Successful allogeneic hematopoietic stem cell transplantation in a patient with type I CD36 deficiency: a case study and literature review
Background CD36-deficient individuals may produce anti-CD36 antibodies through antigenic exposure to CD36, in situations including blood transfusions. Therefore, allogeneic hematopoietic stem cell transplantation (HSCT) from CD36-positive donors to CD36-negative patients remains a challenge. Case re...
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| Published in | International journal of hematology Vol. 118; no. 5; pp. 656 - 660 |
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| Main Authors | , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
Singapore
Springer Nature Singapore
01.11.2023
Springer Nature B.V |
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| Online Access | Get full text |
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| Abstract | Background
CD36-deficient individuals may produce anti-CD36 antibodies through antigenic exposure to CD36, in situations including blood transfusions. Therefore, allogeneic hematopoietic stem cell transplantation (HSCT) from CD36-positive donors to CD36-negative patients remains a challenge.
Case report
A 64-year-old man with acute myeloid leukemia became refractory to platelet transfusions during chemotherapy. Anti-CD36 antibodies without anti-HLA antibodies were detected in serum, and the absence of CD36 expression on platelets and monocytes confirmed type I CD36 deficiency. The patient achieved complete remission, and received maintenance therapy with CD36-negative platelet transfusions. However, he relapsed soon afterward, and thus underwent peripheral blood stem cell transplantation (PBSCT) from a CD36-positive unrelated donor. The anti-CD36 antibody titer had decreased before the transplant, and the PBSCT-course was uneventful. The patient has been well without any complications associated with CD36 status mismatch.
Discussion
The few reports of allogeneic HSCT in patients with CD36 deficiency have suggested that anti-CD36 antibodies could be involved in several post-transplant complications, such as delayed platelet recovery, transfusion refractoriness, and transfusion-related acute lung injury. Our present case confirmed that stem cell transplantation from CD36-positive donors to negative patients is feasible, when it includes careful prior assessment of anti-CD36 antibody titers and interventions to attenuate them. |
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| AbstractList | CD36-deficient individuals may produce anti-CD36 antibodies through antigenic exposure to CD36, in situations including blood transfusions. Therefore, allogeneic hematopoietic stem cell transplantation (HSCT) from CD36-positive donors to CD36-negative patients remains a challenge.
A 64-year-old man with acute myeloid leukemia became refractory to platelet transfusions during chemotherapy. Anti-CD36 antibodies without anti-HLA antibodies were detected in serum, and the absence of CD36 expression on platelets and monocytes confirmed type I CD36 deficiency. The patient achieved complete remission, and received maintenance therapy with CD36-negative platelet transfusions. However, he relapsed soon afterward, and thus underwent peripheral blood stem cell transplantation (PBSCT) from a CD36-positive unrelated donor. The anti-CD36 antibody titer had decreased before the transplant, and the PBSCT-course was uneventful. The patient has been well without any complications associated with CD36 status mismatch.
The few reports of allogeneic HSCT in patients with CD36 deficiency have suggested that anti-CD36 antibodies could be involved in several post-transplant complications, such as delayed platelet recovery, transfusion refractoriness, and transfusion-related acute lung injury. Our present case confirmed that stem cell transplantation from CD36-positive donors to negative patients is feasible, when it includes careful prior assessment of anti-CD36 antibody titers and interventions to attenuate them. Background CD36-deficient individuals may produce anti-CD36 antibodies through antigenic exposure to CD36, in situations including blood transfusions. Therefore, allogeneic hematopoietic stem cell transplantation (HSCT) from CD36-positive donors to CD36-negative patients remains a challenge. Case report A 64-year-old man with acute myeloid leukemia became refractory to platelet transfusions during chemotherapy. Anti-CD36 antibodies without anti-HLA antibodies were detected in serum, and the absence of CD36 expression on platelets and monocytes confirmed type I CD36 deficiency. The patient achieved complete remission, and received maintenance therapy with CD36-negative platelet