Search

Your search keyword '"Pellecchio M"' showing total 4 results
Start Over Author "Pellecchio M" Publication Type Academic Journals
4 results on '"Pellecchio M"'

1. Risk of acute arterial and venous thromboembolic events in eosinophilic granulomatosis with polyangiitis (Churg-Strauss syndrome).

Author

Bettiol A, Sinico RA, Schiavon F, Monti S, Bozzolo EP, Franceschini F, Govoni M, Lunardi C, Guida G, Lopalco G, Paolazzi G, Vacca A, Gregorini G, Leccese P, Piga M, Conti F, Fraticelli P, Quartuccio L, Alberici F, Salvarani C, Bettio S, Negrini S, Selmi C, Sciascia S, Moroni G, Colla L, Manno C, Urban ML, Vannacci A, Pozzi MR, Fabbrini P, Polti S, Felicetti M, Marchi MR, Padoan R, Delvino P, Caporali R, Montecucco C, Dagna L, Cariddi A, Toniati P, Tamanini S, Furini F, Bortoluzzi A, Tinazzi E, Delfino L, Badiu I, Rolla G, Venerito V, Iannone F, Berti A, Bortolotti R, Racanelli V, Jeannin G, Padula A, Cauli A, Priori R, Gabrielli A, Bond M, Tedesco M, Pazzola G, Tomietto P, Pellecchio M, Marvisi C, Maritati F, Palmisano A, Dejaco C, Willeit J, Kiechl S, Olivotto I, Willeit P, Prisco D, Vaglio A, and Emmi G

Subjects
Humans, Churg-Strauss Syndrome, Granulomatosis with Polyangiitis, Venous Thromboembolism, Venous Thrombosis
Abstract

Competing Interests: Conflict of interest: A. Bettiol has nothing to disclose. Conflict of interest: R.A. Sinico has nothing to disclose. Conflict of interest: F. Schiavon has nothing to disclose. Conflict of interest: S. Monti has nothing to disclose. Conflict of interest: E.P. Bozzolo has nothing to disclose. Conflict of interest: F. Franceschini has nothing to disclose. Conflict of interest: M. Govoni has nothing to disclose. Conflict of interest: C. Lunardi has nothing to disclose. Conflict of interest: G. Guida has nothing to disclose. Conflict of interest: G. Lopalco has nothing to disclose. Conflict of interest: G. Paolazzi has nothing to disclose. Conflict of interest: A. Vacca has nothing to disclose. Conflict of interest: G. Gregorini has nothing to disclose. Conflict of interest: P. Leccese has nothing to disclose. Conflict of interest: M. Piga has nothing to disclose. Conflict of interest: F. Conti has nothing to disclose. Conflict of interest: P. Fraticelli has nothing to disclose. Conflict of interest: L. Quartuccio has nothing to disclose. Conflict of interest: F. Alberici has nothing to disclose. Conflict of interest: C. Salvarani has nothing to disclose. Conflict of interest: S. Bettio has nothing to disclose. Conflict of interest: S. Negrini has nothing to disclose. Conflict of interest: C. Selmi has nothing to disclose. Conflict of interest: S. Sciascia has nothing to disclose. Conflict of interest: G. Moroni has nothing to disclose. Conflict of interest: L. Colla has nothing to disclose. Conflict of interest: C. Manno has nothing to disclose. Conflict of interest: M.L. Urban has nothing to disclose. Conflict of interest: A. Vannacci has nothing to disclose. Conflict of interest: M.R. Pozzi has nothing to disclose. Conflict of interest: P. Fabbrini has nothing to disclose. Conflict of interest: S. Polti has nothing to disclose. Conflict of interest: M. Felicetti has nothing to disclose. Conflict of interest: M.R. Marchi has nothing to disclose. Conflict of interest: R. Padoan has nothing to disclose. Conflict of interest: P. Delvino has nothing to disclose. Conflict of interest: R. Caporali has nothing to disclose. Conflict of interest: C. Montecucco has nothing to disclose. Conflict of interest: L. Dagna has nothing to disclose. Conflict of interest: A. Cariddi has nothing to disclose. Conflict of interest: P. Toniati has nothing to disclose. Conflict of interest: S. Tamanini worked at ASST Spedali Civili Brescia, Unit of Rheumatology and Immunology during the conduct of the study, but has since been employed by GlaxoSmithKline. Conflict of interest: F. Furini has nothing to disclose. Conflict of interest: A. Bortoluzzi has nothing to disclose. Conflict of interest: E. Tinazzi has nothing to disclose. Conflict of interest: L. Delfino has nothing to disclose. Conflict of interest: I. Badiu has nothing to disclose. Conflict of interest: G. Rolla has nothing to disclose. Conflict of interest: V. Venerito has nothing to disclose. Conflict of interest: F. Iannone has nothing to disclose. Conflict of interest: A. Berti has nothing to disclose. Conflict of interest: R. Bortolotti has nothing to disclose. Conflict of interest: V. Racanelli has nothing to disclose. Conflict of interest: G. Jeannin has nothing to disclose. Conflict of interest: A. Padula has nothing to disclose. Conflict of interest: A. Cauli has nothing to disclose. Conflict of interest: R. Priori has nothing to disclose. Conflict of interest: A. Gabrielli has nothing to disclose. Conflict of interest: M. Bond has nothing to disclose. Conflict of interest: M. Tedesco has nothing to disclose. Conflict of interest: G. Pazzola has nothing to disclose. Conflict of interest: P. Tomietto has nothing to disclose. Conflict of interest: M. Pellecchio has nothing to disclose. Conflict of interest: C. Marvisi has nothing to disclose. Conflict of interest: F. Maritati has nothing to disclose. Conflict of interest: A. Palmisano has nothing to disclose. Conflict of interest: C. Dejaco has nothing to disclose. Conflict of interest: J. Willeit has nothing to disclose. Conflict of interest: S. Kiechl has nothing to disclose. Conflict of interest: I. Olivotto has nothing to disclose. Conflict of interest: P. Willeit has nothing to disclose. Conflict of interest: D. Prisco has nothing to disclose. Conflict of interest: A. Vaglio has nothing to disclose. Conflict of interest: G. Emmi has nothing to disclose.

