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Henoch-Sch?nlein purpura (HSP) is a common childhood vasculitis. Abdominal pain is a common feature of HSP, often leading to surgical consultation for evaluation of possible intussusception. Appendicitis is a rare complication of HSP, and in each of the 3 reported cases, appendectomy preceded the appearance of the purpuric rash. More often, unnecessary laparotomies are performed on patients in whom appendicitis is suspected, but who subsequently develop the characteristic purpura. This is the first reported case of appendicitis developing in a patient with the established HSP rash. This case is also the first report of perforated appendicitis in HSP. Clinical vigilance and serial physical and ultrasonographic examinations are needed to detect conditions necessitating surgery in patients with HSP. 相似文献
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Davis MA Landesman R Tadmor B Hopmeier M Shenhar G Barker T Pozner CN Binstadt ES Nelson S Look R Shubina M Walls RM 《Annals of emergency medicine》2008,51(4):420-5, 425.e1-5
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Hazen MM Woodward AL Hofmann I Degar BA Grom A Filipovich AH Binstadt BA 《Arthritis and rheumatism》2008,58(2):567-570
The clinical syndromes of hemophagocytic lymphohistiocytosis (HLH) and macrophage activation syndrome (MAS) are both characterized by dysregulated inflammation with prolonged fever, hepatosplenomegaly, coagulopathy, hematologic cytopenias, and evidence of hemophagocytosis in the bone marrow or liver. While HLH is either inherited or acquired, children with severe rheumatic diseases, most notably systemic juvenile idiopathic arthritis, are at risk for MAS. The phenotypic similarity between HLH and MAS raises the possibility that they share common pathogenetic mechanisms. Familial forms of HLH have been attributed to mutations in the genes encoding perforin (PRF1) and Munc13-4 (UNC13D), among others, and are characterized by defective cytotoxic lymphocyte function. While some patients with systemic JIA have decreased levels of perforin protein expression and natural killer (NK) cell function, mutations of HLH-associated genes in patients with systemic JIA have not been reported. We report the case of an 8-year-old girl with systemic JIA without MAS who was found to have compound heterozygous mutations of UNC13D and reduced NK cell cytotoxic function. This case broadens the range of clinical phenotypes attributable to UNC13D mutations and offers new insights into the etiology and pathogenesis of systemic JIA. 相似文献
6.
Abruzzo LV; Schmidt K; Weiss LM; Jaffe ES; Medeiros LJ; Sander CA; Raffeld M 《Blood》1993,82(1):241-246
We describe a patient with angioimmunoblastic lymphadenopathy with dysproteinemia (AILD), who subsequently developed large-cell immunoblastic lymphoma of B-cell immunophenotype. At the time of the initial diagnosis, histologic examination of an inguinal lymph node showed typical features of AILD, and there was no evidence of a monoclonal B-cell population by immunohistochemical analysis. In situ hybridization and Southern blot analysis for Epstein-Barr virus (EBV) were negative. At autopsy 2 years later, the patient had widespread lymph node and organ involvement by large-cell immunoblastic lymphoma of B-cell immunophenotype. Southern blot analysis performed on DNA extracted from lymph nodes, liver, and spleen showed two patterns of Ig heavy chain and kappa light chain gene rearrangements. The T-cell receptor beta chain gene was in the germline configuration. Analysis with an EBV terminal repeat region probe showed two clonal populations that paralleled the Ig gene rearrangement studies. Double-labeling immunohistochemistry and in situ hybridization confirmed the presence of EBV within the neoplastic B cells. The data support the hypothesis that EBV was not etiologically related to AILD in this case, and that EBV proliferation may occur after the onset of the disease. Further, the data suggest that some B-cell lymphomas that arise in the setting of AILD resemble EBV-associated B-cell lymphomas that arise in other immunodeficiency states. 相似文献
7.
Histamine reduces boron neutron capture therapy‐induced mucositis in an oral precancer model 下载免费PDF全文
8.
Valéria Martins Araújo CARNEIRO Ana Cristina Barreto BEZERRA Maria do Carmo Machado GUIMAR?ES Maria Imaculada MUNIZ-JUNQUEIRA 《Journal of applied oral science : revista FOB》2012,20(5):503-509
Phagocytosis by neutrophils and monocytes constitutes the main defense mechanism
against bacterial challenges in periodontitis. Phagocytosis by neutrophils has
already been evaluated, whereas phagocytic function of monocytes has hardly been
addressed so far.
Objectives
The aim of this study was to assess phagocytosis by neutrophils and monocytes in periodontitis.Material and Methods
The sample included 30 subjects with severe periodontitis and 27 control subjects without periodontal disease. The phagocytic index (PhI) was calculated as the mean number of adhered/ingested Saccharomyces cerevisiae per phagocytozing monocyte or neutrophil multiplied by the percentage of phagocytes involved in phagocytosis.Results
A significant reduction in phagocyte functions was observed in individuals with periodontitis. The median of PhI of neutrophils using non-sensitized S. cerevisiae was 3 for the control group, and 1.5 for the periodontitis group (p=0.01, Mann-Whitney test). The median of PhI of monocytes with non-sensitized S. cerevisiae was 26.13 for the control group, and 13.23 for the periodontitis group (p=0.03, Mann Whitney test). The median of PhI of monocytes assessed with sensitized S. cerevisiae was 97.92 for the control group and 60.1 for the periodontitis group (p=0.005, t-test).Conclusion
The data demonstrated a reduction in the function of phagocytes, suggesting a decrease in immune defenses in periodontitis. 相似文献9.
Camila Santos PEREIRA Marcos Vinícius Macedo de OLIVEIRA Lucas Oliveira BARROS Gabriela Alencar BANDEIRA Sérgio Henrique Sousa SANTOS John R. BASILE André Luiz Sena GUIMAR?ES Alfredo Maurício Batista DE PAULA 《Journal of applied oral science : revista FOB》2013,21(5):416-421