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[PMID]:27776448
[Au] Autor:Ye C; Zhang W; Jiang S; Yu Y; Zhou X; Zhu L; Xue D; He R
[Ad] Endereço:a Department of Orthopedic Surgery , the Second Affiliated Hospital, School of Medicine, Zhejiang University , Hangzhou , Zhejiang , China.
[Ti] Título:Platelet-derived growth factor-BB attenuates titanium-particle-induced osteolysis in vivo.
[So] Source:Growth Factors;34(5-6):177-186, 2016 12.
[Is] ISSN:1029-2292
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Inflammation and osteoclastogenesis play critical roles in wear-particle-induced periprosthetic osteolysis (WPO). Platelet-derived growth factor-BB (PDGF-BB) could promote osteogenesis and inhibit inflammatory response. The aim of this study was to investigate the impact of PDGF-BB on WPO. Mice were divided into four groups, namely, sham, vehicle, low-, and high-dose PDGF-BB groups. Mice in the rhPDGF-BB groups were treated with PDGF-BB at 0.25 or 1 mg/ml/kg/day. Mice in the sham and vehicle groups received PBS daily. Two weeks after surgery, calvariae were harvested. Immunohistochemical analysis and µ-CT showed that PDGF-BB significantly reduced osteoclast formation and bone resorption. ELISA showed that rhPDGF-BB decreased the secretion of TNF-α, IL-1ß, and IL-6. Western blotting revealed that rhPDGF-BB stimulated the expression of osteocalcin and osteoprotegerin. Furthermore, more VEGF and CD31 proteins were observed due to PDGF-BB by immunofluorescence. In conclusion, these findings suggest that rhPDGF-BB represents a potential treatment for WPO.
[Mh] Termos MeSH primário: Interface Osso-Implante/patologia
Osteólise/tratamento farmacológico
Proteínas Proto-Oncogênicas c-sis/uso terapêutico
Titânio/efeitos adversos
[Mh] Termos MeSH secundário: Animais
Interleucina-1beta/genética
Interleucina-1beta/metabolismo
Interleucina-6/genética
Interleucina-6/metabolismo
Camundongos
Camundongos Endogâmicos C57BL
Osteólise/etiologia
Molécula-1 de Adesão Celular Endotelial de Plaquetas/genética
Molécula-1 de Adesão Celular Endotelial de Plaquetas/metabolismo
Proteínas Proto-Oncogênicas c-sis/administração & dosagem
Fator de Necrose Tumoral alfa/genética
Fator de Necrose Tumoral alfa/metabolismo
Fator A de Crescimento do Endotélio Vascular/genética
Fator A de Crescimento do Endotélio Vascular/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Interleukin-1beta); 0 (Interleukin-6); 0 (Platelet Endothelial Cell Adhesion Molecule-1); 0 (Proto-Oncogene Proteins c-sis); 0 (Tumor Necrosis Factor-alpha); 0 (Vascular Endothelial Growth Factor A); 1B56C968OA (becaplermin); D1JT611TNE (Titanium)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180307
[Lr] Data última revisão:
180307
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161026
[St] Status:MEDLINE
[do] DOI:10.1080/08977194.2016.1240680


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[PMID]:28464271
[Au] Autor:Yang X; Gao W; Wang B; Wang X; Guo H; Xiao Y; Kong L; Hao D
[Ad] Endereço:Hong-Hui Hospital, Xi'an Jiaotong University College of Medicine, Xi'an, 710054, China.
[Ti] Título:Picroside II Inhibits RANKL-Mediated Osteoclastogenesis by Attenuating the NF-κB and MAPKs Signaling Pathway In Vitro and Prevents Bone Loss in Lipopolysaccharide Treatment Mice.
[So] Source:J Cell Biochem;118(12):4479-4486, 2017 Dec.
