Background and Clinical Significance: Mantle cell lymphoma (MCL) frequently involves bone marrow, gastrointestinal tract, and hepatosplenomegaly, whereas pleural effusions are uncommon. Cases requiring invasive mechanical ventilation and thoracic drainage are rare. We report a case of MCL with persistent massive pleural effusions requiring invasive mechanical ventilation and bilateral continuous thoracic drainage. Case Presentation: A 71-year-old woman presented with dyspnea and was found to have bilateral pleural effusions and generalized lymphadenopathy. Shortly after admission, she developed acute respiratory failure due to pleural effusions and required invasive mechanical ventilation. Right-sided continuous thoracic drainage was initiated. Thereafter, more than 1 L of pleural fluid was drained each day. Flow cytometry of the pleural fluid showed CD5-positive B cells with kappa light-chain restriction. Bone marrow examination revealed abnormal lymphocyte infiltration. Cervical lymph node biopsy demonstrated diffuse proliferation of medium-sized, abnormal B lymphocytes with an immunophenotype of CD5+, CD19+, CD20+, cyclin D1+, SOX11+, and κ+, with a Ki-67 index of 20%, confirming MCL, stage IV. Immunochemotherapy with rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) was commenced under mechanical ventilation. Shortly thereafter, left-sided continuous thoracic drainage was also initiated. However, in response to immunochemotherapy, the bilateral pleural effusions gradually subsided, enabling extubation, and there was no reaccumulation after removal of both chest tubes. Furthermore, generalized lymphadenopathy regressed, and bone marrow examination revealed resolution of lymphoma infiltration, resulting in complete remission. Conclusions: De novo MCL complicated by persistent massive pleural effusions requiring invasive mechanical ventilation and bilateral continuous thoracic drainage is rare. A thorough diagnostic workup followed by prompt initiation of immunochemotherapy can arrest pleural output, enable extubation, and be lifesaving. Clinicians should recognize that MCL rarely presents with persistent massive pleural effusions.

The KMT2A gene is frequently altered in acute myeloid leukemia (AML). KMT2A abnormalities include partial tandem duplication (PTD), single-nucleotide variants (SNVs), and chromosomal rearrangements such as t(9;11)(p21.3;q23.3) and t(v;11q23.3). However, with the widespread adoption of next-generation sequencing (NGS), PTD has been assessed less frequently. We evaluated the clinical features and prognostic impact of PTD and other KMT2A abnormalities. We analyzed the KMT2A abnormalities and coexisting genetic alterations in 585 patients with de novo AML diagnosed across 25 institutions (1991–2020). Using bone marrow and/or peripheral blood samples, we identified PTD by targeted polymerase chain reaction-based assay, chromosomal rearrangements by karyotyping, and SNVs and other genetic alterations by targeted NGS. KMT2A abnormalities were detected in 18.3

We report the case of a 76-year-old man with follicular lymphoma who developed cancer-associated thrombosis (CAT) presenting as multiple brain infarctions during complete remission (CR). After the fourth cycle of R-CHOP (rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisolone) and pegfilgrastim, the patient presented with dysarthria and right upper-limb paresis. Brain magnetic resonance imaging demonstrated multiple brain infarctions with a positive three-territory sign, specific for cancer-associated brain infarctions. Laboratory tests revealed leukocytosis and thrombocytopenia. Whole-body computed tomography demonstrated CR without thrombosis. Anticoagulation with unfractionated heparin, followed by apixaban, resulted in neurological improvements. The patient was discharged without bleeding or any neurological sequelae. This case highlights that CAT can occur even in indolent lymphoma during CR and that anticoagulation is effective and safe despite the presence of thrombocytopenia.

