Database : MEDLINE
Search on : macrophage and activation and syndrome [Words]
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[PMID]: 29516326
[Au] Autor:Du C; Peng L; Kou G; Wang P; Lu L; Li Y
[Ad] Address:Department of Gastroenterology, Linyi People's Hospital, Shandong University, Linyi, 276000, Shandong, People's Republic of China.
[Ti] Title:Assessment of Serum sTREM-1 as a Marker of Subclinical Inflammation in Diarrhea-Predominant Patients with Irritable Bowel Syndrome.
[So] Source:Dig Dis Sci;, 2018 Mar 07.
[Is] ISSN:1573-2568
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:BACKGROUND: Irritable bowel disease (IBS) is viewed upon as a functional disorder of subclinical inflammatory changes in recent years, and there is no reliable biomarker. Triggering receptor expressed on myeloid cells 1 (TREM-1), also produced in a soluble form (sTREM-1), is involved in the activation of inflammatory cascades of intracellular events and may play a role in pathogenesis of IBS. AIM: To investigate whether serum sTREM-1 level can be used as a marker of subclinical inflammation in D-IBS. METHODS: Abdominal pain was quantified by a validated questionnaire. Expression level of TREM-1 in colonic mucosa as well as sTREM-1 level in serum was also detected. Furthermore, we investigated the involvement of TREM-1-associated macrophage activation in IBS-like visceral hypersensitivity. RESULTS: No evidence for obvious inflammation was found in D-IBS patients. Serum sTREM-1 level in D-IBS patients was significantly higher than that in HCs, which was also significantly correlated with abdominal pain scores. We showed a marked increase in the proportion of TREM-1-expressing macrophages in D-IBS, which was significantly correlated with abdominal pain scores. Functionally, gadolinium chloride (GdCl ), a macrophage selective inhibitor, or LP17, the TREM-1-specific peptide, significantly suppressed the visceral hypersensitivity in trinitrobenzene sulfonic acid (TNBS)-treated mice with IBS-like visceral hypersensitivity. CONCLUSIONS: Serum sTREM-1 level is significantly higher in D-IBS patients and positively correlates with abdominal pain, which may be initiated by TREM-1-associated macrophage activation, indicating the existence of subclinical inflammation in D-IBS. Therefore, serum sTREM-1 is a potential marker of subclinical inflammation in D-IBS.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180308
[Lr] Last revision date:180308
[St] Status:Publisher
[do] DOI:10.1007/s10620-018-5002-y

  2 / 7068 MEDLINE  
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[PMID]: 29386593
[Au] Autor:Lieben L
[Ad] Address:Nature Reviews Disease Primers.
[Ti] Title:Autoinflammatory diseases: Free IL-18 causes macrophage activation syndrome.
[So] Source:Nat Rev Rheumatol;, 2018 Feb 01.
[Is] ISSN:1759-4804
[Cp] Country of publication:United States
[La] Language:eng
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180308
[Lr] Last revision date:180308
[St] Status:Publisher
[do] DOI:10.1038/nrrheum.2018.11

  3 / 7068 MEDLINE  
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[PMID]: 29178470
[Au] Autor:Brisse E; Imbrechts M; Mitera T; Vandenhaute J; Berghmans N; Boon L; Wouters C; Snoeck R; Andrei G; Matthys P
[Ad] Address:Laboratory of Immunobiology, Rega Institute, KU Leuven, Leuven, Belgium.
[Ti] Title:Lymphocyte-independent pathways underlie the pathogenesis of murine cytomegalovirus-associated secondary haemophagocytic lymphohistiocytosis.
[So] Source:Clin Exp Immunol;192(1):104-119, 2018 Apr.