[Is] ISSN:1097-4644
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Picroside II, one of the major components isolated from the seed of natural plant picrorhiza, is widely used in traditional Chinese medicine. The present study was performed to define effects of picroside II on nuclear factor-kappaB ligand (RANKL)-stimulated osteoclast differentiation in vitro and on lipopolysaccharide (LPS)-induced bone loss in vivo. The bone marrow cells (BMMs) were harvested and induced with RANKL followed by treatment with picroside II at several doses, and the differentiation of osteoclasts from these cells was evaluated by tartrate-resistant acid phosphatase (TRAP) staining and resorption pit formation assay. The effects of picroside II on osteoclastogenesis were studied by examining RANKL-induced osteoclast F-actin ring formation and osteoclast bone resorption. Moreover, we explored the mechanisms of these downregulation effects by performed Western blotting and quantitative RT-PCR examination. Results demonstrated picroside II strongly inhibited RANKL-induced osteoclast formation when added during the early stage of BMMs cultures, suggesting that it acts on osteoclast precursors to inhibit RANKL/RANK signaling. Moreover, picroside II markedly decreased the phosphorylation of p38, ERK, JNK, p65, and I-κB degradation, and significantly suppressed c-Fos and nuclear factor of activated T-cells cytoplasmic 1 (NFATc1), both the key transcription factors during osteoclastogenesis. Furthermore, in vivo studies verified the bone protection effects of picroside II. These results collectively suggested that picroside II acted as an anti-resorption agent by blocking osteoclast activation. J. Cell. Biochem. 118: 4479-4486, 2017. © 2017 Wiley Periodicals, Inc.
[Mh] Termos MeSH primário: Cinamatos/farmacologia
Glucosídeos Iridoides/farmacologia
Lipopolissacarídeos/toxicidade
Sistema de Sinalização das MAP Quinases/efeitos dos fármacos
NF-kappa B/metabolismo
Osteoclastos/metabolismo
Osteólise
Receptor Ativador de Fator Nuclear kappa-B/metabolismo
[Mh] Termos MeSH secundário: Animais
Camundongos
Osteoclastos/patologia
Osteólise/induzido quimicamente
Osteólise/metabolismo
Osteólise/patologia
Osteólise/prevenção & controle
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cinnamates); 0 (Iridoid Glucosides); 0 (Lipopolysaccharides); 0 (NF-kappa B); 0 (Receptor Activator of Nuclear Factor-kappa B); 0 (Tnfrsf11a protein, mouse); 39012-20-9 (picroside II)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180102
[Lr] Data última revisão:
180102
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170503
[St] Status:MEDLINE
[do] DOI:10.1002/jcb.26105


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[PMID]:28681916
[Au] Autor:Song F; Wei C; Zhou L; Qin A; Yang M; Tickner J; Huang Y; Zhao J; Xu J
[Ad] Endereço:Research Centre for Regenerative Medicine, Guangxi Key Laboratory of Regenerative Medicine, Guangxi Medical University, Nanning, Guangxi, China.
[Ti] Título:Luteoloside prevents lipopolysaccharide-induced osteolysis and suppresses RANKL-induced osteoclastogenesis through attenuating RANKL signaling cascades.
[So] Source:J Cell Physiol;233(2):1723-1735, 2018 Feb.
[Is] ISSN:1097-4652
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Bone destruction or osteolysis marked by excessive osteoclastic bone resorption is a very common medical condition. Identification of agents that can effectively suppress excessive osteoclast formation and function is crucial for prevention and treatment of osteolytic conditions such as periprosthetic joint infection and periprosthetic loosening. Luteoloside, a flavonoid, is a natural bioactive compound with anti-inflammation and anti-tumor properties. However, the effect of Luteoloside on inflammation-induced osteolysis is unknown. Here, we found that Luteoloside exhibited a strong inhibitory effect on lipopolysaccharide (LPS)-induced osteolysis in vivo. In addition, Luteoloside suppressed RANKL-induced osteoclast differentiation and abrogated bone resorption in a dose-dependent manner. Further, we found that the anti-osteoclastic and anti-resorptive actions of Luteoloside are mediated via blocking NFATc1 activity and the attenuation of RANKL-mediated Ca signaling as well as NF-κB and MAPK pathways. Taken together, this study shows that Luteoloside may be a potential therapeutic agent for osteolytic bone diseases associated with abnormal osteoclast formation and function in inflammatory conditions.