Transplant-associated thrombotic microangiopathy (TA-TMA) generally occurs after allogeneic hematopoietic stem cell transplantation (HSCT) and has a high mortality rate. However, TA-TMA after autologous HSCT is rare. In particular, there are almost no accurate reports of TA-TMA after autologous HSCT in adults. Furthermore, there are no reports of such patients being treated with complement-targeting agents, including eculizumab. We report the first adult case of TA-TMA after autologous HSCT treated with eculizumab. A 66-year-old woman in complete remission after the second relapse of follicular lymphoma received autologous HSCT following the MEAM regimen (ranimustine [MCNU], etoposide, cytarabine [Ara-C], and melphalan). Trilineage engraftment was confirmed. However, she developed new-onset hypertension, hemolytic anemia, thrombocytopenia, and renal failure. The screening results were notable for normal coagulation, normal ADAMTS13 activity and inhibitor levels, and negative direct and indirect Coombs tests. No variants appeared in complement regulatory genes such as CFH, CFB, CFHR5, CFI, CD46, C3, THBD, and DGKE. In addition, all other microbiological and autoimmune screening tests were negative. Based on comprehensive diagnostic findings and the onset within 100 days post-HSCT, TA-TMA was diagnosed. She also developed acute respiratory failure requiring >15 L/min of oxygen. Transthoracic echocardiography revealed pulmonary hypertension (PH) and right-sided heart failure (RHF) as complications of TA-TMA. Following the administration of eculizumab, clinical improvement was observed. In conclusion, TA-TMA after first-time autologous HSCT in adults is extremely rare but can occur. Even with serious complications such as PH and RHF, TA-TMA after autologous HSCT may improve with early diagnosis and prompt initiation of complement-targeting agents, such as eculizumab. These findings suggest that complement inhibition may play a critical therapeutic role even in patients with cardiopulmonary complications and raise the possibility that the prognosis of TA-TMA after autologous HSCT may be more favorable than previously reported in allogeneic HSCT, with a lower mortality rate.

We investigated whether reduced intensity-chemotherapy (IC) is associated with decreased toxicity and longer overall survival (OS) in elderly AML patients. Age-dependent dose-reduced IC was administered to 110 AML patients between 2004 and 2021. We assessed myelosuppressive toxicity, clinical efficacy, and safety of our regimen using the depth index (D-index). Patients of 66–79 years of age (younger elderly [YE], n = 52) and ≥ 80 years (older elderly [OE], n = 19) were compared to a control group of patients of ≤ 65 years of age (n = 39). Although no significant differences were observed in the number of days with neutrophil count < 500/µl, the D-index, or the onset of sepsis among the groups, OS significantly differed (median OS: control, 578 days [317 days-NA]; YE, 281 days [158–515 days]; OE, 185 days [72–373 days]; p = 0.0001). IC for elderly AML patients achieved negative treatment outcomes despite a reduction in myelosuppressive toxicity, with no data beyond a median OS of 14.7 months for Azacytidine + Venetoclax therapy in a phase 3 VIALE-A trial. Although the findings were negative, the present results provide insights into appropriate IC regimens for elderly AML patients in the future.

Nucleophosmin1 (NPM1) mutations are the most frequently detected gene mutations in acute myeloid leukemia (AML) and are considered a favorable prognostic factor. We retrospectively analyzed the prognosis of 605 Japanese patients with de novo AML, including 174 patients with NPM1-mutated AML. Although patients with NPM1-mutated AML showed a high remission rate, this was not a favorable prognostic factor for overall survival (OS); this is contrary to generally accepted guidelines. Comprehensive gene mutation analysis showed that mutations in codon R882 of DNA methyltransferase 3A (DNMT3AR882 mutations) were a strong predicative factor indicating poor prognosis in all AML (p < 0.0001) and NPM1-mutated AML cases (p = 0.0020). Furthermore, multivariate analysis of all AML cases showed that DNMT3AR882 mutations and the co-occurrence of internal tandem duplication in FMS-like tyrosine kinase 3 (FLT3-ITD), NPM1 mutations, and DNMT3AR882 mutations (triple mutations) were independent factors predicting a poor prognosis related to OS, with NPM1 mutations being an independent factor for a favorable prognosis (hazard ratios: DNMT3AR882 mutations, 1.946; triple mutations, 1.992, NPM1 mutations, 0.548). Considering the effects of DNMT3AR882 mutations and triple mutations on prognosis and according to the classification of NPM1-mutated AML into three risk groups based on DNMT3AR882 /FLT3-ITD genotypes, we achieved the improved stratification of prognosis (p < 0.0001). We showed that DNMT3AR882 mutations are an independent factor for poor prognosis; moreover, when confounding factors that include DNMT3AR882 mutations were excluded, NPM1 mutations were a favorable prognostic factor. This revealed that ethnological prognostic discrepancies in NPM1 mutations might be corrected through prognostic stratification based on the DNMT3A status.

