The Experts below are selected from a list of 10431 Experts worldwide ranked by ideXlab platform
Nicole Casadevall - One of the best experts on this subject based on the ideXlab platform.
-
antibody mediated pure red cell Aplasia in chronic kidney disease patients receiving erythropoiesis stimulating agents new insights
Kidney International, 2012Co-Authors: Iain C. Macdougall, Huub Schellekens, Angel L M De Francisco, Nicole Casadevall, Simon D Roger, David Goldsmith, Hans C Ebbers, Wolfgang Jelkmann, Gerard M London, Walter H. HörlAbstract:Antibody-mediated pure red cell Aplasia is a very rare but devastating condition affecting patients receiving treatment with erythropoiesis-stimulating agents. New cases continue to emerge, generally in clusters, consistent with an ‘environmental’ trigger to its pathogenesis. Defining the causes of antibody-mediated pure red cell Aplasia is clearly of importance for patients with chronic kidney disease, but any developments in this area may also have relevance to other disease areas as therapeutic delivery of endogenous proteins rapidly increases. This review focuses on the current knowledge regarding the etiology of antibody-mediated pure red cell Aplasia and the current approach to therapy.
-
Pure Red Cell Aplasia Induced by Erythropoiesis-Stimulating Agents
Clinical Journal of The American Society of Nephrology, 2008Co-Authors: Carol A. Pollock, Iain C. Macdougall, Walter H. Hörl, Jerome Rossert, Huub Schellekens, Robert Delage, Angel L M De Francisco, Nicole Casadevall, David W. Johnson, Robin ThorpeAbstract:Pure red cell Aplasia in patients who are treated for anemia of chronic kidney disease with erythropoiesis-stimulating agents such as epoetin was first reported in 1998. Although the incidence of pure red cell Aplasia peaked in 2002, it remains important for nephrologists to know how to investigate a suspected case of pure red cell Aplasia and how to identify other causes of hyporesponsiveness to erythropoiesis-stimulating agents, which account for the vast majority of such cases. The authors reviewed the current status of information in the literature and drew on their personal experiences with patients regarding the diagnosis and management of epoetin-induced pure red cell Aplasia. The mechanism for development of epoetin-induced pure red cell Aplasia remains unconfirmed. It generally occurs after the production of neutralizing anti-erythropoietin antibodies. Elucidation of a suspected pure red cell Aplasia case requires a systematic approach, beginning with simple measurements such as blood cell counts, because most cases of erythropoiesis-stimulating agent hyporesponsiveness are attributable to other causes. If these criteria indicate that the patient9s response to erythropoiesis-stimulating agent therapy is very poor, then bone marrow examination and measurement of anti-erythropoietin antibodies is justified. If pure red cell Aplasia is confirmed, then cessation of erythropoiesis-stimulating agent therapy and initiation of immunosuppressive therapy are recommended. Continued study of epoetin-induced pure red cell Aplasia is needed to help nephrologists prevent or manage future cases and will have implications for the use of other protein-based therapeutic agents.
-
epoetin induced autoimmune pure red cell Aplasia
Journal of The American Society of Nephrology, 2005Co-Authors: Nicole Casadevall, Kaiuwe Eckard, Jerome RosseAbstract:During the first 10 yr of therapy with recombinant human erythropoietin ([EPO]), only three cases of antibody-associated pure red cell Aplasia have been described in patients who were treated with EPO, whereas several millions of patients have received this treatment. Thus, the possibility for epoetin to induce the formation of anti-EPO antibodies was considered extremely low. However, since 1998, a significant increase in the number of cases of EPO-induced pure red cell Aplasia has been found in patients with chronic kidney disease with a peak in 2001 and 2002. The incidence rate seems now to be back to the baseline level. The change in formulation of epoetin a sold outside the United States seems to be the cause of these antibodies.