transfusions. However, he relapsed soon afterward, and thus underwent peripheral blood stem cell transplantation (PBSCT) from a CD36-positive unrelated donor. The anti-CD36 antibody titer had decreased before the transplant, and the PBSCT-course was uneventful. The patient has been well without any complications associated with CD36 status mismatch. Discussion The few reports of allogeneic HSCT in patients with CD36 deficiency have suggested that anti-CD36 antibodies could be involved in several post-transplant complications, such as delayed platelet recovery, transfusion refractoriness, and transfusion-related acute lung injury. Our present case confirmed that stem cell transplantation from CD36-positive donors to negative patients is feasible, when it includes careful prior assessment of anti-CD36 antibody titers and interventions to attenuate them. CD36-deficient individuals may produce anti-CD36 antibodies through antigenic exposure to CD36, in situations including blood transfusions. Therefore, allogeneic hematopoietic stem cell transplantation (HSCT) from CD36-positive donors to CD36-negative patients remains a challenge.BACKGROUNDCD36-deficient individuals may produce anti-CD36 antibodies through antigenic exposure to CD36, in situations including blood transfusions. Therefore, allogeneic hematopoietic stem cell transplantation (HSCT) from CD36-positive donors to CD36-negative patients remains a challenge.A 64-year-old man with acute myeloid leukemia became refractory to platelet transfusions during chemotherapy. Anti-CD36 antibodies without anti-HLA antibodies were detected in serum, and the absence of CD36 expression on platelets and monocytes confirmed type I CD36 deficiency. The patient achieved complete remission, and received maintenance therapy with CD36-negative platelet transfusions. However, he relapsed soon afterward, and thus underwent peripheral blood stem cell transplantation (PBSCT) from a CD36-positive unrelated donor. The anti-CD36 antibody titer had decreased before the transplant, and the PBSCT-course was uneventful. The patient has been well without any complications associated with CD36 status mismatch.CASE REPORTA 64-year-old man with acute myeloid leukemia became refractory to platelet transfusions during chemotherapy. Anti-CD36 antibodies without anti-HLA antibodies were detected in serum, and the absence of CD36 expression on platelets and monocytes confirmed type I CD36 deficiency. The patient achieved complete remission, and received maintenance therapy with CD36-negative platelet transfusions. However, he relapsed soon afterward, and thus underwent peripheral blood stem cell transplantation (PBSCT) from a CD36-positive unrelated donor. The anti-CD36 antibody titer had decreased before the transplant, and the PBSCT-course was uneventful. The patient has been well without any complications associated with CD36 status mismatch.The few reports of allogeneic HSCT in patients with CD36 deficiency have suggested that anti-CD36 antibodies could be involved in several post-transplant complications, such as delayed platelet recovery, transfusion refractoriness, and transfusion-related acute lung injury. Our present case confirmed that stem cell transplantation from CD36-positive donors to negative patients is feasible, when it includes careful prior assessment of anti-CD36 antibody titers and interventions to attenuate them.DISCUSSIONThe few reports of allogeneic HSCT in patients with CD36 deficiency have suggested that anti-CD36 antibodies could be involved in several post-transplant complications, such as delayed platelet recovery, transfusion refractoriness, and transfusion-related acute lung injury. Our present case confirmed that stem cell transplantation from CD36-positive donors to negative patients is feasible, when it includes careful prior assessment of anti-CD36 antibody titers and interventions to attenuate them. BackgroundCD36-deficient individuals may produce anti-CD36 antibodies through antigenic exposure to CD36, in situations including blood transfusions. Therefore, allogeneic hematopoietic stem cell transplantation (HSCT) from CD36-positive donors to CD36-negative patients remains a challenge.Case reportA 64-year-old man with acute myeloid leukemia became refractory to platelet transfusions during chemotherapy. Anti-CD36 antibodies without anti-HLA antibodies were detected in serum, and the absence of CD36 expression on platelets and monocytes confirmed type I CD36 deficiency. The patient achieved complete remission, and received maintenance therapy with CD36-negative platelet transfusions. However, he relapsed soon afterward, and thus underwent peripheral blood stem cell transplantation (PBSCT) from a CD36-positive unrelated donor. The anti-CD36 antibody titer had decreased before the transplant, and the PBSCT-course was uneventful. The patient has been well without any complications associated with CD36 status mismatch.DiscussionThe few reports of allogeneic HSCT in patients with CD36 deficiency have suggested that anti-CD36 antibodies could be involved in several post-transplant complications, such as delayed platelet recovery, transfusion refractoriness, and transfusion-related acute lung injury. Our present case confirmed that stem cell transplantation from CD36-positive donors to negative patients is feasible, when it includes careful prior assessment of anti-CD36 antibody titers and interventions to attenuate them. |
