[A case of gastric follicular lymphoma resected and diagnosed with laparoscopy and endoscopy cooperative surgery].

A woman in her 70s was diagnosed with a protruding mucosa-associated lymphoid tissue (MALT) lymphoma during a secondary health examination. After eradication of Helicobacter pylori, a biopsy revealed gastric follicular lymphoma (FL) and the lesion was still protruding one year later. 18F-fluorodeoxyglucose positron emission tomography showed focal nodular hypermetabolic activity, suggesting that FL may have transformed into a diffuse large B-cell lymphoma. Upper gastrointestinal endoscopy, colonoscopy, and capsule endoscopy showed no other lesions in the gastrointestinal tract, and bone marrow biopsy showed no permeation into the marrow. Therefore, this lesion, which appeared as a submucosal tumor, was limited to the stomach. Laparoscopy and endoscopy cooperative surgery was performed, because it allows for correct pathological diagnosis while removing only a minimal portion of the stomach wall. Histological findings showed follicular structures consisting of abnormal lymphoid cells. Immunohistochemical analysis revealed that neoplastic cells were positive for CD20, CD79a, Bcl-2, CD10, and c-MYC, but negative for CD3, CD5, and cyclin D1. Finally, we diagnosed this lesion as a primary gastric FL.

Lower Risks of Gastrointestinal Perforation and Intestinal Obstruction in Patients with Atypical Antipsychotics in Comparison with Typical Antipsychotics Based on Real-World Data from the MID-NET® in Japan.

Intestinal perforation and obstruction are known to be one of the adverse events caused by antipsychotics; however, warning information on package inserts varies among antipsychotics. To investigate the risks of gastrointestinal perforation and intestinal obstruction in patients prescribed atypical antipsychotics compared with those in patients prescribed typical antipsychotics, a nested case-control study was conducted utilizing real-world data from the MID-NET® medical information database in Japan. The study period spanned from January 1, 2009, to December 31, 2018. We found that the risks of gastrointestinal perforation and intestinal obstruction in patients prescribed atypical antipsychotics were significantly lower than those in patients prescribed typical antipsychotics (adjusted odds ratio, 0.48; 95% confidence interval, 0.29-0.80). This finding was supported with prolonged periods for the exposure definition in the sensitivity analyses. In addition, no major differences in the risks of atypical antipsychotics, such as risperidone, quetiapine, olanzapine, and aripiprazole, were identified in this study. The safety profile regarding the lower risks of gastrointestinal perforation and intestinal obstruction in patients prescribed atypical antipsychotics should be considered when choosing antipsychotics in clinical practice in terms of the proper use of such drugs.

Neuronal injury induces microglial production of macrophage inflammatory protein-1α in rat corticostriatal slice cultures.

Chemokines are potent chemoattractants for immune and hematopoietic cells. In the central nervous system, chemokines play an important role in inflammatory responses through activation of infiltrating leukocytes and/or resident glial cells. We previously demonstrated that N-methyl-D-aspartate (NMDA)-evoked neuronal injury induced astrocytic production of monocyte chemoattractant protein-1 (MCP-1, CCL2) via sustained activation of extracellular signal-regulated kinase (ERK) in rat organotypic slice cultures. In the present study, we examined mRNA expression and protein production of macrophage inflammatory protein-1α (MIP-1α, CCL3) induced by NMDA-evoked neuronal injury in the slice cultures. MIP-1α mRNA expression was transiently increased by NMDA treatment in a concentration-dependent manner. Double-fluorescence immunohistochemistry revealed that MIP-1α was produced predominantly in microglia. Depletion of microglial cells from the slice cultures by pretreatment with liposome-encapsulated clodronate abrogated the increase in MIP-1α mRNA expression after NMDA treatment. NMDA-induced MIP-1α mRNA expression was partially but significantly inhibited by the c-Jun N-terminal kinase inhibitor SP600125; conversely, the p38 mitogen-activated protein (MAP) kinase inhibitor SB203580 enhanced it. U0126, a MAP kinase/ERK kinase inhibitor, did not affect mRNA expression. These results, combined with our previous findings, demonstrate that NMDA-evoked neuronal injury differentially induces MIP-1α and MCP-1 production in microglia and astrocytes, respectively, through activation of different intracellular signaling pathways.

Encephalopathy, disseminated intravascular coagulation, and hemolytic-uremic syndrome after infection with enterohemorrhagic Escherichia coli O111.

An outbreak of enterohemorrhagic Escherichia coli (EHEC) occurred in Toyama and other prefectures in Japan during 2011. Some patients, including adults, showed complications such as encephalopathy, disseminated intravascular coagulation, and hemolytic-uremic syndrome, and the disease course was extremely aggressive. This report describes the clinical features of four patients infected with Escherichia coli (E. coli) O111 who developed very severe to fatal complications. The initial symptoms in all patients included abdominal pain, diarrhea, and bloody stools, and neurological abnormalities started to appear from 1 to 3 days after admission. Vomiting and pyrexia developed in three patients. Leukocyte counts, lactate dehydrogenase (LDH), and fibrin/fibrinogen degradation products were elevated, and thrombocytopenia was evident. Extremely elevated LDH and severe thrombocytopenia were characteristic at the time encephalopathy became apparent. All patients received oral fosfomycin, intravenous antibiotics, and anticoagulant therapy, three received gamma globulin, plasma exchange, and blood transfusion, and two received steroids and dialysis. Three patients required mechanical ventilation, and two adult patients died. E. coli O111 positive for Shiga toxin 2 was detected in stool culture in two patients, and serological tests for E. coli O111 were positive in the other two patients. In conclusion, EHEC O111 can cause severe illness in children and adults, and the prognosis becomes poorer as the severity of complications increases. Close monitoring including platelet counts and LDH are useful. Once these clinical parameters change, intensive treatment should be provided to prevent the development of severe complications.