-
treatment of erythropoietin induced pure red cell Aplasia a retrospective study
The Lancet, 2004Co-Authors: David Verhelst, Jerome Rossert, Anne Kruger, Kai-uwe Eckardt, Nicole Casadevall, Iain C. MacdougallAbstract:Summary Background Recombinant human erythropoietin is the standard treatment for anaemia related to chronic kidney disease, and its widespread use has been favoured by a very high therapeutic index. However, since 1998, more than 200 patients worldwide with chronic kidney disease treated in this way have developed neutralising antibodies to erythropoietin, causing pure red cell Aplasia. We aimed to collate clinical and pathological features in patients unequivocally shown to have erythropoietin-induced pure red cell Aplasia. Methods We retrospectively obtained data from the files of 47 patients with pure red cell Aplasia. We assessed treatment and outcome of patients and defined recovery from pure red cell Aplasia as an increase in reticulocyte counts to more than 20 000 per μL in patients who were no longer transfusion-dependent. Findings When patients developed pure red cell Aplasia, all were receiving erythropoietin subcutaneously, and the product most typically prescribed was epoetin alfa (Eprex, Ortho Biotech). The median delay between start of erythropoietin treatment and occurrence of pure red cell Aplasia was 11 months (IQR 7·5–14). Nine patients received no immunosuppressive treatment, and none of these recovered. Of 37 patients who received immunosuppressive therapy, 29 (78%) recovered. All six patients who received a kidney transplant recovered within 1 month, and recovery rates were between 56% and 88% in patients treated with corticosteroids, corticosteroids plus cyclophosphamide, or ciclosporin. No relapse of pure red cell Aplasia happened after stopping immunosuppressive treatment, but no patient was rechallenged with erythropoietin. Interpretation Immunosuppressive treatment accelerates recovery from erythropoietin-induced pure red cell Aplasia.
-
autoantibodies against erythropoietin in a patient with pure red cell Aplasia
The New England Journal of Medicine, 1996Co-Authors: Nicole Casadevall, Evelyne Dupuy, Pascale Molhosabatie, Gerard Tobelem, Uno Vare, Patrick MayeuAbstract:Autoimmunity is often implicated in pure red-cell Aplasia. Approximately 10 to 15 percent of patients with pure red-cell Aplasia have thymomas,1 and remission of the anemia occurs in 25 to 30 percent of these patients after the thymoma is removed.2 In other patients there are immunologic abnormalities, such as hypogammaglobulinemia,3 monoclonal immunoglobulins,4 antithyroid antibodies,5 antinuclear antibodies,6,7 and autoimmune hemolytic anemia.3,8 Immunosuppressive therapy is successful in many patients,2,9–12 and a good response to plasmapheresis has been reported in two patients.13,14 In 1967 Krantz and Kao reported that plasma from a patient with pure red-cell Aplasia inhibited . . .
Iain C. Macdougall - One of the best experts on this subject based on the ideXlab platform.
-
antibody mediated pure red cell Aplasia in chronic kidney disease patients receiving erythropoiesis stimulating agents new insights
Kidney International, 2012Co-Authors: Iain C. Macdougall, Huub Schellekens, Angel L M De Francisco, Nicole Casadevall, Simon D Roger, David Goldsmith, Hans C Ebbers, Wolfgang Jelkmann, Gerard M London, Walter H. HörlAbstract:Antibody-mediated pure red cell Aplasia is a very rare but devastating condition affecting patients receiving treatment with erythropoiesis-stimulating agents. New cases continue to emerge, generally in clusters, consistent with an ‘environmental’ trigger to its pathogenesis. Defining the causes of antibody-mediated pure red cell Aplasia is clearly of importance for patients with chronic kidney disease, but any developments in this area may also have relevance to other disease areas as therapeutic delivery of endogenous proteins rapidly increases. This review focuses on the current knowledge regarding the etiology of antibody-mediated pure red cell Aplasia and the current approach to therapy.
