antigens and can be responsive to restricted food intake. The aim of this review is to assess whether there is an association between these two pathologies. In the majority of the studies examined, including the studies in pediatric population, the prevalence of eosinophilic esophagitis in subjects with celiac disease was about 10-times that of the general population. We suggest searching for eosinophilic esophagitis in all children undergoing endoscopy for suspicious celiac disease. © 2013 by the authors; licensee MDPI, Basel, Switzerland.

Valoti E.,Irccs Instituto Of Ricerche Farmacologiche Mario Negri | Alberti M.,Irccs Instituto Of Ricerche Farmacologiche Mario Negri | Tortajada A.,CSIC - Biological Research Center | Garcia-Fernandez J.,CSIC - Biological Research Center | And 6 more authors.
Journal of the American Society of Nephrology | Year: 2015

Genomic aberrations affecting the genes encoding factor H (FH) and the five FH-related proteins (FHRs) have been described in patients with atypical hemolytic uremic syndrome (aHUS), a rare condition characterized by microangiopathic hemolytic anemia, thrombocytopenia, and ARF. These genomic rearrangements occur through nonallelic homologous recombinations caused by the presence of repeated homologous sequences in CFH and CFHR1-R5 genes. In this study, we found heterozygous genomic rearrangements among CFH and CFHR genes in 4.5% of patients with aHUS. CFH/CFHR rearrangements were associated with poor clinical prognosis and high risk of post-transplant recurrence. Five patients carried known CFH/CFHR1 genes, but we found a duplication leading to a novel CFHR1/CFH hybrid gene in a family with two affected subjects. The resulting fusion protein contains the first four short consensus repeats of FHR1 and the terminal short consensus repeat 20 of FH. In an FH-dependent hemolysis assay, we showed that the hybrid protein causes sheep erythrocyte lysis. Functional analysis of the FHR1 fraction purified from serum of heterozygous carriers of the CFHR1/CFH hybrid gene indicated that the FHR1/FH hybrid protein acts as a competitive antagonist of FH. Furthermore, sera from carriers of the hybrid CFHR1/CFH gene induced more C5b-9 deposition on endothelial cells than control serum. These results suggest that this novel genomic hybrid mediates disease pathogenesis through dysregulation of complement at the endothelial cell surface. We recommend that genetic screening of aHUS includes analysis of CFH and CFHR rearrangements, particularly before a kidney transplant. Copyright © 2015 by the American Society of Nephrology.

Lodi G.,University of Milan | Pellicano R.,Molinette Hospital | Carrozzo M.,Northumbria University
Oral Diseases | Year: 2010

Objective: Hepatitis C virus (HCV) is one of the major causes of chronic liver disease worldwide but its morbidity is also due to a variety of extra-hepatic manifestations including mixed cryoglubulinemia, non-Hodgkin lymphoma, diabetes, porphyria cutanea tarda and lichen planus. The aims of this study were to conduct a systematic review and a meta-analysis on the prevalence of HCV in lichen planus patients and on the prevalence of lichen planus in chronic HCV infection. Materials and Method: Bibliographic searches were conducted in several electronic databases. Pooled data were analysed by calculating odds ratios, using a random effects model. Results and Conclusions: Thirty-three studies comparing the seroprevalence of HCV in lichen planus patients and six reporting the prevalence of lichen planus in patients with HCV infection were included in the meta-analysis. The summary estimate showed that LP patients have significantly higher risk (odds ratio 4.85; 95% confidence interval 3.58-6.56) than controls of being HCV seropositive. A similar odds ratio of having lichen planus was found among HCV patients (4.47; 95% confidence interval 1.84-10.86). Sub-analyses indicated that variability of HCVlichen planus association seemed only partially depending on geographic effect. © 2010 John Wiley & Sons AS.

Pellicano R.,Molinette Hospital | Guerra L.,Medical Service
Minerva Medica | Year: 2012

Chronic or acute pain related to skin ulcers or their management (medication, debridement) is a typical case of mixed pain, both neuropathic and nociceptive. It represents a disabling clinical condition that deteriorates the patient's quality of life. The pharmaceutical therapy must be based on both, intensity and the type of pain. Although NSAIDs, Non Steroidal Anti-Inflammatory Drugs are notoriously effective on nociceptive pain, do not give great results on neuropathic and mixed pain. Also the consumption of NSAIDs is affected by a series of side effects that may involve several organs. In case of neuropathic pain, the benefit deriving from the use of a single active principle is relative. This sets the rational grounds for the use of combined drugs. The paracetamol/tramadol combination represents an innovative solution in the treatment of both the neuropathic and nociceptive components of the pain, since both active principles have a different action mechanism, multiple targets and different pharmacokinetics. It is very interesting, from the clinical point of view, that tramadol is a pure antagonist, not selective, of μ, δ, and κ receptors and carries out and important inhibition action of serotonin and norepinephrine reuptake. This double mechanism, opioid and non-opioid, explains its analgesic efficacy also on neuropathic pain. Besides, since its opioid action is rather weak, it does not induce the severe side effects typical of traditional opioids. The benefit of such com bination comes from their complementary pharmacokinetic profile, since the first has a quick action insurgence, while tramadol has a more prolonged effect. Therefore, this combination allows to obtain a quick and long lasting effect with a high tolerability profile also when treating skin ulcer pain.