[Is] ISSN:1365-2249
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Haemophagocytic lymphohistiocytosis (HLH) constitutes a spectrum of immunological disorders characterized by uncontrolled immune activation and key symptoms such as fever, splenomegaly, pancytopenia, haemophagocytosis, hyperferritinaemia and hepatitis. In genetic or primary HLH, hyperactivated CD8 T cells are the main drivers of pathology. However, in acquired secondary HLH, the role of lymphocytes remains vague. In the present study the involvement of lymphocytes in the pathogenesis of a cytomegalovirus-induced model of secondary HLH was explored. We have previously reported CD8 T cells to be redundant in this model, and therefore focused on CD4 helper and regulatory T cells. CD4 T cells were activated markedly and skewed towards a proinflammatory T helper type 1 transcription profile in mice displaying a severe and complete HLH phenotype. Counter to expectations, regulatory T cells were not reduced in numbers and were, in fact, more activated. Therapeutic strategies targeting CD25 hyperactivated T cells were ineffective to alleviate disease, indicating that T cell hyperactivation is not a pathogenic factor in cytomegalovirus-induced murine HLH. Moreover, even though T cells were essential in controlling viral proliferation, CD4 T cells, in addition to CD8 T cells, were dispensable in the development of the HLH-like syndrome. In fact, no T or B cells were required for induction and propagation of HLH disease, as evidenced by the occurrence of cytomegalovirus-associated HLH in severe combined immunodeficient (SCID) mice. These data suggest that lymphocyte-independent mechanisms can underlie virus-associated secondary HLH, accentuating a clear distinction with primary HLH.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1711
[Cu] Class update date: 180308
[Lr] Last revision date:180308
[St] Status:In-Data-Review
[do] DOI:10.1111/cei.13084

  4 / 7068 MEDLINE  
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[PMID]: 28453746
[Au] Autor:Zhu C; Mustafa D; Zheng PP; van der Weiden M; Sacchetti A; Brandt M; Chrifi I; Tempel D; Leenen PJM; Duncker DJ; Cheng C; Kros JM
[Ad] Address:Department of Pathology, Erasmus Medical Center, Rotterdam, The Netherlands.
[Ti] Title:Activation of CECR1 in M2-like TAMs promotes paracrine stimulation-mediated glial tumor progression.
[So] Source:Neuro Oncol;19(5):648-659, 2017 05 01.
[Is] ISSN:1523-5866
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Background: The majority of glioma-associated microglia/macrophages have been identified as M2-type macrophages with immune suppressive and tumor supportive action. Recently, the extracellular adenosine deaminase protein Cat Eye Syndrome Critical Region Protein 1 (CECR1) was shown to regulate macrophage maturation. In this study, we investigate the role of CECR1 in the regulation of the glioma-associated macrophage response. Methods: Expression of CECR1 was assessed in human glioma samples. CECR1-mediated macrophage response was studied in vitro, using donor derived CD14+ monocytes and the THP-1 monocytic cell line. The response of the human glioma cell line U87 to conditioned medium of macrophages preconditioned with recombinant human CECR1 or CECR1 silencing was also assessed. Results: CECR1 was strongly expressed in high-grade gliomas (P < .001) and correlated positively with the M2 phenotype markers in tumor-associated microglia/macrophages (TAMs) (overall, P < .05). In vitro studies confirmed the presence of a significantly higher level of CECR1 expression in M2-like macrophages exposed to U87 conditioned medium (P < .001). CECR1 knockdown or stimulation of macrophages affected differentiation toward the M2-like phenotype. Stimulation of U87 cells with conditioned medium of CECR1 knockdown or stimulated macrophages affected tumor cell proliferation and migration, coinciding with altered intracellular signaling of mitogen-activated protein kinase (MAPK). In glioma tissue samples, CECR1 expression correlated with Ki67 and MAPK signaling protein. Conclusions: CECR1 is a potent regulator of TAM polarization and is consistently highly expressed by M2-type TAMs, particularly in high-grade glioma. Paracrine effects induced by CECR1 in M2-like TAMs activate MAPK signaling and stimulate the proliferation and migration of glioma cells.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1704
[Cu] Class update date: 180308
[Lr] Last revision date:180308
[St] Status:In-Process
[do] DOI:10.1093/neuonc/now251

  5 / 7068 MEDLINE  
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[PMID]: 29197110
[Au] Autor:Davies JOJ; Hart AC; De La Fuente J; Bain BJ
[Ad] Address:St Mary's Hospital, Imperial College Healthcare NHS Foundation Trust, Praed Street, London, W2 1NY, United Kingdom.
