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http://dx.doi.org/10.1016/j.medcli.2016.01.011 | DOI Listing |
Hematology Am Soc Hematol Educ Program
December 2024
Department of Internal Medicine and Clinical Immunology, Henri Mondor University Hospital, Assistance Publique-Hôpitaux de Paris, Université Paris-Est Créteil, Créteil, France.
The management of immune thrombocytopenia (ITP) is continuously evolving with the development and introduction of newer therapies and a better understanding of the disease. Corticosteroids still represent the cornerstone of first-line treatment. Patients who fail to achieve remission with a short course of corticosteroids require subsequent therapy.
View Article and Find Full Text PDFClin Case Rep
December 2024
Nephrology Department, Regional University Hospital of Malaga University of Malaga, Biomedical Research Institute of Malaga (IBIMA)-Plataforma BIONAND, RICORS2040 (RD21/0005/0012) Malaga Spain.
Key Clinical Message: The coexistence of rheumatoid arthritis (RA) and PLA2R-associated membranous nephropathy (MN) is uncommon. It is difficult to demonstrate whether the mechanisms of renal pathology are triggered by RA, but it has been observed that the pro-inflammatory molecules present in RA increase the expression of PLA2R. Rituximab could be effective in both conditions.
View Article and Find Full Text PDFSci Rep
November 2024
Department for Health, University of Bath, Bath, BA2 7AY, UK.
Complement-dependent cytotoxicity (CDC) is a primary mechanism-of-action of monoclonal antibody (mAb) immunotherapies used to treat haematological cancers, including rituximab and daratumumab. However, mAb efficacy may be limited by reduced bioavailability of complement C1q - which activates the complement classical pathway following interactions with mAb-opsonised target cells. C1q is secreted by phagocytes upon recruitment to sites of muscle damage to facilitate muscular repair, hence we hypothesised that muscle damaging exercise may increase C1q 'spill-over' into blood.
View Article and Find Full Text PDFJ Immunother Cancer
November 2024
Department of Hematology, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong, China
Neurology
December 2024
From the Department of Neurology (C.J.K., D.D., M.V.P., M.P.S., G.S., M.L.M.), Mayo Clinic, Rochester, MN; Department of Neurology (J.D.T.), Royal Adelaide Hospital, Adelaide, South Australia; Department of Laboratory Medicine and Pathology Mayo Clinic (D.L.M., J.R.M., S.S.), Rochester, MN; Department of Neurology (S.S.), Rambam Medical Center, Haifa, Israel; and Department of Hematology Mayo Clinic Foundation (S.M.A.), Rochester, MN.
Background And Objectives: Patients with typical anti-myelin-associated glycoprotein (anti-MAG) neuropathy have IgM-gammopathy, mimic distal chronic inflammatory demyelinating polyradiculoneuropathy (CIDP), and are treatment resistant. Anti-MAG patients go unrecognized when IgM-gammopathy is undetected or with atypical phenotypes. We investigated an optimal anti-MAG titration cutoff for excluding CIDP and the impact of IgM-gammopathy detection on neuropathy treatment evaluation without anti-MAG antibodies.
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