A case of inflammatory mass resulting from calcium crystal deposition disease around the thoracic spine.

Calcium crystal deposition diseases are transient benign diseases that can cause intense pain. They can sometimes cause masses and soft tissue edema around the calcification, which should be differentiated from tumors and abscesses. We report a case of calcium crystal deposition disease with an enhanced mass on the ventral side of the vertebral bodies resembling tumors and abscesses. A female patient in her 50s visited our hospital complaining of chest pain. Computed tomography revealed a soft tissue mass with polygonal high-density lesions on the ventral side of the thoracic spine. Initially, we suspected it to be a perivertebral tumor and considered a biopsy. However, the pain rapidly improved with the administration of oral acetaminophen (Caronal, Chuo-ku/Tokyo/Japan). Hence, the patient was followed up for the time being. The mass disappeared after 3 months. In addition, polygonal high-density lesions inside the mass disappeared over time. Therefore, it was diagnosed as an inflammatory mass due to calcium crystal deposition disease. Calcium crystal deposition diseases can cause soft tissue edema and inflammatory mass around the calcium crystal deposit that can be confused with a perivertebral tumor. This report elucidates the importance of identifying calcifications within and near the masses to diagnose an inflammatory mass resulting from calcium crystal deposition.

[Concurrent chemo-radiotherapy for localized refractory non-Hodgkin's lymphoma--report of two cases].

Localized refractory diffuse large B-cell lymphomas (DLBCL) were treated with concurrent chemo-radiotherapy. Case 1 had right cervical lymphadenopathy. Lymphoma enlarged even after the fourth courses of chemotherapy consisting of cyclophosphamide, doxorubicin, vincristine, and prednisolone (CHOP). The second case had a pharyngeal tumor and bilateral cervical lymphadenopathy. A lymphoma enlarged after eighth courses of CHOP. Both cases were treated with concurrent chemo-radiotherapy. Chemotherapy consisted of mitoxantrone, methotrexate, ifosfamide,and prednisolone (MMIP). The dose of radiation to the involved sites was 40 Gy. The first case received chemotherapy three days after radiotherapy was started. The second case was treated with chemotherapy, and radiotherapy was begun one day after. Both cases show mucositis and leukopenia. One case received two courses of chemotherapy after chemo-radiotherapy, and the other received no additional chemotherapy. Both cases achieved complete remission after the combined therapy, however, lymphoma in one case recurred three months after the therapy. It is possible that this concurrent chemo-radiotherapy is effective for localized DLBCL which did not disappear after standard chemotherapy.

Imaging findings of gastric calcifying fibrous tumour.

Calcifying fibrous tumours (CFTs) are rare benign lesions that usually affect the soft tissues, the mesentery and the peritoneum. Gastric CFT is particularly rare. Here, we report a CFT found incidentally in a 31-year-old male. The mass was well circumscribed and showed partial calcification on the CT scan, with dark signal intensity seen on T2 weighted MRI. To the best of our knowledge, there is very limited published information concerning imaging findings of CFTs. We discuss the CT scan and MRI findings of this patient, which can be considered typical for gastric CFT, and present a review of the limited literature available.

Accumulating microglia phagocytose injured neurons in hippocampal slice cultures: involvement of p38 MAP kinase.

In this study, microglial migration and phagocytosis were examined in mouse organotypic hippocampal slice cultures, which were treated with N-methyl-D-aspartate (NMDA) to selectively injure neuronal cells. Microglial cells were visualized by the expression of enhanced green fluorescent protein. Daily observation revealed microglial accumulation in the pyramidal cell layer, which peaked 5 to 6 days after NMDA treatment. Time-lapse imaging showed that microglia migrated to the pyramidal cell layer from adjacent and/or remote areas. There was no difference in the number of proliferating microglia between control and NMDA-treated slices in both the pyramidal cell layer and stratum radiatum, suggesting that microglial accumulation in the injured areas is mainly due to microglial migration, not to proliferation. Time-lapse imaging also showed that the injured neurons, which were visualized by propidium iodide (PI), disappeared just after being surrounded by microglia. Daily observation revealed that the intensity of PI fluorescence gradually attenuated, and this attenuation was suppressed by pretreatment with clodronate, a microglia toxin. These findings suggest that accumulating microglia phagocytosed injured neurons, and that PI fluorescence could be a useful indicator for microglial phagocytosis. Using this advantage to examine microglial phagocytosis in living slice cultures, we investigated the involvements of mitogen-activated protein (MAP) kinases in microglial accumulation and phagocytosis. p38 MAP kinase inhibitor SB203580, but not MAP kinase/extracellular signal-regulated kinase inhibitor PD98059 or c-Jun N-terminal kinase inhibitor SP600125, suppressed the attenuation of PI fluorescence. On the other hand, microglial accumulation in the injured areas was not inhibited by any of these inhibitors. These data suggest that p38 MAP kinase plays an important role in microglial phagocytosis of injured neurons.