[Ti] Title:Macrophage activation syndrome and post-transplant microangiopathy following haploidentical bone marrow transplantation for sickle cell anemia.
[So] Source:Am J Hematol;93(4):588-589, 2018 Aug.
[Is] ISSN:1096-8652
[Cp] Country of publication:United States
[La] Language:eng
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1712
[Cu] Class update date: 180307
[Lr] Last revision date:180307
[St] Status:In-Data-Review
[do] DOI:10.1002/ajh.24995

  6 / 7068 MEDLINE  
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[PMID]: 29508239
[Au] Autor:Xin Y; Wang D; Huang M; Yu J; Fang L; Xiao S
[Ad] Address:State Key Laboratory of Agricultural Microbiology, College of Veterinary Medicine, Huazhong Agricultural University, Wuhan, 430070, People's Republic of China.
[Ti] Title:Proteome analysis of differential protein expression in porcine alveolar macrophages regulated by porcine reproductive and respiratory syndrome virus nsp1ß protein.
[So] Source:Virus Genes;, 2018 Mar 05.
[Is] ISSN:1572-994X
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Porcine reproductive and respiratory syndrome virus (PRRSV), an acute infectious disease agent in swine, causes enormous economic losses to the global swine industry. PRRSV nonstructural protein 1ß (nsp1ß) plays a critical role in viral subgenomic mRNA synthesis and host immune regulation. However, the global changes of cellular gene expression in natural target cells regulated by the nsp1ß have not yet been identified. Here, isobaric tags for relative and absolute quantification (iTRAQ) labeling coupled with liquid chromatography-tandem mass spectrometry were used to quantitatively identify cellular proteins in porcine alveolar macrophage (PAM) 3D4/21 cells transduced with recombinant lentivirus expressing PRRSV nsp1ß that are differentially expressed compared with PAM 3D4/21 cells transduced with recombinant lentivirus expressing GFP. Of the 425 cellular proteins detected as differentially expressed, 186 were upregulated and 239 were downregulated. Based on the identities of the differentially expressed cellular proteins and the essential role of nsp1ß in interferon (IFN) activation and inflammatory factor antagonism during PRRSV infection, we propose a potential mechanism in which nsp1ß inhibits IFN induction and nuclear factor κB (NF-κB) signaling pathways. Our results suggest that mitochondrial antiviral signaling (MAVS) protein and translocases of outer membrane complex 70 (TOM70), involved in type I IFN induction, were downregulated, while protein phosphatase 1A (PPM1A), related to the inhibition of NF-κB pathway activation, was upregulated in nsp1ß-overexpressed PAM 3D4/21 cells. These data provide valuable information for better understanding the potential biological function of nsp1ß during PRRSV infection and the mechanism of virus escape from host immune surveillance of viral replication.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180306
[Lr] Last revision date:180306
[St] Status:Publisher
[do] DOI:10.1007/s11262-018-1547-2

  7 / 7068 MEDLINE  
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[PMID]: 29470247
[Au] Autor:Signoff JK; Fitzgerald JC; Teachey DT; Balamuth F; Weiss SL
[Ad] Address:Division of Critical Care, Department of Pediatrics, UC Davis Children's Hospital, Sacramento, CA.
[Ti] Title:Hypofibrinogenemia Is Associated With Poor Outcome and Secondary Hemophagocytic Lymphohistiocytosis/Macrophage Activation Syndrome in Pediatric Severe Sepsis.
[So] Source:Pediatr Crit Care Med;, 2018 Feb 21.