Mutations of CCAAT/enhancer-binding protein alpha (CEBPAmu) are found in 10% to 15% of de novo acute myeloid leukemia (AML) cases. Double-mutated CEBPA (CEBPAdm) is associated with a favorable prognosis; however, single-mutated CEBPA (CEBPAsm) does not seem to improve prognosis. We investigated CEBPAmu for prognosis in 1028 patients with AML, registered in the Multi-center Collaborative Program for Gene Sequencing of Japanese AML. It was found that CEBPAmu in the basic leucine zipper domain (bZIP) was strongly associated with a favorable prognosis, but CEBPAmu out of the bZIP domain was not. The presence of CEBPAmu in bZIP was a strong indicator of a higher chance of achieving complete remission (P < .001), better overall survival (OS; P < .001) and a lower risk of relapse (P < .001). The prognostic significance of CEBPAmu in bZIP was also observed in the subgroup with CEBPAsm (all patients: OS, P = .008; the cumulative incidence of relapse, P = .063; patients aged ≤70 years and with intermediate-risk karyotype: OS, P = .008; cumulative incidence of relapse, P = .026). Multivariate analysis of 744 patients aged ≤70 years showed that CEBPAmu in bZIP was the most potent predictor of OS (hazard ratio, 0.3287; P < .001). CEBPAdm was validated as a cofounding factor, which was overlapping with CEBPAmu in bZIP. In summary, these findings indicate that CEBPAmu in bZIP is a potent marker for AML prognosis. It holds potential in the refinement of treatment stratification and the development of targeted therapeutic approaches in CEBPA-mutated AML.

A 61-year-old man presented with a 3-days' history of fever and headache. On admission, his body temperature was 40°C, pulse rate was 99/min, and respiratory rate was 25/min. Serum CRP was elevated, and chest X-ray showed an opacity in the left upper lung field. Under the suspected diagnosis of community-acquired pneumonia, the patient was initiated on treatment with ampicillin/sulbactam, and oxygen supplementation via a nasal cannula at 2L/min. A review of the history revealed that his current occupation was maintenance of grease traps, which are chambers for removing grease from food waste before it enters the sewer pipe. Four days before onset of his symptoms, he had worked on a very dirty restaurant grease trap while wearing a poorly equipped face mask. Legionnaires' disease was suspected, and urinary antigen testing revealed a positive result. Sputum culture and PCR were also positive for Legionella pneumophila serogroup 1, the most common causative Legionella genus of acute pneumonic illness. The antibiotic was switched to intravenous levofloxacin at 500mg/day on day 2 of admission, and the patient's symptoms improved.

Recent studies have reported that measurable residual disease (MRD) analysis using NPM1 mutations helps determine whether allogeneic hematopoietic stem cell transplantation (allo-HSCT) is indicated in acute myeloid leukemia (AML) patients. However, the optimal timing and cutoff value for measuring MRD using genomic DNA remain undetermined. This study aimed to investigate the optimal timing and cutoff value to ascertain the value of NPM1 mutation in MRD assessment. NPM1-mutated MRD was quantified by real-time polymerase chain reaction of bone marrow samples from 56 patients with NPM1-positive AML who achieved hematological remission. The area under the receiver-operating characteristic curve was greatest when MRD was assessed after two courses of post-remission therapy with a cutoff value of 0.010% (specificity, 68.4%; sensitivity, 87.0%). Patients whose MRD was below the cutoff value throughout the course of treatment had significantly better overall survival and relapse-free survival rates. Of the 33 patients who did not undergo transplantation during the first remission, all of the 11 who were never MRD-negative at any point experienced a relapse. Evaluating MRD with a cutoff value of 0.010% after two courses of post-remission therapy helps predict prognosis and determine the indication for allo-HSCT.

The development of myeloid leukocytosis in leukemia patients during antileukemic treatment requires a differential diagnosis between myeloid leukemoid reaction and leukemia progression. We herein report the case of an 80-year-old Japanese man with chronic myelomonocytic leukemia (CMML) who developed marked myeloid leukocytosis (36.3 × 109/L) with 32.5

Herein, we report the findings of a 79-year-old male patient who presented with multiple extramedullary plasmacytomas following a relapse of primary plasma cell leukemia. He developed thrombotic microangiopathy (TMA) while receiving carfilzomib, lenalidomide, and dexamethasone (KLd) therapy. He was diagnosed with plasma cell leukemia 3 years ago; he demonstrated a very good partial response (VGPR) after undergoing two regimens, including either bortezomib or lenalidomide, and he had been followed up without any other treatment due to complications of infection. Following relapse, KLd was initiated. On day 7 of KLd, TMA developed; therefore, the treatment was discontinued. The TMA improved only with the discontinuation of KLd. A reduced dose of KLd was readministered; the TMA did not relapse. He demonstrated VGPR after three courses of reduced-KLd; he has since remained in remission through ten courses. Therefore, carfilzomib therapy may be useful in relapsing and refractory cases. Drug-induced TMA has been reported to be caused by either immune-mediated or dose-dependent toxicity mechanisms. In patients who develop dose-dependent TMA with carfilzomib, dose reduction could be considered in cases showing an effective response to the treatment.