| Author | Kobayashi, Hironori Ueki, Toshimitsu Takahashi, Daisuke Tsuno, Nelson Hirokazu Shishido, Tsutomu Kobayashi, Hikaru Ishikawa, Ryuto Koyama, Daisuke Sumi, Masahiko Okuyama, Shuhei |
| Author_xml | – sequence: 1 givenname: Shuhei orcidid: 0000-0001-6948-2341 surname: Okuyama fullname: Okuyama, Shuhei email: okuyama442@gmail.com organization: Department of Hematology, Nagano Red Cross Hospital, Department of Hematology, Yamagata Prefectural Central Hospital – sequence: 2 givenname: Masahiko surname: Sumi fullname: Sumi, Masahiko organization: Department of Hematology, Nagano Red Cross Hospital – sequence: 3 givenname: Ryuto surname: Ishikawa fullname: Ishikawa, Ryuto organization: Department of Hematology, Nagano Red Cross Hospital – sequence: 4 givenname: Tsutomu surname: Shishido fullname: Shishido, Tsutomu organization: Department of Hematology, Nagano Red Cross Hospital – sequence: 5 givenname: Daisuke surname: Koyama fullname: Koyama, Daisuke organization: Department of Hematology, Nagano Red Cross Hospital – sequence: 6 givenname: Toshimitsu surname: Ueki fullname: Ueki, Toshimitsu organization: Department of Hematology, Nagano Red Cross Hospital – sequence: 7 givenname: Daisuke surname: Takahashi fullname: Takahashi, Daisuke organization: Central Blood Institute, Blood Service Headquarters, Japanese Red Cross Society – sequence: 8 givenname: Hironori surname: Kobayashi fullname: Kobayashi, Hironori organization: Laboratory Department, Japanese Red Cross Kanto-Koshinetsu Block Blood Center – sequence: 9 givenname: Hikaru surname: Kobayashi fullname: Kobayashi, Hikaru organization: Department of Hematology, Nagano Red Cross Hospital – sequence: 10 givenname: Nelson Hirokazu surname: Tsuno fullname: Tsuno, Nelson Hirokazu organization: Laboratory Department, Japanese Red Cross Kanto-Koshinetsu Block Blood Center |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/37490235$$D View this record in MEDLINE/PubMed |
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| Cites_doi | 10.1038/bmt.2014.331 10.1172/jci.insight.165142 10.1046/j.1537-2995.1995.35996029165.x 10.5551/jat.10603 10.1182/blood-2016-03-643544 10.1038/bmt.2011.131 10.1182/blood.V80.5.1105.1105 10.21307/immunohematology-2020-028 10.1182/blood.V76.9.1698.1698 10.1111/j.1423-0410.2008.01095.x 10.2183/pjab.66.41 10.1182/blood.V83.2.392.392 10.1182/blood.V75.3.684.684 10.1016/j.bbmt.2016.06.017 10.1046/j.1537-2995.1999.39080873.x 10.1182/bloodadvances.2021004862 10.1016/j.exphem.2007.04.003 10.1111/vox.13119 10.1038/emm.2014.38 10.1016/S2352-3026(22)00296-4 10.1182/blood-2016-05-716480 |
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| Keywords | CD36 deficiency Platelet transfusion refractoriness Patient blood management Anti-CD36 Hematopoietic stem cell |
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CD36-deficient individuals may produce anti-CD36 antibodies through antigenic exposure to CD36, in situations including blood transfusions.... CD36-deficient individuals may produce anti-CD36 antibodies through antigenic exposure to CD36, in situations including blood transfusions. Therefore,... BackgroundCD36-deficient individuals may produce anti-CD36 antibodies through antigenic exposure to CD36, in situations including blood transfusions.... |
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| SubjectTerms | Acute myeloid leukemia Antibodies Antigens Blood platelets Blood transfusion Bone marrow transplantation Case Report CD36 antigen Chemotherapy Complications Hematology Hematopoietic stem cells Histocompatibility antigen HLA Leukemia Literature reviews Medicine Medicine & Public Health Monocytes Oncology Patients Peripheral blood Platelets Remission Stem cell transplantation Stem cells Thermal resistance Transfusion Transplantation |
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| Title | Successful allogeneic hematopoietic stem cell transplantation in a patient with type I CD36 deficiency: a case study and literature review |
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