-
Pure Red Cell Aplasia Induced by Erythropoiesis-Stimulating Agents
Clinical Journal of The American Society of Nephrology, 2008Co-Authors: Carol A. Pollock, Iain C. Macdougall, Walter H. Hörl, Jerome Rossert, Huub Schellekens, Robert Delage, Angel L M De Francisco, Nicole Casadevall, David W. Johnson, Robin ThorpeAbstract:Pure red cell Aplasia in patients who are treated for anemia of chronic kidney disease with erythropoiesis-stimulating agents such as epoetin was first reported in 1998. Although the incidence of pure red cell Aplasia peaked in 2002, it remains important for nephrologists to know how to investigate a suspected case of pure red cell Aplasia and how to identify other causes of hyporesponsiveness to erythropoiesis-stimulating agents, which account for the vast majority of such cases. The authors reviewed the current status of information in the literature and drew on their personal experiences with patients regarding the diagnosis and management of epoetin-induced pure red cell Aplasia. The mechanism for development of epoetin-induced pure red cell Aplasia remains unconfirmed. It generally occurs after the production of neutralizing anti-erythropoietin antibodies. Elucidation of a suspected pure red cell Aplasia case requires a systematic approach, beginning with simple measurements such as blood cell counts, because most cases of erythropoiesis-stimulating agent hyporesponsiveness are attributable to other causes. If these criteria indicate that the patient9s response to erythropoiesis-stimulating agent therapy is very poor, then bone marrow examination and measurement of anti-erythropoietin antibodies is justified. If pure red cell Aplasia is confirmed, then cessation of erythropoiesis-stimulating agent therapy and initiation of immunosuppressive therapy are recommended. Continued study of epoetin-induced pure red cell Aplasia is needed to help nephrologists prevent or manage future cases and will have implications for the use of other protein-based therapeutic agents.
-
treatment of erythropoietin induced pure red cell Aplasia a retrospective study
The Lancet, 2004Co-Authors: David Verhelst, Jerome Rossert, Anne Kruger, Kai-uwe Eckardt, Nicole Casadevall, Iain C. MacdougallAbstract:Summary Background Recombinant human erythropoietin is the standard treatment for anaemia related to chronic kidney disease, and its widespread use has been favoured by a very high therapeutic index. However, since 1998, more than 200 patients worldwide with chronic kidney disease treated in this way have developed neutralising antibodies to erythropoietin, causing pure red cell Aplasia. We aimed to collate clinical and pathological features in patients unequivocally shown to have erythropoietin-induced pure red cell Aplasia. Methods We retrospectively obtained data from the files of 47 patients with pure red cell Aplasia. We assessed treatment and outcome of patients and defined recovery from pure red cell Aplasia as an increase in reticulocyte counts to more than 20 000 per μL in patients who were no longer transfusion-dependent. Findings When patients developed pure red cell Aplasia, all were receiving erythropoietin subcutaneously, and the product most typically prescribed was epoetin alfa (Eprex, Ortho Biotech). The median delay between start of erythropoietin treatment and occurrence of pure red cell Aplasia was 11 months (IQR 7·5–14). Nine patients received no immunosuppressive treatment, and none of these recovered. Of 37 patients who received immunosuppressive therapy, 29 (78%) recovered. All six patients who received a kidney transplant recovered within 1 month, and recovery rates were between 56% and 88% in patients treated with corticosteroids, corticosteroids plus cyclophosphamide, or ciclosporin. No relapse of pure red cell Aplasia happened after stopping immunosuppressive treatment, but no patient was rechallenged with erythropoietin. Interpretation Immunosuppressive treatment accelerates recovery from erythropoietin-induced pure red cell Aplasia.
Dennis W Raisch - One of the best experts on this subject based on the ideXlab platform.
-
pure red cell Aplasia and epoetin therapy
The New England Journal of Medicine, 2004Co-Authors: Charles L Bennett, Stefano Luminari, Martin S Tallman, Norene Mcwilliams, June M Mckoy, Allison E Lyons, Steve Trifilio, Stephen A. Klinge, Allen R Nissenson, Dennis W RaischAbstract:Background Between 1988 and 1998, antibody-associated pure red-cell Aplasia was reported in three patients who had undergone treatment with recombinant human erythropoietin (epoetin). Between 1998 and 2000, 13 such cases were reported from France — 12 in patients who had received the Eprex formulation of epoetin alfa and 1 in a patient who had received Neorecormon (a formulation of epoetin beta); both are products that are marketed outside the United States. Methods We obtained reports of epoetin-associated pure red-cell Aplasia from the Food and Drug Administration and from the manufacturers of Eprex, Epogen (another formulation of epoetin alfa), and Neorecormon. The numbers of case reports and estimates of exposure-adjusted incidence were analyzed according to the product, the cause of anemia, the route of administration, the country in which pure red-cell Aplasia was identified, and the date on which pure red-cell Aplasia was reported. Results Between January 1998 and April 2004, 175 cases of epoetin-a...