Pellicano R.,Molinette Hospital
Minerva Gastroenterologica e Dietologica | Year: 2014

Gastrointestinal (GI) damage by non-steroidal anti-inflammatory drugs (NSAIDs) is an important Public Health problem due to morbility and elevated mortality rate. The logic behind the development and sale of molecules which are selective cyclooxeg-nase-2 (COX-2) inhibitors called coxibs, is to limit the undesired effects of traditional NSAIDs, which should theoretically derive from the inhibition of COX-1. With respect to the emphasis of the initial trials, to now epidemiological studies, open-label studies, meta-analyses and reviews of the same data with longer follow-up, have produced opposite conclusions. Indeed, a recent series of meta-analyses has shown that the risks of GI events are similar for coxib and diclofenac, while they are significantly higher during the assumption of ibuprofen or naproxen. Moreover, the presumed lower gastrolesiv-ity of coxibs is based on a highly simplified hypothesis, that the gastroprotective PGs derive from COX-1 and that the phlogistic processes are related to COX-2. Also in geriatric populations, though less tolerated than coxibs, diclofenac presents minor GI side effects when compared with naproxen and ibuprofen. In this context, in the case of moderate pain intensity, it is possible to use combinations with weak opioids, such as paraceta-mol-tramadol. Though intestinal damage by NSAIDs are a nosological entity of growing interest, to now no trial has been conducted with optimal criteria to demonstrate the superiority of coxibs over traditional NSAIDs. For this reason, chronic inflammation of the intestine still represents a contraindication to the administration of coxibs.

Stacchini A.,Molinette Hospital | Demurtas A.,Molinette Hospital | Aliberti S.,Molinette Hospital
Cytometry Part B - Clinical Cytometry | Year: 2012

We report the unusual flow cytometric detection of liposomes in the cerebrospinal fluid of patients with aggressive non-Hodgkin's lymphoma and acute myeloid leukemia, treated with intrathecal liposomal cytarabine. Copyright © 2012 International Clinical Cytometry Society.

Stacchini A.,Molinette Hospital | Aliberti S.,Molinette Hospital | Demurtas A.,Molinette Hospital | Benevolo G.,Molinette Hospital | Godio L.,Molinette Hospital
Cytometry Part B - Clinical Cytometry | Year: 2012

Background: Flow cytometry (FC) is considered a sensitive and specific technique for the detection of occult lymphoma cells in cerebrospinal fluid (CSF). Methods: The diagnostic sensitivity of a FC approach which uses a combination of 10 antibodies, a single-tube evaluation, and a six-color instrument, was evaluated and compared to conventional cytology (CC) for the detection of lymphomatous cells in the CSF of 44 patients affected by B-cell non-Hodgkin's lymphoma (B-NHL) considered at high risk of central nervous system spread. Results: The CSF obtained from 36 newly diagnosed and 8 relapsed patients affected by B-cell lymphoma was assessed by FC and CC on a total of 62 samples; 52/62 (82.6%) were considered paucicellular as they had fewer than 10 cells/μl. All cases were evaluated by both methods. FC gave 15/62 (24%) positive results, CC 10/62 (16%) positive results; none of the samples evaluated had a positive CC with a negative FC result. Conclusions: The use of a multiparameter FC approach, which collects an elevated number of monoclonal antibodies in a single tube and identify different cell populations with a selective gating strategy analysis, allows for the evaluation of lymphocyte subsets and the detection of leptomeningeal disease in B-NHL, even in the presence of paucicellularity of samples. Copyright © 2012 International Clinical Cytometry Society.

Rabbia C.,Molinette Hospital | Pini R.,Molinette Hospital
Journal of Cardiovascular Surgery | Year: 2010

Atherosclerotic renovascular disease is an increasingly recognized cause of severe hypertension and declining kidney function. Patients with atherosclerotic renovascular disease have been demonstrated to have an increased risk of adverse cardiovascular events. Over the course of the last two decades renal artery revascularization for treatment of atherosclerotic renal artery stenosis (RAS) has gained great increase via percutaneous techniques. However the efficacy of contemporary revascularization therapies in the treatment of renal artery stenosis is unproven and controversial. The indication for renal artery stenting is widely questioned due to a not yet proven benefit of renal revascularization compared to best medical therapy. Many authors question the efficacy of percutaneous renal revascularization on clinical outcome parameters, such as preservation of renal function and blood pressure control. None of the so far published randomized controlled trials could prove a beneficial outcome of RAS revascularization compared with medical management. Currently accepted indications for revascularization are significant RAS with progressive or acute deterioration of renal function and/or severe uncontrollable hypertension, renal function decline with the use of agents blocking the reninangiotensin system and recurrent flash pulmonary edema. The key point for success is the correct selection of the patient. This article summarizes the background and the limitations of the so far published and still ongoing controlled trials.

The inflammatory bowel diseases (IBDs) are being seen as a gut inflammatory hub occurring: 1) with inflammatory spots in the eyes, skin, liver, joints (extra-intestinal manifestations); 2) with functionally contiguous disorders such as psoriasis and lung disease (barrier organ diseases); 3) as the consequence of genetic loss of non-redundant cell functions that are critical for gut homeostasis and defense (monogenic IBD). Recent multidisciplinary analysis, fostered by the input of genomic search, has helped hypothesize two pathogenetic models for the main phenotypes of IBDs. In ulcerative colitis, an increased mucosal permeability would prevail, allowing arousal of inflammation from the hyper-reactive underneath lymphoid tissue; an impaired bacterial sensing by innate immunity cells would by contrast place Crohn's disease (CD) in the chapter of the immune deficiency disorders, with the activity phases (the actual target of traditional immune suppressive strategies) representing just "zenith" phases in the continuously waxing-and-waning course of the attempts of the blunted inflammatory machinery to clear the invaders. Studying such errors of innate immunity, a few open-minded investigators have observed that they might not be a CD exclusivity at all: the proven evidence of CD-like pictures in a plethora of granulomatous disorders has thus been consolidated. This scenario calls for a concept of "syndrome" to best be accounted for, and to encourage the envisaging of the future therapy for IBD. © 2016 EDIZIONI MINERVA MEDICA.

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