[Mh] Termos MeSH primário: Anti-Inflamatórios/farmacologia
Glucosídeos/farmacologia
Lipopolissacarídeos
Luteolina/farmacologia
Osteoclastos/efeitos dos fármacos
Osteogênese/efeitos dos fármacos
Osteólise/prevenção & controle
Ligante RANK/metabolismo
Crânio/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Sinalização do Cálcio/efeitos dos fármacos
Modelos Animais de Doenças
Relação Dose-Resposta a Droga
Durapatita/metabolismo
Camundongos
Camundongos Endogâmicos C57BL
Proteínas Quinases Ativadas por Mitógeno/metabolismo
NF-kappa B/metabolismo
Fatores de Transcrição NFATC/metabolismo
Osteoclastos/metabolismo
Osteoclastos/patologia
Osteólise/induzido quimicamente
Osteólise/metabolismo
Osteólise/patologia
Células RAW 264.7
Crânio/metabolismo
Crânio/patologia
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Inflammatory Agents); 0 (Glucosides); 0 (Lipopolysaccharides); 0 (NF-kappa B); 0 (NFATC Transcription Factors); 0 (Nfatc1 protein, mouse); 0 (RANK Ligand); 0 (Tnfsf11 protein, mouse); 91D9GV0Z28 (Durapatite); 98J6XDS46I (luteolin-7-glucoside); EC 2.7.11.24 (Mitogen-Activated Protein Kinases); KUX1ZNC9J2 (Luteolin)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171128
[Lr] Data última revisão:
171128
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170707
[St] Status:MEDLINE
[do] DOI:10.1002/jcp.26084


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[PMID]:28690758
[Au] Autor:Bechir A; Haifa R; Atef BA; Emna B; Asma A; Nesrine BS; Yosra BY; Abdrrahim K
[Ad] Endereço:Department of Hematology, Farhat Hached Hospital, Sousse Tunisia.
[Ti] Título:Osteolytic bone lesions, severe hypercalcemia without circulating blasts: unusual presentation of childhood acute lymphoblastic leukemia.
[So] Source:Pan Afr Med J;26:244, 2017.
[Is] ISSN:1937-8688
[Cp] País de publicação:Uganda
[La] Idioma:eng
[Ab] Resumo:Hypercalcemia and severe osteolytic lesions are rare complications of acute lymphoblastic leukemia (ALL) in childhood. We report a case of a 3 years old boy who presented with prolonged fever, nausea, vomiting and increasing lower limbs pain. Skeletal X-rays and CT scan showed severe osteolytic lesions of the skull and extremities. Her physical examination showed multiple cervical lymph nodes. In laboratory tests, he had severe hypercalcemia. Parathyroid hormone (PTH) was not elevated. Despite the absence of circulating blasts, bone marrow biopsy revealed B-precursor (ALL). Hypercalcemia was initially treated with intravenous isotonic sodium chloride solution and diuretics but the serum calcium level normalized only after the beginning of corticosteroids and chemotherapy. The child responded initially to chemotherapy and eventually relapsed and died of septic shock. Acute leukemia must be considered in differential diagnosis in patients with hypercalcemia. A detailed examination even when there no circulating blasts in their peripheral blood smear, and if in doubt bone marrow aspiration should must be taken into consideration.
[Mh] Termos MeSH primário: Hipercalcemia/etiologia
Osteólise/etiologia
Leucemia-Linfoma Linfoblástico de Células Precursoras/diagnóstico
[Mh] Termos MeSH secundário: Antineoplásicos/administração & dosagem
Biópsia
Pré-Escolar
Diagnóstico Diferencial
Evolução Fatal
Seres Humanos
Masculino
Leucemia-Linfoma Linfoblástico de Células Precursoras/patologia
Tomografia Computadorizada por Raios X
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170906
[Lr] Data última revisão:
170906
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170711
[St] Status:MEDLINE
[do] DOI:10.11604/pamj.2017.26.244.10506


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[PMID]:28675805
[Au] Autor:Lazarus S; Tseng HW; Lawrence F; Woodruff MA; Duncan EL; Pettit AR
[Ad] Endereço:Translational Research Institute, Brisbane, Queensland, Australia; University of Queensland Diamantina Institute, Faculty of Medicine, The University of Queensland, Brisbane, Queensland, Australia; Department of Endocrinology and Diabetes, Royal Brisbane and Women's Hospital, Brisbane, Queensland, A
[Ti] Título:Characterization of Normal Murine Carpal Bone Development Prompts Re-Evaluation of Pathologic Osteolysis as the Cause of Human Carpal-Tarsal Osteolysis Disorders.
[So] Source:Am J Pathol;187(9):1923-1934, 2017 Sep.
