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עמוד בית
Fri, 19.07.24

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November 2014
Evgeni Brotfain MD, Alexander Zlotnik MD PhD, Andrei Schwartz MD, Amit Frenkel MD, Leonid Koyfman MD, Shaun E. Gruenbaum MD and Moti Klein MD

Background: Optimal oxygen supply is the cornerstone of the management of critically ill patients after extubation, especially in patients at high risk for extubation failure. In recent years, high flow oxygen system devices have offered an appropriate alternative to standard oxygen therapy devices such as conventional face masks and nasal prongs.

Objectives: To assess the clinical effects of high flow nasal cannula (HFNC) compared with standard oxygen face masks in Intensive Care Unit (ICU) patients after extubation.

Methods: We retrospectively analyzed 67 consecutive ventilated critical care patients in the ICU over a period of 1 year. The patients were allocated to two treatment groups: HFNC (34 patients, group 1) and non-rebreathing oxygen face mask (NRB) (33 patients, group 2). Vital respiratory and hemodynamic parameters were assessed prior to extubation and 6 hours after extubation. The primary clinical outcomes measured were improvement in oxygenation, ventilation-free days, re-intubation, ICU length of stay, and mortality.

Results: The two groups demonstrated similar hemodynamic patterns before and after extubation. The respiratory rate was slightly elevated in both groups after extubation with no differences observed between groups. There were no statistically significant clinical differences in PaCO2. However, the use of HFNC resulted in improved PaO2/FiO2 post-extubation (P < 0.05). There were more ventilator-free days in the HFNC group (P < 0.05) and fewer patients required re-intubation (1 vs. 6). There were no differences in ICU length of stay or mortality.

Conclusion: This study demonstrated better oxygenation for patients treated with HFNC compared with NRB after extubation. HFNC may be more effective than standard oxygen supply devices for oxygenation in the post-extubation period.

Ari Zimran MD, Gheona Altarescu MD and Deborah Elstein PhD
Ricardo Silvariño MD MSc, Oscar Noboa MD and Ricard Cervera MD PhD FRCP
Basement membranes form an anatomic barrier that contains connective tissue. They are composed of type IV collagen, laminin and proteoglycans. Anti-basement membrane antibodies bind to the non-collagen site of the α3 chain of type IV collagen. A group of renal diseases, pulmonary diseases and perhaps others affecting different organs have long been associated with the presence of antibodies directed against glomerular basement membrane (GBM), alveolar basement membrane and tubular basement membrane. Goodpasture disease has a frequency of 0.5 to 1 case by million/year, and is responsible for up to 20% of crescentic glomerulonephritis in renal biopsy. It has been associated with genetic and immune abnormalities and there are usually environmental triggers preceding clinical onset. Renal disease can occur isolated or in association with pulmonary hemorrhage. In general, renal disease has a rapid progression that determines severe compromise, with rare spontaneous resolution. The diagnosis of Goodpasture disease requires the presence of the anti-GBM antibody, either in circulation or in renal tissue. The prognosis of non-treated patients is poor. The standard of care is plasma exchange combined with prednisone and cyclophosphamide. Anti-GBM antibody levels must be monitored frequently until their disappearance, and then every 6 months to confirm sustained remission in the absence of clinical signs of recurrence. Prognosis of the disease is strongly associated with its initial presentation. Survival rates are related to the degree of renal compromise at onset of the disease. Recurrence of the disease post-transplantation is low.
Stefan M. Kovachev MD PhD, Svetoslav D. Nikolov MD PhD and Anna P. Mihova MD PhD
Eva Zold MD PhD, Edit Bodolay MD PhD, Balazs Dezső MD PhD, Györgyike Soos MD PhD, Britt Nakken PhD and Peter Szodoray MD PhD
October 2014
Rina Aharoni PhD and Ruth Arnon PhD

A fundamental challenge for multiple sclerosis (MS) therapy is to promote repair and remyelination beyond their limited spontaneous extent. Glatiramer acetate (GA, Copaxone®), an approved treatment for MS, has been shown to induce immunomodulation as well as neuroprotection in the inflamed central nervous system (CNS) in MS and in its model, experimental autoimmune encephalomyelitis (EAE). Using electron microscopy, immunohistochemistry, and advanced magnetic resonance imaging, we have demonstrated diminished myelin damage in GA-treated mice, in both relapsing-remitting and chronic EAE, even when treatment was applied late after the disease exacerbation, suggesting repair. Furthermore, quantitative analysis indicated significant elevation in remyelinated axons in GA-treated compared to untreated EAE mice. To further prove that GA can promote myelination, we studied its effect in the developing naïve CNS, when injected postnatally. Immunohistochemical and ultrastructural analyses revealed significant increase in the number of myelinated axons, the thickness of the myelin encircling them, and the resulting g-ratios in the spinal cords of GA-injected mice compared to their phosphate-buffered saline-injected littermates. A prominent elevation in the amount of progenitor oligodendrocytes and their proliferation, as well as in mature oligodendrocytes, implied that the effect of GA is linked to the differentiation along the oligodendroglial cascade. Furthermore, a functional advantage in rotating rod test was exhibited by GA-injected mice over their littermates. These cumulative findings indicate that GA treatment affects myelination under inflammatory as well as non-inflammatory conditions, supporting the notion that the repair process in the CNS can be up-regulated by therapy.

Mathilde Versini MD, Gali Aljadeff BSc, Pierre-Yves Jeandel MD PhD and Yehuda Shoenfeld MD
Paola Triggianese MD, Maria D. Guarino MD, Eleonora Ballanti MD, Maria S. Chimenti MD PhD and Roberto Perricone MD
Yael Bar-On MD, Varda Shalev MD, Dahlia Weitzman PhD, Gabriel Chodick PhD and Howard Amital MD MHA
Tomer Bashi MD, Miri Blank PhD and Yehuda Shoenfeld MD FRCP
Orit Barrett MD, Ella Abramovich MD, Jacob Dreiher MD MPH, Victor Novack MD PhD and Mahmoud Abu-Shakra MD
María-Teresa Arango MSc, Shaye Kivity MD, Joab Chapman MD PhD and Yehuda Shoenfeld MD FRCP
Piercarlo Sarzi-Puttini MD and Fabiola Atzeni MD PhD
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