Treatment with liposome-encapsulated clodronate as a new strategic approach in the management of immune thrombocytopenic purpura in a mouse model.
Identifieur interne : 003888 ( Main/Exploration ); précédent : 003887; suivant : 003889Treatment with liposome-encapsulated clodronate as a new strategic approach in the management of immune thrombocytopenic purpura in a mouse model.
Auteurs : RBID : pubmed:11023519English descriptors
- KwdEn :
- Animals, Autoimmune Diseases (drug therapy), Autoimmune Diseases (physiopathology), Bleeding Time, Blood Platelets (immunology), Blood Platelets (pathology), Clodronic Acid (administration & dosage), Clodronic Acid (pharmacology), Clodronic Acid (therapeutic use), Dose-Response Relationship, Drug, Drug Compounding, Drug Evaluation, Preclinical, Erythrocyte Count, Immune Sera (toxicity), Indium Radioisotopes (diagnostic use), Leukocyte Count, Liposomes, Liver (physiopathology), Macrophages (drug effects), Macrophages (physiology), Mice, Models, Animal, Organ Specificity, Organometallic Compounds (diagnostic use), Oxyquinoline (analogs & derivatives), Oxyquinoline (diagnostic use), Platelet Count, Purpura, Thrombocytopenic, Idiopathic (chemically induced), Purpura, Thrombocytopenic, Idiopathic (drug therapy), Purpura, Thrombocytopenic, Idiopathic (physiopathology), Rabbits, Spleen (physiopathology).
- MESH :
- chemical , administration & dosage : Clodronic Acid.
- chemical , analogs & derivatives : Oxyquinoline.
- chemical , diagnostic use : Indium Radioisotopes, Organometallic Compounds, Oxyquinoline.
- chemically induced : Purpura, Thrombocytopenic, Idiopathic.
- drug effects : Macrophages.
- drug therapy : Autoimmune Diseases, Purpura, Thrombocytopenic, Idiopathic.
- immunology : Blood Platelets.
- pathology : Blood Platelets.
- chemical , pharmacology : Clodronic Acid.
- physiology : Macrophages.
- physiopathology : Autoimmune Diseases, Liver, Purpura, Thrombocytopenic, Idiopathic, Spleen.
- chemical , therapeutic use : Clodronic Acid.
- chemical , toxicity : Immune Sera.
- Animals, Bleeding Time, Dose-Response Relationship, Drug, Drug Compounding, Drug Evaluation, Preclinical, Erythrocyte Count, Leukocyte Count, Liposomes, Mice, Models, Animal, Organ Specificity, Platelet Count, Rabbits.
Abstract
Immune thrombocytopenic purpura (ITP) is an autoimmune disease related to the presence of elevated levels of platelet-associated immunoglobulin, or autoantibodies. In recent years the importance of macrophage Fc gamma receptors in the uptake of platelets in ITP has been confirmed. Although in patients with ITP the platelet destruction occurs in liver and spleen, in this present experimental mouse model the liver was the principal organ of sequestration of sensitized platelets. The uptake in the spleen, bone marrow, lung, and kidneys was negligible and not different from that in control animals. In addition, the trapped platelets did not return to circulation, and new cells derived from the platelet-storage pool or new thrombocytogenesis were necessary to restore the platelet count. The depletion of splenic and hepatic murine macrophages by liposome-encapsulated clodronate (lip-clod) was studied as a new strategy for ITP treatment. Lip-clod inhibits, in a dose-dependent manner, the antibody-induced thrombocytopenia. Moreover, lip-clod treatment rapidly restored (24 hours) the platelet count in thrombocytopenic animals to hematologic safe values, and despite additional antiplatelet antiserum treatment, mice were able to maintain this level of platelets at least up to 48 hours. The bleeding times in lip-clod-treated animals was not different from those in controls, demonstrating that the hemostasis was well controlled in these animals. The results presented in this study demonstrate that lip-clod treatment can be effective in the management of experimental ITP. (Blood. 2000;96:2834-2840)
PubMed: 11023519
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Rooijen</name></author><author><name sortKey="Palermo, M S" uniqKey="Palermo M">M S Palermo</name></author><author><name sortKey="Isturiz, M A" uniqKey="Isturiz M">M A Isturiz</name></author></titleStmt><publicationStmt><date when="2000">2000</date><idno type="RBID">pubmed:11023519</idno><idno type="pmid">11023519</idno><idno type="wicri:Area/Main/Corpus">003B76</idno><idno type="wicri:Area/Main/Curation">003B76</idno><idno type="wicri:Area/Main/Exploration">003888</idno></publicationStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Autoimmune Diseases (drug therapy)</term><term>Autoimmune Diseases (physiopathology)</term><term>Bleeding Time</term><term>Blood Platelets (immunology)</term><term>Blood Platelets (pathology)</term><term>Clodronic Acid (administration & dosage)</term><term>Clodronic Acid (pharmacology)</term><term>Clodronic Acid (therapeutic use)</term><term>Dose-Response Relationship, Drug</term><term>Drug Compounding</term><term>Drug Evaluation, Preclinical</term><term>Erythrocyte Count</term><term>Immune Sera (toxicity)</term><term>Indium Radioisotopes (diagnostic use)</term><term>Leukocyte Count</term><term>Liposomes</term><term>Liver (physiopathology)</term><term>Macrophages (drug effects)</term><term>Macrophages (physiology)</term><term>Mice</term><term>Models, Animal</term><term>Organ Specificity</term><term>Organometallic Compounds (diagnostic use)</term><term>Oxyquinoline (analogs & derivatives)</term><term>Oxyquinoline (diagnostic use)</term><term>Platelet Count</term><term>Purpura, Thrombocytopenic, Idiopathic (chemically induced)</term><term>Purpura, Thrombocytopenic, Idiopathic (drug therapy)</term><term>Purpura, Thrombocytopenic, Idiopathic (physiopathology)</term><term>Rabbits</term><term>Spleen (physiopathology)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="administration & dosage" xml:lang="en"><term>Clodronic Acid</term></keywords><keywords