{"title":"[Analysis of anti-SARS-CoV-2 IgG antibody titers after mRNA booster vaccination in patients with nonmalignant hematological disorders].","authors":"Masao Hagihara, Tomiyuki Sugi, Hiroyoshi Hayashi, Shiori Nakashima, Shin Ohara, Yui Imai, Hirofumi Nakano, Tomoyuki Uchida, Morihiro Inoue, Keiko Mitamura","doi":"10.11406/rinketsu.64.133","DOIUrl":"https://doi.org/10.11406/rinketsu.64.133","url":null,"abstract":"<p><p>In our facility, anti-SARS-CoV-2 mRNA vaccines were given to 21 patients, including 8 with aplastic anemia (AA), 3 with pure red cell aplasia (PRCA), and 10 with immune thrombocytopenic purpura (ITP), and IgG antibody titers were assessed one month after vaccinations. After receiving both a second vaccine and a booster shot, all patients with AA/PRCA treated with cyclosporine A aside from one, had IgG titers that were lower than the median levels of healthy controls. Even if prednisolone (PSL) doses did not go over 10 mg/day, ITP patients receiving PSL therapy were unable to achieve adequate levels of IgG after booster immunizations.</p>","PeriodicalId":6352,"journal":{"name":"[Rinsho ketsueki] The Japanese journal of clinical hematology","volume":"64 2","pages":"133-136"},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9220909","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"","authors":"","doi":"10.11406/rinketsu.64.155","DOIUrl":"https://doi.org/10.11406/rinketsu.64.155","url":null,"abstract":"","PeriodicalId":6352,"journal":{"name":"[Rinsho ketsueki] The Japanese journal of clinical hematology","volume":"64 2","pages":"155-156"},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9245144","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"[Thrombotic microangiopathy with gastrointestinal hemorrhage during carfilzomib therapy for multiple myeloma].","authors":"Shuhei Matsumoto, Hiromichi Takahashi, Takashi Hamada, Katsuhiro Miura, Masaru Nakagwa, Kazuya Kurihara, Toshihide Endo, Takashi Koike, Kazuhide Iizuka, Noriyoshi Iriyama, Tomohiro Nakayama, Yoshihiro Hatta, Hideki Nakamura","doi":"10.11406/rinketsu.64.255","DOIUrl":"https://doi.org/10.11406/rinketsu.64.255","url":null,"abstract":"<p><p>A 70-year-old woman was admitted to the hospital with loss of appetite and melena. She was diagnosed with multiple myeloma 7 years ago and had been on carfilzomib, lenalidomide, and dexamethasone (KRd) therapy for a month because her disease had a relapsed/refractory. On admission, her laboratory tests revealed hemolytic anemia with schizocytes, thrombocytopenia, and acute renal dysfunction. TMA (thrombotic microangiography) caused by carfilzomib was suspected. The possibility of thrombotic thrombocytopenia was considered, and steroid pulse therapy was initiated. Her condition improved significantly after she stopped taking carfilzomib, plasma exchange, hemodiafiltration, steroid pulse therapy, and abstaining from food. The previously reported cases of carfilzomib-induced TMA included fever, gastrointestinal symptoms (nausea/vomiting, diarrhea), and acute renal disorders (lower extremity edema, decreasing urine output). As far as we know, this is the first case of carfilzomib-induced TMA with bleeding as the first symptom.</p>","PeriodicalId":6352,"journal":{"name":"[Rinsho ketsueki] The Japanese journal of clinical hematology","volume":"64 4","pages":"255-259"},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9384944","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"[Hematological immune-related adverse events of immune checkpoint inhibitors and their management].","authors":"Yoshiki Akatsuka","doi":"10.11406/rinketsu.64.782","DOIUrl":"https://doi.org/10.11406/rinketsu.64.782","url":null,"abstract":"Immune checkpoints suppress inappropriate immune responses to self-molecules or cells. Cytotoxic T-lymphocyte-associated protein 4 (CTLA-4) and programmed cell death protein 1 (PD-1) expressed in T cells are representative molecules involved in the immune checkpoint system. The recent advent of immune checkpoint inhibitors (ICIs) has drastically changed cancer immunotherapy because a substantial proportion of patients with advanced cancers have responded to ICIs and some of them have been cured. This benefit is due to T-cell rescue from immune suppression in their tumor microenvironment by blocking cluster of differentiation 80/CTLA-4 and PD-L1/PD-1 interactions. However, blocking these interactions also liberates T cells that are reactive to self-antigens from tolerance, resulting in the occurrence of autoimmune diseases, that is, immune-related adverse events. Although the primary target organs are the lungs, gastrointestinal tract, and endocrine glands, hematopoietic cells are also affected in 0.5-3% of patients, potentially resulting in anemia or thrombocytopenia. Because hematopoietic system homeostasis is critical to maintaining life support, the occurrence of grade 3-4 irAEs in the hematopoietic system is directly life-threatening. Herein, we review the relationship between ICIs and toxicities in patients with cancer and describe the characteristics and management strategies for hematological immune-related adverse events.","PeriodicalId":6352,"journal":{"name":"[Rinsho ketsueki] The Japanese journal of clinical hematology","volume":"64 8","pages":"782-790"},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10181328","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"[Diagnosis and management of EBV-positive lymphoproliferative disorders].","authors":"Ayako Arai","doi":"10.11406/rinketsu.64.764","DOIUrl":"https://doi.org/10.11406/rinketsu.64.764","url":null,"abstract":"<p><p>Epstein-Barr virus (EBV) has the ability to immortalize not only B cells but also T and natural killer (NK) cells. The virus may also contribute to the onset of EBV-positive lymphoproliferative disorders (EBV-LPDs) by inducing the introduction of gene mutations. It is known that B cell EBV-LPDs (B-EBV-LPDs) develop with preexisting immunodeficiency, but the onset mechanism of T cell and NK cell EBV-LPDs (T-EBV-LPDs and NK-EBV-LPDs), also known as chronic active EBV disease and associated diseases, is unclear. The diagnosis of both EBV-LPDs requires the quantitative examination of EBV-DNA in the peripheral blood. Eliminating the cause of immunodeficiency or administering rituximab is effective in treating B-EBV-LPDs, but some B-EBV-LPDs and T-EBV-LPDs/NK-EBV-LPDs are resistant to pharmacotherapy. Therefore, further research is needed to explicate the pathophysiology of EBV-LPDs and develop a drug for its treatment.</p>","PeriodicalId":6352,"journal":{"name":"[Rinsho ketsueki] The Japanese journal of clinical hematology","volume":"64 8","pages":"764-771"},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10183269","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"[Acute myeloid leukemia with t (8;21) translocation diagnosed at 21 weeks of gestation resulting in full-term delivery without chemotherapy].","authors":"Yuka Norihama, Moe Nomura, Yuki Oda, Yuki Kasuya, Tomomi Takei, Kota Sato, Mizuki Ogura, Taku Kikuchi, Yu Abe, Tadao Ishida, Yasuyo Kasai, Nobuhiro Tsukada","doi":"10.11406/rinketsu.64.731","DOIUrl":"https://doi.org/10.11406/rinketsu.64.731","url":null,"abstract":"<p><p>A 28-year-old female was diagnosed with acute myeloid leukemia (AML) due to t (8;21) (q22;q22.1); RUNX1-RUNX1T1 at 21 weeks of gestation. Because no adverse prognostic genetic mutations were discovered, we decided to continue the pregnancy without chemotherapy for as long as possible. After careful monitoring with blood tests every two weeks, the disease did not progress until full-term, and a cesarean section was performed at 39 weeks of gestation. About two months after delivery, blasts in the peripheral blood increased to 46.5%, and myeloblasts in the bone marrow increased to 21.2%. The patient received idarubicin and cytarabine induction therapy, followed by three cycles of high-dose cytarabine consolidation therapy, and complete remission was maintained. Here we report a rare case who could avoid chemotherapy until full-term labor without progression of AML.