[Is] ISSN:1529-7535
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:OBJECTIVES: Some children with sepsis exhibit a sustained hyperinflammatory response that can trigger secondary hemophagocytic lymphohistiocytosis/macrophage activation syndrome. Although hypofibrinogenemia is a shared feature of sepsis and hemophagocytic lymphohistiocytosis, there are no data about fibrinogen as a biomarker to identify children with sepsis/secondary hemophagocytic lymphohistiocytosis/macrophage activation syndrome overlap. We hypothesized that hypofibrinogenemia is associated with poor outcomes and secondary hemophagocytic lymphohistiocytosis/macrophage activation syndrome and has utility as a screening biomarker for this sepsis phenotype. DESIGN: A retrospective cohort study of patients less than or equal to 21 years treated for severe sepsis from January 2012 to December 2014. SETTING: Emergency department and PICU at a single academic children's hospital. PATIENTS: Consecutive patients with greater than or equal to one episode of hypofibrinogenemia (serum fibrinogen < 150 mg/dL) within 7 days of sepsis were compared with a random sample of patients without hypofibrinogenemia using an a priori sample size target of 190. Thirty-eight patients with hypofibrinogenemia were compared with 154 without hypofibrinogenemia. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: The primary outcome was "complicated course" (composite of 28-d mortality or ≥ two organ failures at 7 d). Secondary outcomes were 28-day mortality and fulfillment of diagnostic criteria for secondary hemophagocytic lymphohistiocytosis/macrophage activation syndrome. We used Wilcoxon rank-sum, Fisher exact test, and multivariable logistic regression to compare patients with versus without hypofibrinogenemia. Patients with hypofibrinogenemia were more likely to have a complicated course (73.7% vs 29.2%; p < 0.001), 28-day mortality (26.3% vs 7.1%, p = 0.002), and meet diagnostic criteria for secondary hemophagocytic lymphohistiocytosis/macrophage activation syndrome (21.1% vs 1.3%; p < 0.001). After controlling for confounders, hypofibrinogenemia remained associated with complicated course (adjusted odds ratio, 8.8; 95% CI, 3.5-22.4), mortality (adjusted odds ratio, 6.0; 95% CI, 2.0-18.1), and secondary hemophagocytic lymphohistiocytosis/macrophage activation syndrome (adjusted odds ratio, 27.6; 95% CI, 4.4-173). CONCLUSIONS: Hypofibrinogenemia was independently associated with poor outcome and secondary hemophagocytic lymphohistiocytosis/macrophage activation syndrome in pediatric sepsis. Measurement of fibrinogen may provide a pragmatic biomarker to identify children with possible sepsis/secondary hemophagocytic lymphohistiocytosis/macrophage activation syndrome overlap for whom further diagnostic testing and consideration of adjunctive immunomodulatory therapies should be considered.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180306
[Lr] Last revision date:180306
[St] Status:Publisher
[do] DOI:10.1097/PCC.0000000000001507

  8 / 7068 MEDLINE  
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[PMID]: 29339744
[Au] Autor:Lagrange B; Benaoudia S; Wallet P; Magnotti F; Provost A; Michal F; Martin A; Di Lorenzo F; Py BF; Molinaro A; Henry T
[Ad] Address:CIRI, Centre International de Recherche en Infectiologie, Inserm, U1111, Université Claude Bernard Lyon 1, CNRS, UMR5308, École Normale Supérieure de Lyon, Univ Lyon, F-69007, Lyon, France.
[Ti] Title:Human caspase-4 detects tetra-acylated LPS and cytosolic Francisella and functions differently from murine caspase-11.
[So] Source:Nat Commun;9(1):242, 2018 01 16.
