A case of Philadelphia chromosome‐positive acute lymphocytic leukaemia with type I CD36 deficiency
Background CD36 is a glycoprotein expressed on platelets and monocytes of the blood. There are two types of CD36 deficiency, type I and type II. Individuals with type I‐deficiency do not express CD36 in any cell type and can produce the CD36 antibody, which causes pathological conditions, such as fe...
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| Veröffentlicht in: | Vox sanguinis 2022-01, Vol.117 (1), p.128-132 |
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| creator | Matsui, Marina Kajiwara, Koichi Tsukada, Masao Iwama, Kanichi Yamada, Kazunari Kodo, Hideki Seto, Katsuya Tonami, Kaoru Ando, Moe Matsuhashi, Mika Watanabe‐Okochi, Naoko Tsuno, Nelson Hirokazu Kozai, Yasuji |
| description | Background
CD36 is a glycoprotein expressed on platelets and monocytes of the blood. There are two types of CD36 deficiency, type I and type II. Individuals with type I‐deficiency do not express CD36 in any cell type and can produce the CD36 antibody, which causes pathological conditions, such as fetal/neonatal alloimmune thrombocytopenia (FNAIT) and platelet transfusion refractory (PTR), through antigenic exposure via transfusion or pregnancy.
Case presentation
We experienced a case of Philadelphia‐positive acute lymphoblastic leukaemia with PTR. In addition to the CD36 antibody, multiple‐specificity HLA antibodies were present in the patient's plasma, requiring transfusion of HLA‐compatible and CD36‐negative platelets (PC‐HLA). Since the number of donors was limited, it was necessary to set‐up a blood transfusion schedule so that hyper‐fractionated cyclophosphamide, vincristine and doxorubicin therapy (hyper‐CVAD) and ponatinib combination chemotherapy could be safely administered to achieve molecular remission. Rituximab administration resulted in reduced levels of both CD36 antibody and HLA antibody. Given the expression of CD36 on haematopoietic stem cells and the limited availability of CD36‐negative PC‐HLA, haematopoietic stem cell transplantation (HSCT) was not considered to be an option.
Conclusion
If CD36‐negative, allogeneic haematopoietic stem cell donors are unable to be found, the indications for HSCT in patients with type I CD36‐deficiency should be carefully weighed. In the present case, molecular remission has been able to be maintained to the present day after completion of a two‐year maintenance regimen. |
| doi_str_mv | 10.1111/vox.13119 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_2541321834</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2541321834</sourcerecordid><originalsourceid>FETCH-LOGICAL-c3539-809f00c079d6241ecf94fec0490d23f8c9c43ce564de0e80bcaf28d9aab30cee3</originalsourceid><addsrcrecordid>eNp10M1u1DAQB3ALgehSOPACyBIXOKQdf2TXPlZbPipVKgdA3CzvZKy4JOsQJy258Qg8I0-CYQsHJOYyl9_8Nfoz9lTAiShzepO-ngglhL3HVkJLVYEWcJ-tALSsLMDmiD3K-RoAjDT1Q3aktJC1rTcr1pxx9Jl4CvxdGzvfUDe00XNsx9SnnHr68e37kHKc4g1xj_NEvFv6oU24TBF5R_NnT325uI1Ty6dlIH7Bt-dqzRsKESPtcXnMHgTfZXpyt4_Zh9ev3m_fVpdXby62Z5cVqlrZyoANAAgb26ylFoTB6kAI2kIjVTBoUSukeq0bAjKwQx-kaaz3OwVIpI7Zi0PuMKYvM-XJ9TEjdZ3fU5qzk7UWSgqjdKHP_6HXaR735Tsn10UYo3Vd1MuDwjHlPFJwwxh7Py5OgPtVvSvVu9_VF_vsLnHe9dT8lX-6LuD0AG5jR8v_k9zHq0-HyJ_hN47F</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2618388445</pqid></control><display><type>article</type><title>A case of Philadelphia chromosome‐positive acute lymphocytic leukaemia with type I CD36 deficiency</title><source>MEDLINE</source><source>Access via Wiley Online Library</source><creator>Matsui, Marina ; Kajiwara, Koichi ; Tsukada, Masao ; Iwama, Kanichi ; Yamada, Kazunari ; Kodo, Hideki ; Seto, Katsuya ; Tonami, Kaoru ; Ando, Moe ; Matsuhashi, Mika ; Watanabe‐Okochi, Naoko ; Tsuno, Nelson Hirokazu ; Kozai, Yasuji</creator><creatorcontrib>Matsui, Marina ; Kajiwara, Koichi ; Tsukada, Masao ; Iwama, Kanichi ; Yamada, Kazunari ; Kodo, Hideki ; Seto, Katsuya ; Tonami, Kaoru ; Ando, Moe ; Matsuhashi, Mika ; Watanabe‐Okochi, Naoko ; Tsuno, Nelson Hirokazu ; Kozai, Yasuji</creatorcontrib><description>Background
CD36 is a glycoprotein expressed on platelets and monocytes of the blood. There are two types of CD36 deficiency, type I and type II. Individuals with type I‐deficiency do not express CD36 in any cell type and can produce the CD36 antibody, which causes pathological conditions, such as fetal/neonatal alloimmune thrombocytopenia (FNAIT) and platelet transfusion refractory (PTR), through antigenic exposure via transfusion or pregnancy.
