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Cucca A.,University of Trieste | Stragapede L.,University of Trieste | Antonutti L.,University of Trieste | Catalan M.,University of Trieste | And 7 more authors.
Journal of NeuroVirology | Year: 2016

A 21-year-old woman presented with acute-onset spastic paraparesis. The MRI spinal scan revealed a contrast-enhanced T2 hyperintensity between C5–T2. The most common neurotropic pathogens were excluded by first level tests. Under suspicion of an acute immune-mediated myelitis, a corticosteroid therapy was administered. However, a seropositivity for both human immunodeficiency virus (HIV) type 1 and human T-lymphotropic virus (HTLV) subsequently emerged. An antiretroviral therapy was started while steroids discontinued. Patient’s clinical conditions remained unchanged. HIV-HTLV-1 co-infection should be included in the differential diagnosis of any acute myelitis, even in patients with a preserved immune status and no risk factors. © 2016 Journal of NeuroVirology, Inc. Source

Taddio A.,University of Trieste | Taddio A.,Institute for Maternal and Child HealthIRCCS Burlo Garofolo | Rossi E.D.,University of Trieste | Monasta L.,Institute for Maternal and Child HealthIRCCS Burlo Garofolo | And 10 more authors.
Clinical Rheumatology | Year: 2016

Kawasaki shock syndrome (KSS) is a rare manifestation of Kawasaki disease (KD) characterized by systolic hypotension or clinical signs of poor perfusion. The objectives of the study are to describe the main clinical presentation, echocardiographic, and laboratory findings, as well as the treatment options and clinical outcomes of KSS patients when compared with KD patients. This is a retrospective study. All children referred to two pediatric rheumatology units from January 1, 2012, to December 31, 2014, were enrolled. Patients were divided into patients with or without KSS. We compared the two groups according to the following variables: sex, age, type of KD (classic, with less frequent manifestations, or incomplete), clinical manifestations, cardiac involvement, laboratory findings, therapy administered, response to treatment, and outcome. Eighty-four patients with KD were enrolled. Of these, five (6 %) met the criteria for KSS. Patients with KSS had higher values of C-reactive protein (p = 0.005), lower hemoglobin levels (p = 0.003); more frequent hyponatremia (p = 0.004), hypoalbuminemia (p = 0.004), and coagulopathy (p = 0.003); and increase in cardiac troponins (p = 0.000). Among the KSS patients, three had a coronary artery involvement, but none developed a permanent aneurysm. Intravenous immunoglobulin resistance was more frequent in the KSS group, although not significantly so (3/5, 60 % vs. 23/79, 30 %, P = NS). None of the five cases was fatal, and all recovered without sequelae. KSS patients are more likely to have higher rates of cardiac involvement. However, most cardiovascular abnormalities resolved promptly with therapy. © 2016 International League of Associations for Rheumatology (ILAR) Source

Davanzo R.,Institute for Maternal and Child HealthIRCCS Burlo Garofolo | Bua J.,Institute for Maternal and Child HealthIRCCS Burlo Garofolo | De Cunto A.,Institute for Maternal and Child HealthIRCCS Burlo Garofolo | Farina M.L.,Poison Control Center | And 5 more authors.
Journal of Human Lactation | Year: 2016

The use of medications by the nursing mother is a common reason for interrupting breastfeeding. Few drugs have been demonstrated to be absolutely contraindicated during breastfeeding. Excessive caution may lead health professionals to unnecessarily advise to interrupt breastfeeding, without assessing the latest evidence or considering the risk-benefit ratio of taking a medication versus terminating breastfeeding. To foster an appropriate approach toward the use of medications in breastfeeding women, the Italian Society of Perinatal Medicine created the following policy statement. © International Lactation Consultant Association. Source

Marcuzzi A.,University of Trieste | Piscianz E.,Institute for Maternal and Child HealthIRCCS Burlo Garofolo | Loganes C.,University of Trieste | Brumatti L.V.,Institute for Maternal and Child HealthIRCCS Burlo Garofolo | And 5 more authors.
International Journal of Molecular Sciences | Year: 2015

The cholesterol pathway is an essential biochemical process aimed at the synthesis of bioactive molecules involved in multiple crucial cellular functions. The end products of this pathway are sterols, such as cholesterol, which are essential components of cell membranes, precursors of steroid hormones, bile acids and other molecules such as ubiquinone. Several diseases are caused by defects in this metabolic pathway: the most severe forms of which cause neurological involvement (psychomotor retardation and cerebellar ataxia) as a result of a variety of cellular impairments, including mitochondrial dysfunction. These pathologies are induced by convergent mechanisms in which the mitochondrial unit plays a pivotal role contributing to defective apoptosis, autophagy and mitophagy processes. Unraveling these mechanisms would contribute to the development of effective drug treatments for these disorders. In addition, the development of biochemical models could have a substantial impact on the understanding of the mechanism of action of drugs that act on this pathway in multifactor disorders. In this review we will focus in particular on inhibitors of cholesterol synthesis, mitochondria-targeted drugs and inhibitors of the inflammasome. © 2015 by the authors; licensee MDPI, Basel, Switzerland. Source

Marcuzzi A.,University of Trieste | Piscianz E.,Institute for Maternal and Child HealthIRCCS Burlo Garofolo | Zweyer M.,University of Trieste | Bortul R.,University of Trieste | And 5 more authors.
International Journal of Molecular Sciences | Year: 2016

Deregulation of the cholesterol pathway is an anomaly observed in human diseases, many of which have in common neurological involvement and unknown pathogenesis. In this study we have used Mevalonate Kinase Deficiency (MKD) as a disease-model in order to investigate the link between the deregulation of the mevalonate pathway and the consequent neurodegeneration. The blocking of the mevalonate pathway in a neuronal cell line (Daoy), using statins or mevalonate, induced an increase in the expression of the inflammasome gene (NLRP3) and programmed cell death related to mitochondrial dysfunction. The morphology of the mitochondria changed, clearly showing the damage induced by oxidative stress and the decreased membrane potential associated with the alterations of the mitochondrial function. The co-administration of geranylgeraniol (GGOH) reduced the inflammatory marker and the damage of the mitochondria, maintaining its shape and components. Our data allow us to speculate about the mechanism by which isoprenoids are able to rescue the inflammatory marker in neuronal cells, independently from the block of the mevalonate pathway, and about the fact that cell death is mitochondria-related. © 2016 by the authors; licensee MDPI, Basel, Switzerland. Source

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