Published
2021
Full Text
View/download PDF

2. Update upon the infection risk in patients receiving TNF alpha inhibitors.

Author

Murdaca G, Negrini S, Pellecchio M, Greco M, Schiavi C, Giusti F, and Puppo F

Subjects
Animals, Antirheumatic Agents administration & dosage, Antirheumatic Agents adverse effects, Etanercept administration & dosage, Etanercept adverse effects, Humans, Immune System Diseases immunology, Immunologic Factors administration & dosage, Immunologic Factors adverse effects, Infections epidemiology, Infliximab administration & dosage, Infliximab adverse effects, Opportunistic Infections epidemiology, Opportunistic Infections etiology, Risk Factors, Immune System Diseases drug therapy, Infections etiology, Tumor Necrosis Factor-alpha antagonists & inhibitors
Abstract

Introduction: TNF-α inhibitors can be administered either as monotherapy or in combination with other anti-inflammatory drugs or DMARDs in the treatment of chronic immune-mediated diseases., Areas Covered: Patients receiving TNF-α inhibitors are at high risk of infections. An update is made on the risk of infection in patients receiving TNF-α inhibitors and the strategies for mitigating against the development of these serious adverse events., Expert Opinion: Infliximab than etanercept appears to be responsible for the increased risk of infections. Re-activation of latent tuberculosis infection and the overall risk of opportunistic infections should be considered before beginning a course of TNF-α inhibitors. A careful medical history, Mantoux test/quantiferon-TB Gold In-tube Test and chest-X-ray should always be performed before starting TNF-α inhibitors. Particular attention should be paid to risk factors for Pneumocystis jirovecii infection. Hepatitis B and C virological follow-up should be considered during TNF-α inhibitors treatment. Finally, appropriate vaccinations for influenza, S. pneumoniae, and HBV should be administered to decrease the risk of infection, and patients who are at high risk of herpes zoster reactivation would benefit from a second vaccination in adulthood.

Published
2019
Full Text
View/download PDF

3. Update upon efficacy and safety of etanercept for the treatment of spondyloarthritis and juvenile idiopathic arthritis.