Case presentation
We experienced a case of Philadelphia‐positive acute lymphoblastic leukaemia with PTR. In addition to the CD36 antibody, multiple‐specificity HLA antibodies were present in the patient's plasma, requiring transfusion of HLA‐compatible and CD36‐negative platelets (PC‐HLA). Since the number of donors was limited, it was necessary to set‐up a blood transfusion schedule so that hyper‐fractionated cyclophosphamide, vincristine and doxorubicin therapy (hyper‐CVAD) and ponatinib combination chemotherapy could be safely administered to achieve molecular remission. Rituximab administration resulted in reduced levels of both CD36 antibody and HLA antibody. Given the expression of CD36 on haematopoietic stem cells and the limited availability of CD36‐negative PC‐HLA, haematopoietic stem cell transplantation (HSCT) was not considered to be an option.
Conclusion
If CD36‐negative, allogeneic haematopoietic stem cell donors are unable to be found, the indications for HSCT in patients with type I CD36‐deficiency should be carefully weighed. In the present case, molecular remission has been able to be maintained to the present day after completion of a two‐year maintenance regimen.</description><identifier>ISSN: 0042-9007</identifier><identifier>EISSN: 1423-0410</identifier><identifier>DOI: 10.1111/vox.13119</identifier><identifier>PMID: 34125957</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Publishing Ltd</publisher><subject>Acute lymphoblastic leukemia ; Antibodies ; antibody‐function ; Antigen presentation ; Antigens ; Blood Platelet Disorders ; Blood transfusion ; CD36 antigen ; Chemotherapy ; Cyclophosphamide ; Doxorubicin ; Female ; Fetuses ; Genetic Diseases, Inborn ; Glycoproteins ; haematopoietic stem cell ; Hematopoietic stem cells ; Histocompatibility antigen HLA ; Humans ; Leukemia ; Monocytes ; Neonates ; patient blood management ; Philadelphia Chromosome ; Platelets ; Precursor Cell Lymphoblastic Leukemia-Lymphoma ; Pregnancy ; refractoriness (platelets) ; Remission ; Rituximab ; Stem cell transplantation ; Stem cells ; Thrombocytopenia ; Thrombocytopenia, Neonatal Alloimmune ; Transfusion ; Transplantation ; Vincristine</subject><ispartof>Vox sanguinis, 2022-01, Vol.117 (1), p.128-132</ispartof><rights>2021 International Society of Blood Transfusion.</rights><rights>Copyright Vox Sanguinis © 2022 International Society of Blood Transfusion</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3539-809f00c079d6241ecf94fec0490d23f8c9c43ce564de0e80bcaf28d9aab30cee3</citedby><cites>FETCH-LOGICAL-c3539-809f00c079d6241ecf94fec0490d23f8c9c43ce564de0e80bcaf28d9aab30cee3</cites><orcidid>0000-0002-2362-257X ; 0000-0002-6514-9127 ; 0000-0002-7619-6500</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2Fvox.13119$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Fvox.13119$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,780,784,1417,27924,27925,45574,45575</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/34125957$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Matsui, Marina</creatorcontrib><creatorcontrib>Kajiwara, Koichi</creatorcontrib><creatorcontrib>Tsukada, Masao</creatorcontrib><creatorcontrib>Iwama, Kanichi</creatorcontrib><creatorcontrib>Yamada, Kazunari</creatorcontrib><creatorcontrib>Kodo, Hideki</creatorcontrib><creatorcontrib>Seto, Katsuya</creatorcontrib><creatorcontrib>Tonami, Kaoru</creatorcontrib><creatorcontrib>Ando, Moe</creatorcontrib><creatorcontrib>Matsuhashi, Mika</creatorcontrib><creatorcontrib>Watanabe‐Okochi, Naoko</creatorcontrib><creatorcontrib>Tsuno, Nelson Hirokazu</creatorcontrib><creatorcontrib>Kozai, Yasuji</creatorcontrib><title>A case of Philadelphia chromosome‐positive acute lymphocytic leukaemia with type I CD36 deficiency</title><title>Vox sanguinis</title><addtitle>Vox Sang</addtitle><description>Background
CD36 is a glycoprotein expressed on platelets and monocytes of the blood. There are two types of CD36 deficiency, type I and type II. Individuals with type I‐deficiency do not express CD36 in any cell type and can produce the CD36 antibody, which causes pathological conditions, such as fetal/neonatal alloimmune thrombocytopenia (FNAIT) and platelet transfusion refractory (PTR), through antigenic exposure via transfusion or pregnancy.