Patrick Mayeu - One of the best experts on this subject based on the ideXlab platform.
-
autoantibodies against erythropoietin in a patient with pure red cell Aplasia
The New England Journal of Medicine, 1996Co-Authors: Nicole Casadevall, Evelyne Dupuy, Pascale Molhosabatie, Gerard Tobelem, Uno Vare, Patrick MayeuAbstract:Autoimmunity is often implicated in pure red-cell Aplasia. Approximately 10 to 15 percent of patients with pure red-cell Aplasia have thymomas,1 and remission of the anemia occurs in 25 to 30 percent of these patients after the thymoma is removed.2 In other patients there are immunologic abnormalities, such as hypogammaglobulinemia,3 monoclonal immunoglobulins,4 antithyroid antibodies,5 antinuclear antibodies,6,7 and autoimmune hemolytic anemia.3,8 Immunosuppressive therapy is successful in many patients,2,9–12 and a good response to plasmapheresis has been reported in two patients.13,14 In 1967 Krantz and Kao reported that plasma from a patient with pure red-cell Aplasia inhibited . . .
Walter H. Hörl - One of the best experts on this subject based on the ideXlab platform.
-
antibody mediated pure red cell Aplasia in chronic kidney disease patients receiving erythropoiesis stimulating agents new insights
Kidney International, 2012Co-Authors: Iain C. Macdougall, Huub Schellekens, Angel L M De Francisco, Nicole Casadevall, Simon D Roger, David Goldsmith, Hans C Ebbers, Wolfgang Jelkmann, Gerard M London, Walter H. HörlAbstract:Antibody-mediated pure red cell Aplasia is a very rare but devastating condition affecting patients receiving treatment with erythropoiesis-stimulating agents. New cases continue to emerge, generally in clusters, consistent with an ‘environmental’ trigger to its pathogenesis. Defining the causes of antibody-mediated pure red cell Aplasia is clearly of importance for patients with chronic kidney disease, but any developments in this area may also have relevance to other disease areas as therapeutic delivery of endogenous proteins rapidly increases. This review focuses on the current knowledge regarding the etiology of antibody-mediated pure red cell Aplasia and the current approach to therapy.
-
Pure Red Cell Aplasia Induced by Erythropoiesis-Stimulating Agents
Clinical Journal of The American Society of Nephrology, 2008Co-Authors: Carol A. Pollock, Iain C. Macdougall, Walter H. Hörl, Jerome Rossert, Huub Schellekens, Robert Delage, Angel L M De Francisco, Nicole Casadevall, David W. Johnson, Robin ThorpeAbstract:Pure red cell Aplasia in patients who are treated for anemia of chronic kidney disease with erythropoiesis-stimulating agents such as epoetin was first reported in 1998. Although the incidence of pure red cell Aplasia peaked in 2002, it remains important for nephrologists to know how to investigate a suspected case of pure red cell Aplasia and how to identify other causes of hyporesponsiveness to erythropoiesis-stimulating agents, which account for the vast majority of such cases. The authors reviewed the current status of information in the literature and drew on their personal experiences with patients regarding the diagnosis and management of epoetin-induced pure red cell Aplasia. The mechanism for development of epoetin-induced pure red cell Aplasia remains unconfirmed. It generally occurs after the production of neutralizing anti-erythropoietin antibodies. Elucidation of a suspected pure red cell Aplasia case requires a systematic approach, beginning with simple measurements such as blood cell counts, because most cases of erythropoiesis-stimulating agent hyporesponsiveness are attributable to other causes. If these criteria indicate that the patient9s response to erythropoiesis-stimulating agent therapy is very poor, then bone marrow examination and measurement of anti-erythropoietin antibodies is justified. If pure red cell Aplasia is confirmed, then cessation of erythropoiesis-stimulating agent therapy and initiation of immunosuppressive therapy are recommended. Continued study of epoetin-induced pure red cell Aplasia is needed to help nephrologists prevent or manage future cases and will have implications for the use of other protein-based therapeutic agents.