[Is] ISSN:1525-2191
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Multicentric carpal-tarsal osteolysis; multicentric osteolysis, nodulosis, and arthropathy; and Winchester syndromes, skeletal dysplasias characterized by carpal/tarsal and epiphyseal abnormalities, are caused by mutations in v-maf musculoaponeurotic fibrosarcoma oncogene ortholog B (MAFB), matrix metalloproteinase (MMP) 2, and MMP14, respectively; however, the underlying pathophysiology is unclear. Osteoclast-mediated osteolysis has been regarded as the main mechanism, but does not explain the skeletal distribution. We hypothesized that MAFB, MMP-2, and MMP-14 have integral roles in carpal/tarsal and epiphyseal bone development. Normal neonatal mouse forepaws were imaged by micro-computed tomography and examined histologically. Murine forepaw ossification occurred sequentially. Subarticular regions of endochondral ossification showed morphologic and calcification patterns that were distinct from archetypical physeal endochondral ossification. This suggests that two different forms of endochondral ossification occur. The skeletal sites showing the greatest abnormality in the carpal-tarsal osteolysis syndromes are regions of subarticular ossification. Thus, abnormal bone formation in areas of subarticular ossification may explain the site-specific distribution of the carpal-tarsal osteolysis phenotype. MafB, Mmp-2, and Mmp-14 were expressed widely, and tartrate-resistant acid phosphatase staining notably was absent in the subarticular regions of the cartilage anlagen and entheses at a time point most relevant to the human osteolysis syndromes. Thus, abnormal peri-articular skeletal development and modeling, rather than excessive bone resorption, may be the underlying pathophysiology of these skeletal syndromes.
[Mh] Termos MeSH primário: Ossos do Carpo/crescimento & desenvolvimento
Lâmina de Crescimento/patologia
Osteólise/patologia
[Mh] Termos MeSH secundário: Animais
Proteínas de Arabidopsis
Ossos do Carpo/diagnóstico por imagem
Ossos do Carpo/metabolismo
Pré-Escolar
Lâmina de Crescimento/diagnóstico por imagem
Lâmina de Crescimento/metabolismo
Seres Humanos
Liases Intramoleculares
Fator de Transcrição MafB/metabolismo
Metaloproteinase 14 da Matriz/metabolismo
Metaloproteinase 2 da Matriz/metabolismo
Camundongos
Osteogênese
Osteólise/diagnóstico por imagem
Osteólise/metabolismo
Microtomografia por Raio-X
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Arabidopsis Proteins); 0 (MafB Transcription Factor); 0 (Mafb protein, mouse); EC 3.4.24.24 (Matrix Metalloproteinase 2); EC 3.4.24.80 (Matrix Metalloproteinase 14); EC 5.5.- (Intramolecular Lyases); EC 5.5.1.6 (CHIL protein, Arabidopsis)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170914
[Lr] Data última revisão:
170914
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170705
[St] Status:MEDLINE


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[PMID]:28591104
[Au] Autor:O'Donnell EK; Raje NS
[Ad] Endereço:Harvard Medical School, Boston, Massachusetts.
[Ti] Título:Myeloma bone disease: pathogenesis and treatment.
[So] Source:Clin Adv Hematol Oncol;15(4):285-295, 2017 Apr.
[Is] ISSN:1543-0790
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Bone involvement manifesting as osteolytic bone disease (OBD) or osteopenia is one of the defining features of multiple myeloma (MM). Osteolytic lesions develop in nearly 90% of patients with MM, and these are frequently complicated by skeleton-related events (SREs) such as severe bone pain, pathologic fractures, vertebral collapse, hypercalcemia, and spinal cord compression. SREs have a negative effect on patients' quality of life and affect their long-term outcomes, including survival. In MM, the delicate balance between bone formation and bone destruction is perturbed. OBD is a consequence of increased osteoclast activation along with osteoblast inhibition, which alter bone remodeling. Although MM remains incurable, tremendous progress has been made in the treatment of the disease. As such, there is a need to address the symptoms of the disease that affect quality of life and, ultimately, overall survival. Novel agents targeting OBD are promising therapeutic strategies not only for the treatment of MM OBD but also for the treatment of MM itself. In addition to bisphosphonates, several novel agents are currently under investigation for their positive effect on bone remodeling via osteoclast inhibition or osteoblast stimulation. Future studies will look to combine or sequence all of these agents to improve quality of life, decrease the symptoms of MM OBD, and enhance antitumor activity.
