A case of follicular lymphoma complicated with mesenteric panniculitis

Mesenteric panniculitis (MP) is a rare disease occasionally complicated with lymphoma. A 55-year old female presented with MP accompanied by malignant lymphoma. This patient was first treated for follicular lymphoma and subsequently for panniculitis. After 6 courses of R-CHOP chemotherapy, the treatment response was partial. An additional course of salvage chemotherapy led to a complete response. Since the mesenteric mass progressed simultaneously with the regression of other lymphoma lesions, we performed a biopsy of the mesenteric mass and pathologically confirmed an MP lesion without lymphoma. Subsequent high-dose chemotherapy led to CR and the MP lesion remained stable. In the present case, MP progressed with chemotherapy. We concluded that mesenteric lesions suspected of progressing or recurring should be diagnosed pathologically even if asymptomatic

Thalamic posterior ventral neurons with bifurcating axons to the first and second somatosensory areas in the cat, demonstrated by the fluorescent retrograde double labeling technique.

The thalamic posterior ventral neurons with bifurcating axons to both the first and second somatosensory cortical areas (SI and SII) in the cat were examined by the fluorescent retrograde double labeling technique. After injection of Evans blue (EB) into the SI, and of 4',6-diamidino-2-phenylindol.2HCl (DAPI) into the SII of the same hemisphere, EB- and DAPI-labeled cells were observed predominantly in both the posterolateral ventral and the posteromedial ventral nuclei of the thalamus. Although EB single-labeled and DAPI single-labeled cells tended to occupy separate regions within the posterior ventral nuclei, a small number of cells double-labeled with both EB and DAPI were detected in the border zone between two single-labeled cell groups. These observations indicate that some cells in the posteromedial and posterolateral ventral nuclei project both to the SI and SII by bifurcating axons.</p

Negative Impact of Gemtuzumab Ozogamicin on CD33-Positive Early T-Cell Precursor Acute Lymphoblastic Leukemia: A Case Report

Introduction: Early T-cell precursor acute lymphoblastic leukemia (ETP-ALL) is a rare subtype of T-cell leukemia that phenotypically expresses mature T-cell markers and immature myeloid markers such as CD33. Gemtuzumab ozogamicin (GO) is a novel agent for the CD33 molecular targeting antibody conjugated to the cytotoxic agent calicheamicin. GO is anticipated to be effective against ETP-ALL. In vivo studies promise antileukemic effects in cell lines; however, clinical reports to support this research are lacking. We treated a patient who suffered from CD33-positive ETP-ALL using GO. Case Presentation: We treated an 81-year-old man who suffered from ETP-ALL. The patient’s leukemia expressed T cell and myeloid markers including cyCD3, CD5, CD7, CD33, and HLA-DR. Initially, the patient was treated using a standard chemotherapy regimen for acute lymphoblastic leukemia comprising cyclophosphamide, daunorubicin, vincristine, l-asparaginase, and prednisolone. The induction chemotherapy produced the expected complete hematological response; however, bone marrow blasts remained. Following consolidation chemotherapy, the patient maintained a full hematological response. Thereafter, we changed the consolidation regimen to nelarabine, which did not reduce bone marrow blasts effectively. After two courses of nelarabine therapy, we finally used GO at an 8 mg/m2 weekly dose after confirming that CD33 expression was still positive in the patient’s residual leukemic cells. GO was ineffective in treating the patient’s leukemia, and peripheral blasts increased 30 days following treatment. The patient died 81 days after initiating GO therapy. Conclusion: This is the first clinical case of GO having a negative impact on ETP-ALL. Because the GO resistance mechanism for ETP-ALL has not been fully elucidated, treatment modification should be considered to achieve optimal clinical efficacy

Central Nervous System Peripheral T Cell Lymphoma Manifesting as Lymphomatosis Cerebri That Was Misdiagnosed as Neuro-Behçet’s Disease: A Case Report