Case presentation
We experienced a case of Philadelphia‐positive acute lymphoblastic leukaemia with PTR. In addition to the CD36 antibody, multiple‐specificity HLA antibodies were present in the patient's plasma, requiring transfusion of HLA‐compatible and CD36‐negative platelets (PC‐HLA). Since the number of donors was limited, it was necessary to set‐up a blood transfusion schedule so that hyper‐fractionated cyclophosphamide, vincristine and doxorubicin therapy (hyper‐CVAD) and ponatinib combination chemotherapy could be safely administered to achieve molecular remission. Rituximab administration resulted in reduced levels of both CD36 antibody and HLA antibody. Given the expression of CD36 on haematopoietic stem cells and the limited availability of CD36‐negative PC‐HLA, haematopoietic stem cell transplantation (HSCT) was not considered to be an option.
Conclusion
If CD36‐negative, allogeneic haematopoietic stem cell donors are unable to be found, the indications for HSCT in patients with type I CD36‐deficiency should be carefully weighed. In the present case, molecular remission has been able to be maintained to the present day after completion of a two‐year maintenance regimen.</description><subject>Acute lymphoblastic leukemia</subject><subject>Antibodies</subject><subject>antibody‐function</subject><subject>Antigen presentation</subject><subject>Antigens</subject><subject>Blood Platelet Disorders</subject><subject>Blood transfusion</subject><subject>CD36 antigen</subject><subject>Chemotherapy</subject><subject>Cyclophosphamide</subject><subject>Doxorubicin</subject><subject>Female</subject><subject>Fetuses</subject><subject>Genetic Diseases, Inborn</subject><subject>Glycoproteins</subject><subject>haematopoietic stem cell</subject><subject>Hematopoietic stem cells</subject><subject>Histocompatibility antigen HLA</subject><subject>Humans</subject><subject>Leukemia</subject><subject>Monocytes</subject><subject>Neonates</subject><subject>patient blood management</subject><subject>Philadelphia Chromosome</subject><subject>Platelets</subject><subject>Precursor Cell Lymphoblastic Leukemia-Lymphoma</subject><subject>Pregnancy</subject><subject>refractoriness (platelets)</subject><subject>Remission</subject><subject>Rituximab</subject><subject>Stem cell transplantation</subject><subject>Stem cells</subject><subject>Thrombocytopenia</subject><subject>Thrombocytopenia, Neonatal Alloimmune</subject><subject>Transfusion</subject><subject>Transplantation</subject><subject>Vincristine</subject><issn>0042-9007</issn><issn>1423-0410</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2022</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp10M1u1DAQB3ALgehSOPACyBIXOKQdf2TXPlZbPipVKgdA3CzvZKy4JOsQJy258Qg8I0-CYQsHJOYyl9_8Nfoz9lTAiShzepO-ngglhL3HVkJLVYEWcJ-tALSsLMDmiD3K-RoAjDT1Q3aktJC1rTcr1pxx9Jl4CvxdGzvfUDe00XNsx9SnnHr68e37kHKc4g1xj_NEvFv6oU24TBF5R_NnT325uI1Ty6dlIH7Bt-dqzRsKESPtcXnMHgTfZXpyt4_Zh9ev3m_fVpdXby62Z5cVqlrZyoANAAgb26ylFoTB6kAI2kIjVTBoUSukeq0bAjKwQx-kaaz3OwVIpI7Zi0PuMKYvM-XJ9TEjdZ3fU5qzk7UWSgqjdKHP_6HXaR735Tsn10UYo3Vd1MuDwjHlPFJwwxh7Py5OgPtVvSvVu9_VF_vsLnHe9dT8lX-6LuD0AG5jR8v_k9zHq0-HyJ_hN47F</recordid><startdate>202201</startdate><enddate>202201</enddate><creator>Matsui, Marina</creator><creator>Kajiwara, Koichi</creator><creator>Tsukada, Masao</creator><creator>Iwama, Kanichi</creator><creator>Yamada, Kazunari</creator><creator>Kodo, Hideki</creator><creator>Seto, Katsuya</creator><creator>Tonami, Kaoru</creator><creator>Ando, Moe</creator><creator>Matsuhashi, Mika</creator><creator>Watanabe‐Okochi, Naoko</creator><creator>Tsuno, Nelson Hirokazu</creator><creator>Kozai, Yasuji</creator><general>Blackwell Publishing Ltd</general><general>S. Karger AG</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QL</scope><scope>7T5</scope><scope>7TM</scope><scope>7U9</scope><scope>C1K</scope><scope>H94</scope><scope>K9.