[Mh] Termos MeSH primário: Doenças Ósseas/etiologia
Doenças Ósseas/terapia
Mieloma Múltiplo/complicações
[Mh] Termos MeSH secundário: Animais
Biomarcadores
Conservadores da Densidade Óssea/administração & dosagem
Conservadores da Densidade Óssea/efeitos adversos
Conservadores da Densidade Óssea/uso terapêutico
Doenças Ósseas/diagnóstico
Doenças Ósseas/metabolismo
Diagnóstico por Imagem
Seres Humanos
Células Mesenquimais Estromais/metabolismo
Terapia de Alvo Molecular
Mieloma Múltiplo/diagnóstico
Osteoblastos/metabolismo
Osteoclastos/metabolismo
Osteócitos/metabolismo
Osteólise
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Biomarkers); 0 (Bone Density Conservation Agents)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171019
[Lr] Data última revisão:
171019
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170608
[St] Status:MEDLINE


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[PMID]:28569732
[Au] Autor:Mbalaviele G; Novack DV; Schett G; Teitelbaum SL
[Ad] Endereço:Department of Medicine, Division of Bone and Mineral Diseases, and.
[Ti] Título:Inflammatory osteolysis: a conspiracy against bone.
[So] Source:J Clin Invest;127(6):2030-2039, 2017 Jun 01.
[Is] ISSN:1558-8238
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:There are many causes of inflammatory osteolysis, but regardless of etiology and cellular contexts, the osteoclast is the bone-degrading cell. Thus, the impact of inflammatory cytokines on osteoclast formation and function was among the most important discoveries advancing the treatment of focal osteolysis, leading to development of therapeutic agents that either directly block the bone-resorptive cell or do so indirectly via cytokine arrest. Despite these advances, a substantial number of patients with inflammatory arthritis remain resistant to current therapies, and even effective anti-inflammatory drugs frequently do not repair damaged bone. Thus, insights into events such as those impacted by inflammasomes, which signal through cytokine-dependent and -independent mechanisms, are needed to optimize treatment of inflammatory osteolysis.
[Mh] Termos MeSH primário: Osso e Ossos/patologia
Osteólise/metabolismo
[Mh] Termos MeSH secundário: Animais
Osso e Ossos/imunologia
Osso e Ossos/metabolismo
Citocinas/fisiologia
Seres Humanos
Inflamassomos/metabolismo
Osteoclastos/fisiologia
Osteócitos/fisiologia
Osteólise/imunologia
Osteólise/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Cytokines); 0 (Inflammasomes)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170926
[Lr] Data última revisão:
170926
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170602
[St] Status:MEDLINE


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[PMID]:28553103
[Au] Autor:Deng Z; Jin J; Wang Z; Wang Y; Gao Q; Zhao J
[Ad] Endereço:Department of Orthopedics, Jinling Hospital, School of Medicine, Nanjing University.
[Ti] Título:The metal nanoparticle-induced inflammatory response is regulated by SIRT1 through NF-κB deacetylation in aseptic loosening.
[So] Source:Int J Nanomedicine;12:3617-3636, 2017.
[Is] ISSN:1178-2013
[Cp] País de publicação:New Zealand
[La] Idioma:eng
[Ab] Resumo:Aseptic loosening is the most common cause of total hip arthroplasty (THA) failure, and osteolysis induced by wear particles plays a major role in aseptic loosening. Various pathways in multiple cell types contribute to the pathogenesis of osteolysis, but the role of Sirtuin 1 (SIRT1), which can regulate inflammatory responses through its deacetylation, has never been investigated. We hypothesized that the downregulation of SIRT1 in macrophages induced by metal nanoparticles was one of the reasons for osteolysis in THA failure. In this study, the expression of SIRT1 was examined in macrophages stimulated with metal nanoparticles from materials used in prosthetics and in specimens from patients suffering from aseptic loosening. To address whether SIRT1 downregulation triggers these inflammatory responses, the effects of the SIRT1 activator resveratrol on the expression of inflammatory cytokines in metal nanoparticle-stimulated macrophages were tested. The results demonstrated that SIRT1 expression was significantly downregulated in metal nanoparticle-stimulated macrophages and clinical specimens of prosthesis loosening. Pharmacological activation of SIRT1 dramatically reduced the particle-induced expression of inflammatory cytokines in vitro and osteolysis in vivo. Furthermore, SIRT1 regulated particle-induced inflammatory responses through nuclear factor kappa B (NF-κB) acetylation. Thus, the results of this study suggest that SIRT1 plays a key role in metal nanoparticle-induced inflammatory responses and that targeting the SIRT1 pathway may lead to novel therapeutic approaches for the treatment of aseptic prosthesis loosening.