</p>","PeriodicalId":6352,"journal":{"name":"[Rinsho ketsueki] The Japanese journal of clinical hematology","volume":"64 8","pages":"731-734"},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10236203","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"[Primary mediastinal large B-cell lymphoma, spindle cell variant demonstrating atypical image findings].","authors":"Sayaka Ohno, Hiroaki Tanaka, Kiyohito Hayashi, Ryo Shimizu, Hideki Kuwano, Yoshio Suzuki","doi":"10.11406/rinketsu.64.30","DOIUrl":"https://doi.org/10.11406/rinketsu.64.30","url":null,"abstract":"<p><p>The patient was a 40-year-old woman referred to our hospital after an anterior mediastinal tumor was detected. Imaging findings revealed a tumor with irregular margins and a marked tendency to infiltrate, with some calcification. Rather than malignant lymphoma, thymic carcinoma or high-grade invasive thymoma was suspected. Endobronchial ultrasound-guided transbronchial needle aspiration biopsy and computed tomography-guided needle biopsy were performed, but no diagnosis was made. Mediastinal tumor biopsy by video-assisted thoracic surgery led to the diagnosis of primary mediastinal large B-cell lymphoma, spindle cell variant. A retrospective examination of the needle biopsy specimens revealed that some tissues considered to have been crushed were composed of spindle-shaped lymphoma cells. This study indicates that it is crucial to note that there is a subtype of primary mediastinal large B-cell lymphoma with an unusual pathological morphology.</p>","PeriodicalId":6352,"journal":{"name":"[Rinsho ketsueki] The Japanese journal of clinical hematology","volume":"64 1","pages":"30-34"},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10764161","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"[Classic Hodgkin lymphoma].","authors":"Shinichi Makita","doi":"10.11406/rinketsu.64.504","DOIUrl":"https://doi.org/10.11406/rinketsu.64.504","url":null,"abstract":"<p><p>Classic Hodgkin lymphoma (cHL) is one of the common subtypes of malignant lymphoma in Western countries. Although patients with HL showed unsatisfactory results in the 1960s, the clinical development in radiotherapy and chemotherapy based on several clinical trials over the last 50 years has made cHL a curable disease with a favorable outcome. As a result, late-onset treatment-related toxicities such as second primary malignancies and cardiac events are thought to be a significant issue especially in early-stage patients. To minimize the toxic effects while maximizing the antitumor efficacy, several clinical trials to evaluate response-adapted strategies using interim PET scans and novel agents, such as brentuximab vedotin (BV) and/or immune checkpoint inhibitor (ICI) are currently underway. In this review, the author summarizes currently available data on PET-adapted and BV and/or ICI-containing therapies for untreated cHL, and discusses their future prospects in cHL treatment.</p>","PeriodicalId":6352,"journal":{"name":"[Rinsho ketsueki] The Japanese journal of clinical hematology","volume":"64 6","pages":"504-513"},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9803680","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"","authors":"","doi":"10.11406/rinketsu.64.698","DOIUrl":"https://doi.org/10.11406/rinketsu.64.698","url":null,"abstract":"","PeriodicalId":6352,"journal":{"name":"[Rinsho ketsueki] The Japanese journal of clinical hematology","volume":"64 7","pages":"698-705"},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10046256","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"","authors":"","doi":"10.11406/rinketsu.64.816","DOIUrl":"https://doi.org/10.11406/rinketsu.64.816","url":null,"abstract":"","PeriodicalId":6352,"journal":{"name":"[Rinsho ketsueki] The Japanese journal of clinical hematology","volume":"64 8","pages":"816-825"},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10183278","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}