[Is] ISSN:2041-1723
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Caspase-4/5 in humans and caspase-11 in mice bind hexa-acylated lipid A, the lipid moeity of lipopolysaccharide (LPS), to induce the activation of non-canonical inflammasome. Pathogens such as Francisella novicida express an under-acylated lipid A and escape caspase-11 recognition in mice. Here, we show that caspase-4 drives inflammasome responses to F. novicida infection in human macrophages. Caspase-4 triggers F. novicida-mediated, gasdermin D-dependent pyroptosis and activates the NLRP3 inflammasome. Inflammasome activation could be recapitulated by transfection of under-acylated LPS from different bacterial species or synthetic tetra-acylated lipid A into cytosol of human macrophage. Our results indicate functional differences between human caspase-4 and murine caspase-11. We further establish that human Guanylate-binding proteins promote inflammasome responses to under-acylated LPS. Altogether, our data demonstrate a broader reactivity of caspase-4 to under-acylated LPS than caspase-11, which may have important clinical implications for management of sepsis.
[Mh] MeSH terms primary: Caspases, Initiator/metabolism
Caspases/metabolism
Francisella/metabolism
Lipopolysaccharides/metabolism
Macrophages/metabolism
[Mh] MeSH terms secundary: Acylation
Animals
Caspases/genetics
Caspases, Initiator/genetics
Cells, Cultured
Cytosol/microbiology
Francisella/physiology
Humans
Inflammasomes/genetics
Inflammasomes/metabolism
Macrophages/microbiology
Mice, Inbred C57BL
Mice, Knockout
NLR Family, Pyrin Domain-Containing 3 Protein/genetics
NLR Family, Pyrin Domain-Containing 3 Protein/metabolism
RNA Interference
Species Specificity
U937 Cells
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Name of substance:0 (Inflammasomes); 0 (Lipopolysaccharides); 0 (NLR Family, Pyrin Domain-Containing 3 Protein); EC 3.4.22.- (CASP4 protein, human); EC 3.4.22.- (Casp11 protein, mouse); EC 3.4.22.- (Caspases); EC 3.4.22.- (Caspases, Initiator)
[Em] Entry month:1803
[Cu] Class update date: 180305
[Lr] Last revision date:180305
[Js] Journal subset:IM
[Da] Date of entry for processing:180118
[St] Status:MEDLINE
[do] DOI:10.1038/s41467-017-02682-y

  9 / 7068 MEDLINE  
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[PMID]: 28460454
[Au] Autor:Shan X; Zhang Y; Chen H; Dong L; Wu B; Xu T; Hu J; Liu Z; Wang W; Wu L; Feng Z; Liang G
[Ad] Address:Chemical Biology Research Center at School of Pharmaceutical Sciences, Wenzhou Medical University, Wenzhou, Zhejiang, China.
[Ti] Title:Inhibition of epidermal growth factor receptor attenuates LPS-induced inflammation and acute lung injury in rats.
[So] Source:Oncotarget;8(16):26648-26661, 2017 Apr 18.
[Is] ISSN:1949-2553
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Acute lung injury (ALI) and its severe form acute respiratory distress syndrome remain the leading cause of morbidity and mortality in intensive care units. Inhibition of epidermal growth factor receptor (EGFR) has been found to be able to reduce inflammatory response. However, it is still unclear whether EGFR inhibition can prevent ALI. This study aimed to validate the EGFR's role in ALI and investigated the effects of EGFR inhibition on lipopolysaccharides (LPS)-induced ALI in rats. In vitro, both pharmacological inhibitors (AG1478 and 451) and si-RNA silencing of EGFR significantly inhibited LPS-induced EGFR signaling activation and inflammatory response in human lung epithelial cells or macrophages. Mechanistically, LPS induced EGFR activation via TLR4 and c-Src signaling. In vivo, rat model with ALI induced by intratracheal instillation of LPS was treated by oral administration of AG1478 and 451. It was observed that AG1478 and 451 blocked the activation of EGFR signaling in lung tissue and reduced the LPS-induced infiltration of inflammatory cells, inflammatory gene expression, and lung injuries. This study demonstrates that TLR4/c-Src-dependent EGFR signaling plays an important role in LPS-induced ALI, and that EGFR may be a potential target in treating ALI.