</scope><scope>M7N</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0002-2362-257X</orcidid><orcidid>https://orcid.org/0000-0002-6514-9127</orcidid><orcidid>https://orcid.org/0000-0002-7619-6500</orcidid></search><sort><creationdate>202201</creationdate><title>A case of Philadelphia chromosome‐positive acute lymphocytic leukaemia with type I CD36 deficiency</title><author>Matsui, Marina ; Kajiwara, Koichi ; Tsukada, Masao ; Iwama, Kanichi ; Yamada, Kazunari ; Kodo, Hideki ; Seto, Katsuya ; Tonami, Kaoru ; Ando, Moe ; Matsuhashi, Mika ; Watanabe‐Okochi, Naoko ; Tsuno, Nelson Hirokazu ; Kozai, Yasuji</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3539-809f00c079d6241ecf94fec0490d23f8c9c43ce564de0e80bcaf28d9aab30cee3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2022</creationdate><topic>Acute lymphoblastic leukemia</topic><topic>Antibodies</topic><topic>antibody‐function</topic><topic>Antigen presentation</topic><topic>Antigens</topic><topic>Blood Platelet Disorders</topic><topic>Blood transfusion</topic><topic>CD36 antigen</topic><topic>Chemotherapy</topic><topic>Cyclophosphamide</topic><topic>Doxorubicin</topic><topic>Female</topic><topic>Fetuses</topic><topic>Genetic Diseases, Inborn</topic><topic>Glycoproteins</topic><topic>haematopoietic stem cell</topic><topic>Hematopoietic stem cells</topic><topic>Histocompatibility antigen HLA</topic><topic>Humans</topic><topic>Leukemia</topic><topic>Monocytes</topic><topic>Neonates</topic><topic>patient blood management</topic><topic>Philadelphia Chromosome</topic><topic>Platelets</topic><topic>Precursor Cell Lymphoblastic Leukemia-Lymphoma</topic><topic>Pregnancy</topic><topic>refractoriness (platelets)</topic><topic>Remission</topic><topic>Rituximab</topic><topic>Stem cell transplantation</topic><topic>Stem cells</topic><topic>Thrombocytopenia</topic><topic>Thrombocytopenia, Neonatal Alloimmune</topic><topic>Transfusion</topic><topic>Transplantation</topic><topic>Vincristine</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Matsui, Marina</creatorcontrib><creatorcontrib>Kajiwara, Koichi</creatorcontrib><creatorcontrib>Tsukada, Masao</creatorcontrib><creatorcontrib>Iwama, Kanichi</creatorcontrib><creatorcontrib>Yamada, Kazunari</creatorcontrib><creatorcontrib>Kodo, Hideki</creatorcontrib><creatorcontrib>Seto, Katsuya</creatorcontrib><creatorcontrib>Tonami, Kaoru</creatorcontrib><creatorcontrib>Ando, Moe</creatorcontrib><creatorcontrib>Matsuhashi, Mika</creatorcontrib><creatorcontrib>Watanabe‐Okochi, Naoko</creatorcontrib><creatorcontrib>Tsuno, Nelson Hirokazu</creatorcontrib><creatorcontrib>Kozai, Yasuji</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Immunology Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Environmental Sciences and Pollution Management</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>MEDLINE - Academic</collection><jtitle>Vox sanguinis</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Matsui, Marina</au><au>Kajiwara, Koichi</au><au>Tsukada, Masao</au><au>Iwama, Kanichi</au><au>Yamada, Kazunari</au><au>Kodo, Hideki</au><au>Seto, Katsuya</au><au>Tonami, Kaoru</au><au>Ando, Moe</au><au>Matsuhashi, Mika</au><au>Watanabe‐Okochi, Naoko</au><au>Tsuno, Nelson Hirokazu</au><au>Kozai, Yasuji</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>A case of Philadelphia chromosome‐positive acute lymphocytic leukaemia with type I CD36 deficiency</atitle><jtitle>Vox sanguinis</jtitle><addtitle>Vox Sang</addtitle><date>2022-01</date><risdate>2022</risdate><volume>117</volume><issue>1</issue><spage>128</spage><epage>132</epage><pages>128-132</pages><issn>0042-9007</issn><eissn>1423-0410</eissn><abstract>Background
