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עמוד בית
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July 2017
Claudia Fabiani MD PhD, Giacomo Emmi MD PhD, Giuseppe Lopalco MD, Lorenzo Vannozzi MD PhD, Daniela Bacherini MD, Silvana Guerriero MD PhD, Rossella Franceschini MD, Bruno Frediani MD, Florenzo Iannone MD PhD, Gian Marco Tosi MD, Donato Rigante MD and Luca Cantarini MD

Background: The evidence on the use of dexamethasone implants in the treatment of Behçet’s disease (BD)-related uveitis is limited to a few cases. 

Objectives: To evaluate the efficacy of dexamethasone implants on ocular functional, morphological, and clinical parameters in BD patients with severe refractory uveitis. 

Methods: Five eyes from five BD patients were enrolled. A single intravitreal dexamethasone injection was applied to each eye. Best corrected visual acuity (BCVA), central macular thickness (CMT) assessed with optical coherence tomography, retinal vasculitis assessed by fluorescein angiography, vitreous haze score (Nussenblatt scale), intraocular pressure (IOP), and lens status (LOCS III, Lens Opacities Classification System III) were recorded at baseline and at 1, 3, and 6 month follow-up visits.

Results: At baseline, all eyes showed marked macular edema and 4/5 had concomitant active retinal vasculitis. Mean BCVA was increased from baseline at each control visit with a mean improvement of 0.26 ± 0.18 lines at 6 months follow-up. Mean CMT decreased from baseline at each control visit with a mean improvement at 6 months follow-up of 198.80 ± 80.08 µm. At the end of the study, none of the eyes showed macular edema and the mean CMT was 276.80 ± 24.94 µm. Retinal vasculitis resolved in all eyes. One eye experienced an IOP spike during treatment that resolved spontaneously, and one eye developed a clinically significant lens opacity at 6 months follow-up. 

Conclusions: Treatment with a dexamethasone implant in BD-uveitis and inflammatory macular edema was safe and effective as an additional treatment combined with systemic immunomodulatory drugs.

 

November 2014
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.
October 2014
Elisabetta Borella MD, Lavinia Palma MD, Margherita Zen MD, Silvano Bettio MD, Linda Nalotto MD, Mariele Gatto MD, Marta Domeneghetti MD, Luca Iaccarino MD, Leonardo Punzi and Andrea Doria MD
Autoinflammatory (AIF) and autoimmune (AIM) diseases are chronic immune disorders characterized by dysregulation of the immune system. Most AIF diseases are monogenic diseases which lead to hyperactivation of the inflammasome and release of pro-inflammatory cytokines, such as interleukin-1 (IL-1) and IL-18, resulting in tissue inflammation. Besides, the main feature of autoimmune diseases is the loss of tolerance of the adaptive immune cells against self antigens. Most AIF diseases are polygenic and numerous immune pathogens are involved in organ damage. The involvement of some AIF-associated mechanisms in AIM diseases, i.e., the activation of the inflammasome and the role of IL-1, was recently recognized. Moreover, some single nucleotide polymorphisms of the inflammasome genes have been proven to be involved in the development of AIF-related inflammatory features in autoimmune patients. These observations raise the possibility of using some anti-inflammatory drugs, like IL-1 antagonists, in autoimmune diseases with autoinflammatory features. 
October 2002
Veronica Silva Vilela, MD, Nilson Ramirez de Jesus, MD and Roger Abramino Levy, MD, PhD
November 2001
Anna Ghirardello, PhD, Andrea Doria, MD, Sandra Zampieri SciBiol, Pier Franca Gambari, MD and Silvano Todesco, MD
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