Background: Nucleophosmin 1 (NPM1) mutations are considered a favorable factor of acute myeloid leukemia (AML). However, their clinical significance in non-European regions remains unclear. DNA methyltransferase 3A (DNMT3A) mutations have been reported as a factor for poor prognosis in many cohort analyses. However, they were excluded among major prognostic factors even in the European Leukemia Net 2017 (ELN2017) classification. In this study, we analyzed the effects of NPM1 and concurrent mutations, particularly DNMT3A mutations, on prognosis. Methods: All patients in this analysis were enrolled and selected by the gene sequencing of Japanese AML (GS-JAML) conducted by Nippon Medical School. We targeted only patients aged 70 years or younger who were diagnosed after 2010 and who received standard induction therapy consisting of 7 days of standard-dose cytarabine (100-200 mg/m2 continuous infusion) and 3 days of an anthracycline antibiotic infusion (idarubicin 12 mg/m2 or daunorubicin 60-90 mg/m2). Mutation screening were performed with target-captured sequencing for the AML gene panel. We also conducted agarose gel electrophoresis for the FMS-like tyrosine kinase 3 (FLT3-ITD) mutations and used the Sanger method to screen for CEBPA and NPM1 mutations. This study was reviewed and approved by the Human Subjects Institutional Review Board (project approval number 29-07-783) of the Nippon Medical School (Tokyo, Japan). Informed consent was obtained in accordance with the Declaration of Helsinki from all participants. Results: We retrospectively analyzed the prognosis in 605 Japanese patients with de novo AML, including 174 patients with NPM1-mutated, 125 patients with DNMT3A-mutated and 127 patients with FLT3-ITD mutated AML. NPM1 mutation was not a prognostic factor either overall or in subgroups based on NPM1/tandem duplication in FLT3-ITD genotypes. Comprehensive gene mutation analysis showed that mutations in codon R882 of DNMT3A(DNMT3AR882) were a strong factor of poor prognosis for AML overall and NPM1-mutated AML. Furthermore, multivariate analysis of all AML showed that DNMT3AR882 mutations and the cooccurrence of FLT3-ITD, NPM1 mutations, and DNMT3AR882 mutations (triple mutation) were independent factors for poor prognosis related to overall survival, with NPM1 mutations being an independent factor for favorable prognosis (hazard ratio: DNMT3AR882 mutations, 1.946; triple mutation, 1.992, NPM1 mutations, 0.548). Furthermore, we evaluated the prognostic impacts of DNMT3AR882 and triple mutation and demonstrated that NPM1-mutated AML patients could be more clearly stratified into three risk groups based on DNMT3AR882/FLT3-ITD genotypes than the ELN 2017 classification. Conclusion: Our study showed that the addition of DNMT3AR882 mutations to existing prognostic models allowed for further stratification of NPM1-mutated AML. This new prognostic model might provide important clinical guidance. Figure 1View largeDownload PPTFigure 1View largeDownload PPT Close modal

The measurement of corrected count increment at 1-h post-transfusion (CCI-1 h) of platelet concentrate (PC) transfusion is recommended, but in the revised Japanese Guideline (2017) it was changed to "after 10-min to 1-h", following the revision of the guidelines from Western countries. Here, we aimed to investigate on the feasibility to apply the CCI measured at 10-min or 30-min post-transfusion as the surrogate of CCI-1 h. Peripheral blood was collected at 10-min, 30-min and 1-h post-transfusion of PC and the effectiveness of the transfusion was analyzed based on the CCI. In the period from December 2017 to February 2020, 8 patients, who received multiple PC transfusion (total 208) at our institution, were analyzed. We performed the univariate analyses to examine the relationship between CCI value and the categorical variables, p-value <0.1 was obtained for gender (p = 2.91 × 10-19), fever after transfusion (p = 0.0163). The qualitative variables, namely measurement time (p = 0.0553), also showed p-value <0.1. Using these factors as covariates in the mixed effect model, we found that the measurement time (p = 0.0007) had a significant effect on the CCI value when looking at fixed effects. Although there is a tendency for decreased CCI values with time progression, the slope of the change in the mixed model was -0.00307, indicating that the CCI difference among the 3 measurements was small. Here we provide evidence that CCI measured at 10-min and 30-min post-transfusion give results comparable to those measured at 1-h post-transfusion, under the Japanese practice of platelet transfusion, which relies on 100 % single-donor apheresis PC, and ABO-identical whenever possible.