[Mh] Termos MeSH primário: Inflamação/metabolismo
Nanopartículas Metálicas/toxicidade
NF-kappa B/metabolismo
Falha de Prótese
Sirtuína 1/metabolismo
[Mh] Termos MeSH secundário: Acetilação
Idoso de 80 Anos ou mais
Animais
Artroplastia de Quadril/efeitos adversos
Citocinas/metabolismo
Feminino
Seres Humanos
Inflamação/induzido quimicamente
Macrófagos/efeitos dos fármacos
Macrófagos/metabolismo
Masculino
Camundongos Endogâmicos C57BL
Meia-Idade
Osteólise/metabolismo
Próteses e Implantes/efeitos adversos
Sirtuína 1/genética
Estilbenos/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cytokines); 0 (NF-kappa B); 0 (Stilbenes); EC 3.5.1.- (SIRT1 protein, human); EC 3.5.1.- (Sirtuin 1); Q369O8926L (resveratrol)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170906
[Lr] Data última revisão:
170906
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170530
[St] Status:MEDLINE
[do] DOI:10.2147/IJN.S124661


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[PMID]:28476105
[Au] Autor:Lehur AC; Zielinski M; Pluvy J; Grégoire V; Diamantis S; Bleibtreu A; Rioux C; Picard A; Vallois D
[Ad] Endereço:Infectious and Tropical Diseases Department, University Hospital Bichat-Claude Bernard, APHP, 46 rue Henri Huchard, 75018, Paris, France.
[Ti] Título:Case of disseminated histoplasmosis in a HIV-infected patient revealed by nasal involvement with maxillary osteolysis.
[So] Source:BMC Infect Dis;17(1):328, 2017 May 05.
[Is] ISSN:1471-2334
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Disseminated Histoplasmosis (DH) is a rare manifestation of Acquired Immune Deficiency Syndrome (AIDS) in European countries. Naso-maxillar osteolysis due to Histoplasma capsulatum var. capsulatum (Hcc) is unusual in endemic countries and has never been reported in European countries. Differential diagnoses such as malignant tumors, cocaine use, granulomatosis, vasculitis and infections are more frequently observed and could delay and/or bias the final diagnosis. CASE PRESENTATION: We report the case of an immunocompromised patient infected by Human Immunodeficiency Virus (HIV) with naso-maxillar histoplasmosis in a non-endemic country. Our aim is to describe the clinical presentation, the diagnostic and therapeutic issues. A 53-year-old woman, originated from Haiti, was admitted in 2016 for nasal deformation with alteration of general condition evolving for at least 6 months. HIV infection was diagnosed in 2006 and classified at AIDS stage in 2008 due to cytomegalovirus infection associated with pulmonary histoplasmosis. At admission, CD4 cell count was 9/mm . Surgical biopsies were performed and ruled out differential or associated diagnoses. Mycological cultures identified Hcc and Blood Polymerase Chain Reaction (PCR) for Hcc was positive. The patient was given daily Amphothericin B liposomal infusion during 1 month. Hcc PCR became negative in the blood under treatment, and then oral switch by itraconazole was introduced. Antiretroviral treatment was reintroduced after a 3-week histoplasmosis treatment. Normalization of naso-maxillar mucosa enabled a palatal prosthesis. CONCLUSION: Naso-maxillar histoplasmosis is extremely rare; this is the first case ever reported in a non-endemic country. Differential diagnoses must be ruled out by conducting microbiologic tools and histological examinations on surgical biopsies. Early antifungal treatment should be initiated in order to prevent DH severe outcomes.
