We present a notable case of a 15-year-old male infected with influenza B virus who showed the clinical manifestations of myocardial ischemia. He was admitted to our hospital with sudden chest pain. He had febrile illness for the past 2 days. Rapid antigen test for influenza revealed positive influenza B virus antigen. The initial electrocardiogram showed elevation of the ST-segments in leads II, II, aVF and reciprocal depression in leads V1 and V2. Serum test showed elevation of creatine kinase and troponin T. Gadlinium-enchanced magnetic resonance imaging, Tl-201 and I-123 beta-methyl-p-iodephenyl-pentadecanoic acid scintigram, coronary angiography revealed no abnormality. Follow-up electrocardiogram showed ST-segment change improvement over the course. Myocarditis associated with influenza B virus seemed to be caused by endothelial impairment and disturbance of microcirculation rather than direct injury to cardiac myocytes.

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Circulating numbers of CD27(+) B cells, rather than CD4(+) T cells, may predict the effective PCV responses in immunocompromised children.

Acquired thrombotic thrombocytopenic purpura (TTP) is characterized by the coemergence of microangiopathic hemolytic anemia, thrombocytopenia, and thrombosis-mediated ischemic injuries of various organs, such as the central nervous system and kidneys. Acute myocardial infarction (AMI) has also occasionally been reported as a complication with TTP as the secondary thrombotic event; however, its emergence as the initial thrombotic event in TTP is extremely rare. This report describes an 80-year-old male patient with acquired TTP, who was affected by AMI without any clinically apparent damage to other organs or abnormal laboratory findings that would be suggestive of TTP at the first presentation. Although AMI was successfully treated by percutaneous coronary intervention (PCI), the patient developed marked thrombocytopenia with acute kidney injury and hemolytic anemia 5 days after PCI. The patient was diagnosed as having acquired TTP based on decreased ADAMTS13 (a disintegrin-like and metalloproteinase with thrombospondin type 1 motifs 13) below the level of detection and the presence of the inhibitor against ADAMTS13, and eventually died of multiorgan failure due to TTP despite undergoing repeated plasma exchanges and immunosuppressive therapies, including corticosteroid and rituximab. Although caution is often paid to therapy-related thrombocytopenia or renal damage after PCI, that is, those caused by antiplatelet drugs, heparin, or contrast agents, our report alerts us to the presence of TTP as an extremely rare, but underlying cause for AMI that could be subclinical at the initial presentation.

The aim of this study is to confirm the usefulness of sputum sampling from the hypopharynx through the nose to identify causative bacteria of pediatric community-acquired lower respiratory tract infection (CA-LRTI) and compare its features between the patients with and without underlying diseases. A retrospective study was performed on 244 pediatric patients hospitalized for CA-LRTI of suspected bacterial etiology. Sputum sample was obtained from these patients by aspirating airway secretion through the nose or the tracheostomy orifice, or coughing up by themselves. Sputum samples were assessed as suitable in 119 (74.4%) of 160 patients with CA-LRTI of suspected pure bacterial etiology. Ninety-six (70.1%) of 137 samples suctioned from the hypopharynx through the nose were suitable for bacterial examination. Seventy-eight (73.6%) of 106 patients identified with causative bacteria had some underlying diseases, and the other 28 patients did not have any underlying diseases. Proportions and antibiotics susceptibility profiles of the identified causative bacteria were almost similar in the patients with and without underlying diseases. Sputum sampling from the hypopharynx through the nose might be significant in pediatric CA-LRTI of suspected bacterial etiology. The initial treatment for patients without underlying diseases would be applicable to those with underlying diseases in the CA-LRTI of children.

Diffuse large B‐cell lymphoma (DLBCL), which is the most prevalent disease subtype of non‐Hodgkin lymphoma, is highly heterogeneous in terms of cytogenetic and molecular features. This study retrospectively investigated the clinical impact of G‐banding‐defined chromosomal abnormality on treatment outcomes of DLBCL in the era of rituximab‐containing immunochemotherapy. Of 181 patients who were diagnosed with DLBCL and treated with R‐CHOP or an R‐CHOP‐like regimen between January 2006 and April 2014, metaphase spreads were evaluable for G‐banding in 120. In these 120 patients, 40 were found to harbor a single chromosomal aberration type; 63 showed chromosomal abnormality variations (CAVs), which are defined by the presence of different types of chromosomal abnormalities in G‐banding, including 19 with two CAVs and 44 with ≥3 CAVs; and 17 had normal karyotypes. No specific chromosomal break point or numerical abnormality was associated with overall survival (OS) or progression‐free survival (PFS), but the presence of ≥3 CAVs was significantly associated with inferior OS rates (hazard ratio (HR): 2.222, 95% confidence interval (CI): 1.056–4.677, P = 0.031) and tended to be associated with shorter PFS (HR: 1.796, 95% CI: 0.965–3.344, P = 0.061). In addition, ≥3 CAVs more frequently accumulated in high‐risk patients, as defined by several conventional prognostic indices, such as the revised International Prognostic Index. In conclusion, our results suggest that the emergence of more CAVs, especially ≥3, based on chromosomal instability underlies the development of high‐risk disease features and a poor prognosis in DLBCL.

Extranodal marginal zone lymphoma (EMZL) of mucosa-associated lymphoid tissue (MALT) of the uterus is rare, and the etiology, pathophysiology and cytogenetic features remain unknown at present. The present study reports a case of a 71-year-old female with EMZL of the uterine cervix that was 80 mm in diameter and invaded directly into the rectal serosa. Complete remission was successfully induced by 6 courses of immunochemotherapy with rituximab plus cyclophosphamide, doxorubicin, vincristine and prednisolone. Although the metaphase spread of the tumor cells was unavailable for whole cytogenetic analysis, fluorescence in situ hybridization (FISH) detected triple signals for MALT1 and B-cell lymphoma 2, located at chromosome 18q21, and the centromere of chromosome 18, which was suggestive of trisomy 18, and in combination with previous studies, suggested a possible association between trisomy 18 and the large tumor at initial presentation in the present patient. In addition, FISH examination detected immunoglobulin heavy chain gene rearrangement, although the translocation partner was unconfirmed. A total of 18 previously-studied patients with EMZL of the uterus, including that of the present study, were reviewed with respect to their clinical features and treatment and cytogenetic abnormality. In the evaluation of the English scientific literature, this is the first reported patient with EMZL of the uterus with partly determined cytogenetic abnormalities.

We herein report a rare case of Burkitt lymphoma (BL) preceded by autoimmune hemolytic anemia (AIHA) caused by autoantibodies against D antigen. After a partial response to AIHA with prednisolone (PSL) treatment for 7 months, the patient developed BL with a t(8;22)(q24;q11.2) chromosomal translocation. Intensive immunochemotherapy, including rituximab, led to a complete response (CR) of BL; however, anti-D antibody remained detectable in the plasma and antibody-dissociated solution from erythrocytes, thus continuous therapy with PSL was necessary even after achievement of the CR. BL with AIHA is extremely rare, with only one previously reported case in the literature.