What is known and objective 5-Azacitidine (AZA) is an agent widely used to treat myelodysplastic syndrome (MDS). Case description We herein report an 83-year-old woman diagnosed with MDS who was treated with AZA. She tolerated the first cycle of AZA; however, severe adverse events involving haemorrhagic enteritis with multiple intestinal ulcers developed after the second and third cycles. Additionally, the interval between the administration of AZA and the development of haematochezia shortened with each cycle of AZA. What is new and Conclusion We herein report as-yet-undescribed potential side effects, AZA-associated haemorrhagic enteritis that should be kept in mind.

Primary splenic malignant lymphoma is very rare, and few reports have examined the diagnostic utility of endoscopic ultrasound-guided fine-needle biopsy (EUS-FNB) for this disease. Here we report an extremely rare case of hepatosplenic T-cell lymphoma (HSTCL). Although HSTCL has been previously documented in patients with inflammatory bowel disease, this is the first report of it being diagnosed by splenic biopsy using EUS-FNB. HSTCL is an extranodal cytotoxic T-cell lymphoma that is located in the liver or spleen, and easily invades the bone marrow; it is characterized by marked hepatosplenomegaly and B symptoms. This disease is more common in young men, and has an aggressive course and poor prognosis. The patient was a 44-year-old woman who was admitted to our hospital with complaints of fever and abdominal pain. Hematologic examination revealed thrombocytopenia, a prolonged blood coagulation time, and an increased serum lactate dehydrogenase level. The platelet count was 73,000/mm (normal range, 158,000–348,000/mm), the international normalized ratio of prothrombin time was 1.37 (normal range, 0.85–1.15), the activated partial prothrombin time was 47.1 sec (normal range, 20.0–40.0 sec), and the serum lactate dehydrogenase level was 593 IU/L (normal range, 124–222 IU/L). Abdominal computed tomography (CT) showed marked splenomegaly (Fig. 1A). F-Fluorodeoxyglucose (F-FDG) positron emission tomography/CT showed preferential accumulation of F-FDG in the spleen (Fig. 1B), as well as in the liver and bone marrow, but there was no accumulation in the lymph nodes. EUS revealed that the spleen was markedly enlarged, with small isoechoic to hypoechoic areas throughout, but no noticeable mass formation was observed (Fig. 1C). The decision was made to perform EUSFNB to confirm a suspected diagnosis of splenic lymphoma. Written informed consent was obtained from the patient after providing a detailed explanation of the procedure. The splenic lesion was punctured transgastrically (Fig. 1C) and the tissue was collected under slight negative pressure using the slow-pull method by slowly withdrawing the stylet. Five punctures were performed using a 22-gauge reverse bevel FNB needle (EchoTip ProCore; Cook Medical, Bloomington, IN, USA) to obtain tissue for immunohistochemistry analysis. There were no procedure-related adverse events. Histopathologic analysis showed diffuse infiltration of medium-sized atypical lymphocytes, with clear cytoplasm, into the sinusoids of the spleen (Fig. 2A). Immunohistochemistry analysis revealed markedly abnormal lymphoid infiltrates in the splenic sinuses that were positive for CD3 (Fig. 2B) and negative for CD4 (Fig. 2C), CD8 (Fig. 2D), and CD20 (Fig. 2E), which is characteristic of HSTCL. The results of bone marrow analysis using flow cytometry also supported this diagnosis, and this case was found to be of the αβ T-cell receptor type (with the αβ type being less dominant than the γδ type). Using a 22-gauge core biopsy needle allowed the collection of a tissue sample with a length of 579.4 μm, which was sufficient to meet the fifth criterion (sufficient material for good quality histological interpretation) in the standard microscopic scorReceived: September 18, 2019 Revised: January 19, 2020 Accepted: January 20, 2020 Correspondence: Yoshiaki Shibata Division of Gastroenterology, Tama-Hokubu Medical Center, Tokyo Metropolitan Health and Medical Treatment Corporation, 1-7-1 Aobacho, Higashimurayamashi, Tokyo 189-0002, Japan Tel: +81-42-396-3811, Fax: +81-42-396-3076, E-mail: yshibatathk@gmail.com ORCID: https://orcid.org/0000-0002-3559-8546