scheme="MESH" type="chemical" qualifier="analogs & derivatives" xml:lang="en"><term>Oxyquinoline</term></keywords><keywords scheme="MESH" type="chemical" qualifier="diagnostic use" xml:lang="en"><term>Indium Radioisotopes</term><term>Organometallic Compounds</term><term>Oxyquinoline</term></keywords><keywords scheme="MESH" qualifier="chemically induced" xml:lang="en"><term>Purpura, Thrombocytopenic, Idiopathic</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Macrophages</term></keywords><keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Autoimmune Diseases</term><term>Purpura, Thrombocytopenic, Idiopathic</term></keywords><keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Blood Platelets</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Blood Platelets</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Clodronic Acid</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Macrophages</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Autoimmune Diseases</term><term>Liver</term><term>Purpura, Thrombocytopenic, Idiopathic</term><term>Spleen</term></keywords><keywords scheme="MESH" type="chemical" qualifier="therapeutic use" xml:lang="en"><term>Clodronic Acid</term></keywords><keywords scheme="MESH" type="chemical" qualifier="toxicity" xml:lang="en"><term>Immune Sera</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Bleeding Time</term><term>Dose-Response Relationship, Drug</term><term>Drug Compounding</term><term>Drug Evaluation, Preclinical</term><term>Erythrocyte Count</term><term>Leukocyte Count</term><term>Liposomes</term><term>Mice</term><term>Models, Animal</term><term>Organ Specificity</term><term>Platelet Count</term><term>Rabbits</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Immune thrombocytopenic purpura (ITP) is an autoimmune disease related to the presence of elevated levels of platelet-associated immunoglobulin, or autoantibodies. In recent years the importance of macrophage Fc gamma receptors in the uptake of platelets in ITP has been confirmed. Although in patients with ITP the platelet destruction occurs in liver and spleen, in this present experimental mouse model the liver was the principal organ of sequestration of sensitized platelets. The uptake in the spleen, bone marrow, lung, and kidneys was negligible and not different from that in control animals. In addition, the trapped platelets did not return to circulation, and new cells derived from the platelet-storage pool or new thrombocytogenesis were necessary to restore the platelet count. The depletion of splenic and hepatic murine macrophages by liposome-encapsulated clodronate (lip-clod) was studied as a new strategy for ITP treatment. Lip-clod inhibits, in a dose-dependent manner, the antibody-induced thrombocytopenia. Moreover, lip-clod treatment rapidly restored (24 hours) the platelet count in thrombocytopenic animals to hematologic safe values, and despite additional antiplatelet antiserum treatment, mice were able to maintain this level of platelets at least up to 48 hours. The bleeding times in lip-clod-treated animals was not different from those in controls, demonstrating that the hemostasis was well controlled in these animals. The results presented in this study demonstrate that lip-clod treatment can be effective in the management of experimental ITP. (Blood. 2000;96:2834-2840)</div></front></TEI><pubmed><MedlineCitation Owner="NLM" Status="MEDLINE"><PMID Version="1">11023519</PMID><DateCreated><Year>2000</Year><Month>11</Month><Day>09</Day></DateCreated><DateCompleted><Year>2000</Year><Month>11</Month><Day>09</Day></DateCompleted><DateRevised><Year>2013</Year><Month>11</Month><Day>21</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0006-4971</ISSN><JournalIssue CitedMedium="Print"><Volume>96</Volume><Issue>8</Issue><PubDate><Year>2000</Year><Month>Oct</Month><Day>15</Day></PubDate></JournalIssue><Title>Blood</Title><ISOAbbreviation>Blood</ISOAbbreviation></Journal><ArticleTitle>Treatment with liposome-encapsulated clodronate as a new strategic approach in the management of immune thrombocytopenic purpura in a mouse model.</ArticleTitle><Pagination><MedlinePgn>2834-40</MedlinePgn></Pagination><Abstract><AbstractText>Immune thrombocytopenic purpura (ITP) is an autoimmune disease related to the presence of elevated levels of platelet-associated immunoglobulin, or autoantibodies. In recent years the importance of macrophage Fc gamma receptors in the uptake of platelets in ITP has been confirmed. Although in patients with ITP the platelet destruction occurs in liver and spleen, in this present experimental mouse model the liver was the principal organ of sequestration of sensitized platelets. The uptake in the spleen, bone marrow, lung, and kidneys was negligible and not different from that in control animals. In addition, the trapped platelets did not return to circulation, and new cells derived from the platelet-storage pool or new thrombocytogenesis were necessary to restore the platelet count. The depletion of splenic and hepatic murine macrophages by liposome-encapsulated clodronate (lip-clod) was studied as a new strategy for ITP treatment. Lip-clod inhibits, in a dose-dependent manner, the antibody-induced thrombocytopenia. Moreover, lip-clod treatment rapidly restored (24 hours) the platelet count in thrombocytopenic animals to hematologic safe values, and despite additional antiplatelet antiserum treatment, mice were able to maintain this level of platelets at least up to 48 hours. The bleeding times in lip-clod-treated animals was not different from those in controls, demonstrating that the hemostasis was well controlled in these animals. The results presented in this study demonstrate that lip-clod treatment can be effective in the management of experimental ITP. 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