[Mh] MeSH terms primary: Acute Lung Injury/etiology
Acute Lung Injury/metabolism
Lipopolysaccharides/adverse effects
Receptor, Epidermal Growth Factor/metabolism
[Mh] MeSH terms secundary: Acute Lung Injury/drug therapy
Acute Lung Injury/pathology
Animals
Cell Line
Cytokines/genetics
Cytokines/metabolism
Inflammation Mediators/metabolism
Macrophages/immunology
Macrophages/metabolism
Protein Kinase Inhibitors/pharmacology
Quinazolines/pharmacology
Rats
Receptor, Epidermal Growth Factor/antagonists & inhibitors
Signal Transduction/drug effects
Toll-Like Receptor 4/metabolism
Tyrphostins/pharmacology
src-Family Kinases/metabolism
[Pt] Publication type:JOURNAL ARTICLE
[Nm] Name of substance:0 (Cytokines); 0 (Inflammation Mediators); 0 (Lipopolysaccharides); 0 (Protein Kinase Inhibitors); 0 (Quinazolines); 0 (Toll-Like Receptor 4); 0 (Tyrphostins); 170449-18-0 (tyrphostin AG 1478); EC 2.7.10.1 (Receptor, Epidermal Growth Factor); EC 2.7.10.2 (CSK tyrosine-protein kinase); EC 2.7.10.2 (src-Family Kinases)
[Em] Entry month:1803
[Cu] Class update date: 180305
[Lr] Last revision date:180305
[Js] Journal subset:IM
[Da] Date of entry for processing:170503
[St] Status:MEDLINE
[do] DOI:10.18632/oncotarget.15790

  10 / 7068 MEDLINE  
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[PMID]: 29342508
[Au] Autor:Borgia RE; Gerstein M; Levy DM; Silverman ED; Hiraki LT
[Ad] Address:The Hospital for Sick Children and University of Toronto, Toronto, Ontario, Canada.
[Ti] Title:Features, Treatment, and Outcomes of Macrophage Activation Syndrome in Childhood-Onset Systemic Lupus Erythematosus.
[So] Source:Arthritis Rheumatol;, 2018 Jan 17.
[Is] ISSN:2326-5205
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:OBJECTIVE: To describe the features and treatment of macrophage activation syndrome (MAS) in a single-center cohort of patients with childhood-onset systemic lupus erythematosus (SLE), and to compare childhood-onset SLE manifestations and outcomes between those with and those without MAS. METHODS: We included all patients with childhood-onset SLE followed up at The Hospital for Sick Children from 2002 to 2012, and identified those also diagnosed as having MAS. Demographic, clinical, and laboratory features of MAS and SLE, medication use, hospital and pediatric intensive care unit (PICU) admissions, as well as damage indices and mortality data were extracted from the Lupus database. Student's t-tests and Fisher's exact tests were used to compare continuous and categorical variables, respectively. We calculated incidence rate ratios of hospital and PICU admissions comparing patients with and those without MAS, using Poisson models. Kaplan-Meier survival analysis was used to examine the time to disease damage accrual. RESULTS: Of the 403 patients with childhood-onset SLE, 38 (9%) had MAS. The majority (68%) had concomitant MAS and SLE diagnoses. Fever was the most common MAS clinical feature. The frequency of renal and central nervous system disease, hospital admissions, the average daily dose of steroids, and time to disease damage were similar between those with and those without MAS. We observed a higher mortality rate among those with MAS (5%) than those without MAS (0.2%) (P = 0.02). CONCLUSION: MAS was most likely to develop concomitantly with childhood-onset SLE diagnosis. The majority of the MAS patients were successfully treated with corticosteroids with no MAS relapses. Although the numbers were small, there was a higher risk of death associated with MAS compared to SLE without MAS.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1801
[Cu] Class update date: 180302
[Lr] Last revision date:180302
[St] Status:Publisher
[do] DOI:10.1002/art.40417


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