Background: Lymphomatosis cerebri (LC) is a unique form of primary central nerves lymphoma (PCNSL), which presents as diffuse infiltration of lymphoma cells characteristically in the white matter rather than tumor formation. However, the involvement of central nervous system (CNS) is unclear because of the lack of contrast enhancement. Case Presentation: We treated a 53-year-old woman with LC and brain lesions resembling neuro-Behcet’s disease. She had a past history of acute uveitis and current symptoms of somnolence and gait disturbances progressing for one month. Cranial magnetic resonance imaging (MRI) revealed high signal lesions in the brain stem. Based on her past history and present clinical findings, she was clinically diagnosed with neuro-Behcet’s disease, which was treated with 1 g of methylprednisolone (mPSL) pulse therapy. Repeated mPSL pulse therapy resulted in a minor response, but the cerebral lesions persisted. After a short remission of several months, signal changes of the brain stem lesion recurred and her consciousness level worsened at 4 months after diagnosis. Upon admission to our hospital, positron emission tomography with 2-deoxy-2-[fluorine-18]fluoro-D-glucose integrated with computed tomography revealed abnormal uptake in the systemic lymph nodes (LNs), including the bilateral inguinal LNs. A diagnosis based on a biopsy of the left inguinal LNs was primary central nervous system lymphoma with inguinal LN lesions, manifesting as LC from malignant peripheral T cell lymphoma, not otherwise specified. Four courses of high-dose methotrexate (3.5 g/m2) therapy lead to temporary recovery of consciousness, but there was no improvement in other neurological findings. All nodal lesions tentatively regressed. Serum soluble interleukin-2 receptor (sIL-2R) (normal range: 121–613 U/mL) was constitutively decreased from 8,520 U/mL before chemotherapy to 740 U/mL after chemotherapy. We observed cerebral micro-bleeds in the center of LC lesions during chemotherapy, but no surgical intervention was required. Two months later, LC recurred in the brain, which was fatal. Conclusions: Neuro-Behçet’s disease is difficult to distinguish from LC when other clinical findings, including human leukocyte antigen disparity, serum sIL-2R, or cerebrospinal IL-6, are lacking. LC should be differentiated from CNS lymphoma before corticosteroid therapy

Erythroleukemia Relapsing as Precursor B-cell Lymphoblastic Leukemia

AML relapsing as ALL has rarely been reported. We describe the case of a 62-yr-old man who was diagnosed with erythroleukemia with a complex karyotype and achieved complete hematologic and cytogenetic remission after induction chemotherapy. However, 4 months after the initial diagnosis, he showed relapse with blasts showing a different morphology and immunophenotype and was diagnosed with precursor B-cell ALL. The relapsing precursor B-cell ALL presented with the same leukemic clones as the primary erythroleukemia. Cytogenetic analysis of his bone marrow (BM) at the time of the primary erythroleukemia showed complex karyotypic abnormalities, including monosomy 5 and monosomy 7. At relapse, his BM showed reemergence of these leukemic clones of complex karyotypic abnormalities with clonal switch. To our knowledge, this is the first case of a lineage switch from erythroleukemia to ALL

Development of early neutropenic fever, with or without bacterial infection, is still a significant complication after reduced-intensity stem cell transplantation

AbstractLittle information is available on the clinical characteristics of infectious complications that occur in the early period after reduced-intensity stem cell transplantation (RIST). We retrospectively investigated the clinical features of neutropenic fever and infectious episodes within 30 days after RIST in 76 patients who had received fluoroquinolones as part of their antibacterial prophylaxis. Preparative regimens included cladribine 0.66 mg/kg or fludarabine 180 mg/m2 plus busulfan 8 mg/kg. All but 1 patient survived 30 days after transplantation, and 75 patients (99%) became neutropenic within a median duration of 9 days. Neutropenic fever was observed in 29 patients (38%), and bacterial infection was confirmed in 15 (20%) of these, including bacteremia (n = 13), bacteremia plus pneumonia (n = 1), and urinary tract infection (n = 1). The causative organisms were gram-positive (n = 9) and gram-negative organisms (n = 7), with a mortality rate of 6%. Neither viral nor fungal infection was documented. Multivariate analysis showed that the presence of neutropenia at the initiation of preparative regimens was an independent risk factor for subsequent documented bacterial infections (P = .026; 95% confidence interval, 1.25–35.1). We conclude that neutropenic fever and bacteremia remain common complications in RIST