The efficacy of 30 platelet concentrate (PC) products transfused to a patient with myelodysplastic syndrome (MDS) was evaluated by calculating the 1-hour post-transfusion corrected count increment (1h-CCI). Of the 30 transfusions, all HLA-A/B-matched, the cross-match (CM) test was negative in 23 (CM(-)-PC) and weakly positive (CM(+)-PC) in 2, and the CM test was not conducted in 5 (non-CM-PC). The effective rate was higher with CM(-)-PC compared to non-CM-PC (82.6% vs 60%), but statistical significance was not achieved, which suggested that the CM test of PC may still be a not satisfactorily effective predictor of PC refractoriness. Studies are ongoing in Japan to confirm on the importance of CM test of PC.

A rare case of non-Hodgkin's lymphoma (NHL) complicated with marked hypercalcemia caused by parathyroid hormone related protein (PTHrP) and presenting with Adams-Stokes attack is reported. A 72-year-old woman was involved in a traffic accident, and was transferred to our hospital. Blood examination revealed marked hypercalcemia (5.3 mmol/l (21.3 mg/dl)). A diagnosis of NHL (B-cell lymphoma, clinical stage IVA) was made by the results of the bone marrow biopsy, CT features showing multiple masses, and the gallium scintigraphy showing strong accumulation. Because of high blood level of PTHrP, hypercalcemia was considered to be due to PTHrP as a mediator acting on calcium metabolism. Hypercalcemia complicated with malignancy has a risk resulting in a fatal outcome. In the cases of malignant lymphoma complicated with hypercalcemia, we should pay attention to PTHrP as a mediator.

To retrospectively evaluate the efficacy and toxicity of radioimmunotherapy with yttrium 90 (90Y)-ibritumomab tiuxetan in patients with relapsed and refractory low-grade B-cell and mantle cell lymphoma. Eight patients (7 males, 1 female) with relapsed and refractory low-grade B-cell lymphoma were treated with 90Y-ibritumomab tiuxetan. Their mean age was 69 years (range, 56-82). The histological subtypes were follicular lymphoma, mantle cell lymphoma, and small lymphocytic lymphoma in 3, 3, and 1 patients, respectively. The median number of chemotherapy cycles was 2.5 (range, 1-6). The median duration from the last treatment was 3.5 months (range, 2-25 months). The 90Y-ibritumomab tiuxetan regimen was as follows: intravenous infusion of rituximab at a dose of 250 mg/m2 and 111In-ibritumomab tiuxetan 130 MBq on day 1. Eligibility was assessed using scintigraphy, followed by infusion of a second dose of rituximab at 250 mg/m2 and 90Y-ibritumomab tiuxetan at a dose of 11.1 or 14.8 MBq/kg on day 8. A response was observed in 4 out of the 8 patients (3 complete responses, 1 partial response). The median progression-free survival was 9 months. All patients could be treated without major side effects, except for myelosuppression. The side effects did not differ according to age. The dose of 90Y-ibritumomab tiuxetan was reduced to 11.1 MBq/kg in 5 out of the 8 cases, owing to thrombocytopenia. Decreases in the white blood cells, platelets, and hemoglobin were observed 5 (range, 3-6), 5.5 (range, 3-6), and 9.5 weeks (range, 5-10 weeks) after the treatment, respectively, and platelet transfusion was needed in one patient each with small lymphocytic lymphoma and mantle cell lymphoma pretreated with 6 cycles of chemotherapy. Treatment with 90Y-ibritumomab tiuxetan showed some effectiveness, especially for patients with small tumor masses. The associated hematological toxicity was controllable, and this toxicity was milder in patients treated with fewer cycles.

We report a rare case of adult varicella complicated by marked thrombocytopenia. A 49-year-old woman presented with fever and rash for 3 days. Blood examination revealed marked thrombocytopenia (2.7 × 104/μL). Varicella infection was diagnosed after elevated levels of varicella zoster virus IgM and IgG antibodies were observed 2 weeks later. In this case, thrombocytopenia was due to varicella infection, and the mechanism was estimated to be non-immunological. Because varicella infection complicated by thrombocytopenia may result in fatal bleeding, thrombocytopenia in patients with varicella warrants close attention.