Intravenous alemtuzumab is an effective and well-tolerated treatment for T-cell prolymphocytic leukemia (T-PLL). Alemtuzumab given intravenously as first-line treatment in 32 patients resulted in an overall response rate of 91% with 81% complete responses. Studies in B-cell chronic lymphocytic leukemia have shown subcutaneous alemtuzumab to be equally as effective as intravenous alemtuzumab. The UKCLL05 pilot study examined the efficacy and toxicity of this more convenient method of administration in 9 previously untreated patients with T-PLL. Only 3 of 9 patients (33%) responded to treatment. Furthermore, 2 of 9 patients (22%) died while on treatment. Recruitment was terminated because of these poor results. After rescue therapy with intravenous alemtuzumab and/or pentostatin, median progression-free survival and overall survival were similar to the intravenous group. Alemtuzumab delivered intravenously, but not subcutaneously, remains the treatment of choice for previously untreated T-PLL.
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http://dx.doi.org/10.1182/blood-2011-08-372854 | DOI Listing |
Ther Adv Neurol Disord
November 2024
Sanofi, Cambridge, MA, USA.
Background: Alemtuzumab is administered intravenously (IV) for relapsing-remitting multiple sclerosis (RRMS), with limited studies of subcutaneous (SC) treatment.
Objectives: We sought to evaluate the pharmacodynamics (PD), pharmacokinetics (PK), and safety profile of SC-administered alemtuzumab in people with progressive multiple sclerosis (PMS).
Design: SCALA was a phase I, open-label, randomized, parallel-group study with two 12-month periods and a safety monitoring phase to 60 months.
Cardiovasc Diagn Ther
August 2024
Institute of Traditional Chinese Medicine, Heilongjiang University of Chinese Medicine, Harbin, China.
Background And Objective: Immune checkpoint inhibitors (ICIs) have become one of the cornerstones of current oncology treatment, and immune checkpoint inhibitor-related myocarditis (IRM) is the most fatal of all immune checkpoint inhibitor-related adverse events (irAEs). Methylprednisolone pulse therapy (500-1,000 mg/day) is the initial treatment for IRM recommended by almost all relevant guidelines. However, subsequent treatment regimens remain unclear for patients who do not respond to methylprednisolone pulse therapy (who are defined as steroid-refractory patients).
View Article and Find Full Text PDFMult Scler
August 2024
CORe, Department of Medicine, The University of Melbourne, Melbourne, VIC, Australia; Neuroimmunology Centre, Department of Neurology, The Royal Melbourne Hospital, Melbourne, VIC, Australia.
Background: Comparisons between cladribine and other potent immunotherapies for multiple sclerosis (MS) are lacking.
Objectives: To compare the effectiveness of cladribine against fingolimod, natalizumab, ocrelizumab and alemtuzumab in relapsing-remitting MS.
Methods: Patients with relapsing-remitting MS treated with cladribine, fingolimod, natalizumab, ocrelizumab or alemtuzumab were identified in the global MSBase cohort and two additional UK centres.
Heliyon
March 2024
Bursa Uludag University, Faculty of Medicine, Department of Neurology, Turkey.
Background: Alemtuzumab (ATZ) is an anti-CD52 humanized monoclonal antibody indicated for treating highly active relapsing-remitting MS (RRMS). It alters the regulation of the immune system by depleting circulating lymphocytes. Changes in blood cell count, infusion-related reactions, and changes in vital parameters can be seen in the early period with ATZ.
View Article and Find Full Text PDFTranspl Immunol
December 2023
Department of Pneumonology and Allergology, Medical University of Gdansk, Poland.
Lung transplantation, like other transplants, carries a risk of graft rejection due to genetic differences between the donor and the recipient. In this paper, we focus on antibody-mediated rejection, which can cause acute and more importantly chronic graft dysfunction and subsequently shortened allograft survival. We present the case of a 46-year-old patient who, two months after lung transplantation (LTx), developed AMR manifested by the deterioration of graft function and de novo production of donor-specific antibodies (DSA): DQ3 (DQ7, DQ8, DQ9).
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