Other Helicobacters, gastric and gut microbiota

The current article is a review of the most important and relevant literature published in 2016 and early 2017 on non-Helicobacter pylori Helicobacter infections in humans and animals, as well as interactions between H. pylori and the microbiota of the stomach and other organs. Some putative new Helicobacter species were identified in sea otters, wild boars, dogs, and mice. Many cases of Helicobacter fennelliae and Helicobacter cinaedi infection have been reported in humans, mostly in immunocompromised patients. Mouse models have been used frequently as a model to investigate human Helicobacter infection, although some studies have investigated the pathogenesis of Helicobacters in their natural host, as was the case for Helicobacter suis infection in pigs. Our understanding of both the gastric and gut microbiome has made progress and, in addition, interactions between H. pylori and the microbiome were demonstrated to go beyond the stomach. Some new approaches of preventing Helicobacter infection or its related pathologies were investigated and, in this respect, the probiotic properties of Saccharomyces, Lactobacillus and Bifidobacterium spp. were confirmed

An Urban Neo-Poverty Population-Based Quality of Life and Related Social Characteristics Investigation from Northeast China

OBJECTIVE: To investigate quality of life (QOL) and related characteristics among an urban neo-poverty population in northeast China, and to compare this population with a traditional poverty cohort. DESIGN: The research was a cross-sectional survey executed from June 2005 to October 2007, with a sample of 2940 individuals ages 36 to 55 in three different industrial cities of northeast China. Data were collected on QOL status and sociodemographic characteristics. QOL was assessed using the 36-item Short Form Health Survey (Chinese version). Multiple regression analysis was employed to analyze association between sociodemographic variables and QOL. RESULTS: The scores for QOL in the neo-poverty group were higher than those in the traditional poverty group, but lower than those in the general population. When the neo-poverty population was divided into two subgroups by age, 36-45 years and 46-55 years, the differences in QOL scores were not significant. However, there were significant differences in several dimensions between two subgroups according to unemployment time (<5 years and >5 years). Additionally, stepwise regression analysis indicated that disease burden, including disease and medical expenditures, was a common risk factor for declining QOL in the neo-poverty group. CONCLUSIONS: Despite some limitations, this study provides initial evidence that the QOL of the urban neo-poverty population lies between that of the general population and traditional poverty. QOL of the neo-poverty group approached QOL of the traditional poverty group with increased unemployment years. In addition to decreased income, disease burden is the most important factor influencing QOL status in urban neo-poverty

Ex Vivo Expansion of Human CD8+ T Cells Using Autologous CD4+ T Cell Help

Background: Using in vivo mouse models, the mechanisms of CD4+ T cell help have been intensively investigated. However, a mechanistic analysis of human CD4+ T cell help is largely lacking. Our goal was to elucidate the mechanisms of human CD4+ T cell help of CD8+ T cell proliferation using a novel in vitro model. Methods/Principal Findings: We developed a genetically engineered novel human cell-based artificial APC, aAPC/mOKT3, which expresses a membranous form of the anti-CD3 monoclonal antibody OKT3 as well as other immune accessory molecules. Without requiring the addition of allogeneic feeder cells, aAPC/mOKT3 enabled the expansion of both peripheral and tumor-infiltrating T cells, regardless of HLA-restriction. Stimulation with aAPC/mOKT3 did not expand Foxp3+ regulatory T cells, and expanded tumor infiltrating lymphocytes predominantly secreted Th1-type cytokines, interferon-γ and IL-2. In this aAPC-based system, the presence of autologous CD4+ T cells was associated with significantly improved CD8+ T cell expansion in vitro. The CD4+ T cell derived cytokines IL-2 and IL-21 were necessary but not sufficient for this effect. However, CD4+ T cell help of CD8+ T cell proliferation was partially recapitulated by both adding IL-2/IL-21 and by upregulation of IL-21 receptor on CD8+ T cells. Conclusions: We have developed an in vitro model that advances our understanding of the immunobiology of human CD4+ T cell help of CD8+ T cells. Our data suggests that human CD4+ T cell help can be leveraged to expand CD8+ T cells in vitro