Author

Murdaca G, Negrini S, Magnani O, Penza E, Pellecchio M, Gulli R, Mandich P, and Puppo F

Subjects
Adolescent, Antirheumatic Agents administration & dosage, Antirheumatic Agents therapeutic use, Child, Etanercept administration & dosage, Etanercept therapeutic use, Humans, Antirheumatic Agents adverse effects, Arthritis, Juvenile drug therapy, Etanercept adverse effects, Spondylitis, Ankylosing drug therapy
Abstract

TNF-α inhibitors have demonstrated efficacy both as monotherapy and in combination with disease-modifying anti-rheumatic drugs (DMARDs) in the treatment of chronic inflammatory immune-mediated diseases such as rheumatoid arthritis, Crohn's disease, ulcerative colitis, ankylosing spondylitis (AS), psoriasis (Ps) and/or psoriatic arthritis (PsA) and may be administered off-label to treat disseminated granuloma annulare, systemic lupus erythematosus and systemic sclerosis. There are several TNF-α inhibitors available for clinical use including infliximab, adalimumab, golimumab, certolizumab pegol and etanercept. In this article, we discuss the efficacy and safety of etanercept in the treatment of spondyloarthritis and juvenile idiopathic arthritis (JIA). Etanercept is effective in the treatment of PsA, AS, JIA and uveitis. Independent predictors of achieving a sustained clinical improvement or MDA in children with JIA include shorter disease duration, no concurrent oral corticosteroid use, history of chronic anterior uveitis and age <9 years. IBD incidence was lower in patients receiving etanercept plus MTX. Intra-articular administration of etanercept seems to favor a prompt target joint improvement without serious adverse events. Etanercept improve endothelial function reducing the risk of acute cardiovascular and/or cerebrovascular events. The most commonly reported adverse events were nasopharyngitis, epidermal and dermal conditions, upper respiratory tract infection, cough, headache and fatigue.

Published
2018
Full Text
View/download PDF

4. Impact of pharmacogenomics upon the therapeutic response to etanercept in psoriasis and psoriatic arthritis.

Author

Murdaca G, Negrini S, Magnani O, Penza E, Pellecchio M, and Puppo F

Subjects
Antirheumatic Agents pharmacology, Antirheumatic Agents therapeutic use, Arthritis, Psoriatic genetics, Etanercept pharmacology, Humans, Immunosuppressive Agents pharmacology, Immunosuppressive Agents therapeutic use, Pharmacogenetics, Polymorphism, Single Nucleotide, Psoriasis genetics, Research Design, Treatment Outcome, Tumor Necrosis Factor-alpha antagonists & inhibitors, Tumor Necrosis Factor-alpha genetics, Arthritis, Psoriatic drug therapy, Etanercept therapeutic use, Psoriasis drug therapy
Abstract

Introduction: TNF-α inhibitors have demonstrated efficacy both as monotherapy and in combination with disease-modifying anti-rheumatic drugs (DMARDs) in the treatment of chronic inflammatory immune-mediated diseases. Etanercept is a decoy receptor" for TNF-α and it is composed of two p75 TNF-α receptors fused to human IgG1. Areas covered: We discuss the potential role of pharmacogenetics in predicting the response to etanercept in patients with Ps and PsA. Expert opinion: Pharmacogenetics represents the new frontier for the discovery of potential genetic markers of biological response to TNF-α inhibitors. Clinical studies showed that TNF-α -308 G/G, +489 GG and the +489 GA, TNF-α -857C (rs1799724), TNFRSF1B 676T (rs1061622), TNFAIP3 G SNP (rs610604), FcγRIIIA-V158F, HLA-C*06, IL-17 A (rs2275913 and rs10484879), IL-17F (rs763780) and IL17RA (rs4819554) SNPs favor the response to etanercept. However, most of these studies are often small and not sufficiently powered to detect an effect and markers tend to be more prognostic than predictive of therapeutic response. Furthermore, studies often examines only the effects of a single SNP, while it would be more useful to analyze more haplotypes in contemporary in the same patients. Appropriately designed clinical trials are needed before a pharmacogenetic approach may be applicable in daily clinical therapeutic practice.

Published
2017
Full Text
View/download PDF

Catalog

Books, media, physical & digital resources
See catalog results