[Mh] Termos MeSH primário: Infecções Oportunistas Relacionadas com a AIDS/etiologia
Histoplasmose/tratamento farmacológico
Histoplasmose/etiologia
Osteólise/etiologia
[Mh] Termos MeSH secundário: Infecções Oportunistas Relacionadas com a AIDS/tratamento farmacológico
Infecções Oportunistas Relacionadas com a AIDS/microbiologia
Síndrome de Imunodeficiência Adquirida/tratamento farmacológico
Fármacos Anti-HIV/uso terapêutico
Antifúngicos/uso terapêutico
Contagem de Linfócito CD4
Infecções por Citomegalovirus/diagnóstico
Infecções por Citomegalovirus/etiologia
Diagnóstico Diferencial
Feminino
Infecções por HIV/complicações
Infecções por HIV/tratamento farmacológico
Haiti
Histoplasmose/diagnóstico
Seres Humanos
Hospedeiro Imunocomprometido
Itraconazol/uso terapêutico
Pneumopatias Fúngicas/diagnóstico
Pneumopatias Fúngicas/tratamento farmacológico
Pneumopatias Fúngicas/etiologia
Doenças Maxilares/tratamento farmacológico
Doenças Maxilares/etiologia
Doenças Maxilares/microbiologia
Meia-Idade
Osteólise/microbiologia
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-HIV Agents); 0 (Antifungal Agents); 304NUG5GF4 (Itraconazole)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170807
[Lr] Data última revisão:
170807
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170507
[St] Status:MEDLINE
[do] DOI:10.1186/s12879-017-2419-4


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[PMID]:28407736
[Au] Autor:Guo J; Gao JZ; Guo LJ; Yin ZX; He EX
[Ad] Endereço:Spine Surgery, The First Affiliated Hospital of Guangzhou Medical University, 151 Yanjiang West Road, Guangzhou, 510000, China.
[Ti] Título:Large enchondroma of the thoracic spine: a rare case report and review of the literature.
[So] Source:BMC Musculoskelet Disord;18(1):155, 2017 Apr 13.
[Is] ISSN:1471-2474
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Enchondroma, a subtype of chondroma, originates from the medullary cavity of the bone and produces an expansile growth pattern. Enchondroma located in the spine is rare and a few cases of large thoracic enchondroma have been reported. The authors document a rare case of large enchondroma in the thoracic spine of a 49-year-old woman, and discuss its clinical, radiological and histopathological characteristics. CASE PRESENTATION: The patient presented with rapidly progressive and severe pain on her upper back. Magnetic resonance imaging revealed an expansile lesion at the posterior elements of T3 that was hypointense on T1-weighted images and mixed iso- to hyperintense on T2-weighted images. Administration of gadolinium-diethylenetriamine pentaacetic acid (Gd-DTPA) resulted in heterogeneous enhancement. During surgery, a large tumor of 4.2cm × 4.7cm × 2.1cm was resected along with the lamina and spinous process. Histological examination revealed that the tumor consisted of mature hyaline cartilage with typical chondrocytes, indicating that it was an enchondroma. CONCLUSIONS: Despite its benign-growing nature, enchondroma should be examined closely for signs of enchondromatosis and enchondrosarcoma. Complete surgical resection is the treatment of choice for immediate relief of symptoms and avoidance of recurrence.
[Mh] Termos MeSH primário: Dor nas Costas/cirurgia
Condroma/diagnóstico
Recidiva Local de Neoplasia/prevenção & controle
Neoplasias da Coluna Vertebral/diagnóstico
Vértebras Torácicas/patologia
[Mh] Termos MeSH secundário: Dor nas Costas/etiologia
Condroma/complicações
Condroma/patologia
Condroma/cirurgia
Meios de Contraste
Feminino
Gadolínio DTPA/administração & dosagem
Seres Humanos
Cartilagem Hialina/patologia
Imagem por Ressonância Magnética
Meia-Idade
Procedimentos Ortopédicos
Osteólise/diagnóstico por imagem
Osteólise/etiologia
Radiografia Torácica
Neoplasias da Coluna Vertebral/complicações
Neoplasias da Coluna Vertebral/patologia
Neoplasias da Coluna Vertebral/cirurgia
Vértebras Torácicas/diagnóstico por imagem
Tomografia Computadorizada por Raios X
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Contrast Media); K2I13DR72L (Gadolinium DTPA)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170713
[Lr] Data última revisão:
170713
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170415
[St] Status:MEDLINE
[do] DOI:10.1186/s12891-017-1519-z



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