CD36 is a glycoprotein expressed on platelets and monocytes of the blood. There are two types of CD36 deficiency, type I and type II. Individuals with type I‐deficiency do not express CD36 in any cell type and can produce the CD36 antibody, which causes pathological conditions, such as fetal/neonatal alloimmune thrombocytopenia (FNAIT) and platelet transfusion refractory (PTR), through antigenic exposure via transfusion or pregnancy.
Case presentation
We experienced a case of Philadelphia‐positive acute lymphoblastic leukaemia with PTR. In addition to the CD36 antibody, multiple‐specificity HLA antibodies were present in the patient's plasma, requiring transfusion of HLA‐compatible and CD36‐negative platelets (PC‐HLA). Since the number of donors was limited, it was necessary to set‐up a blood transfusion schedule so that hyper‐fractionated cyclophosphamide, vincristine and doxorubicin therapy (hyper‐CVAD) and ponatinib combination chemotherapy could be safely administered to achieve molecular remission. Rituximab administration resulted in reduced levels of both CD36 antibody and HLA antibody. Given the expression of CD36 on haematopoietic stem cells and the limited availability of CD36‐negative PC‐HLA, haematopoietic stem cell transplantation (HSCT) was not considered to be an option.
Conclusion
If CD36‐negative, allogeneic haematopoietic stem cell donors are unable to be found, the indications for HSCT in patients with type I CD36‐deficiency should be carefully weighed. In the present case, molecular remission has been able to be maintained to the present day after completion of a two‐year maintenance regimen.</abstract><cop>Oxford, UK</cop><pub>Blackwell Publishing Ltd</pub><pmid>34125957</pmid><doi>10.1111/vox.13119</doi><tpages>5</tpages><orcidid>https://orcid.org/0000-0002-2362-257X</orcidid><orcidid>https://orcid.org/0000-0002-6514-9127</orcidid><orcidid>https://orcid.org/0000-0002-7619-6500</orcidid></addata></record> |
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| ispartof | Vox sanguinis, 2022-01, Vol.117 (1), p.128-132 |
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| source | MEDLINE; Access via Wiley Online Library |
| subjects | Acute lymphoblastic leukemia Antibodies antibody‐function Antigen presentation Antigens Blood Platelet Disorders Blood transfusion CD36 antigen Chemotherapy Cyclophosphamide Doxorubicin Female Fetuses Genetic Diseases, Inborn Glycoproteins haematopoietic stem cell Hematopoietic stem cells Histocompatibility antigen HLA Humans Leukemia Monocytes Neonates patient blood management Philadelphia Chromosome Platelets Precursor Cell Lymphoblastic Leukemia-Lymphoma Pregnancy refractoriness (platelets) Remission Rituximab Stem cell transplantation Stem cells Thrombocytopenia Thrombocytopenia, Neonatal Alloimmune Transfusion Transplantation Vincristine |
| title | A case of Philadelphia chromosome‐positive acute lymphocytic leukaemia with type I CD36 deficiency |
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