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Pesquisa : C14.907.075 [Categoria DeCS]
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[PMID]:27778439
[Au] Autor:Randi AM; Laffan MA
[Ad] Endereço:National Heart and Lung Institute, Imperial College, London, UK.
[Ti] Título:Von Willebrand factor and angiogenesis: basic and applied issues.
[So] Source:J Thromb Haemost;15(1):13-20, 2017 01.
[Is] ISSN:1538-7836
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The recent discovery that von Willebrand factor (VWF) regulates blood vessel formation has opened a novel perspective on the function of this complex protein. VWF was discovered as a key component of hemostasis, capturing platelets at sites of endothelial damage and synthesized in megakaryocytes and endothelial cells (EC). In recent years, novel functions and binding partners have been identified for VWF. The finding that loss of VWF in EC results in enhanced, possibly dysfunctional, angiogenesis is consistent with the clinical observations that in some patients with von Willebrand disease (VWD), vascular malformations can cause severe gastrointestinal (GI) bleeding. In vitro and in vivo studies indicate that VWF can regulate angiogenesis through multiple pathways, both intracellular and extracellular, although their relative importance is still unclear. Investigation of these pathways has been greatly facilitated by the ability to isolate EC from progenitors circulating in the peripheral blood of normal controls and patients with VWD. In the next few years, these will yield further evidence on the molecular pathways controlled by VWF and shed light on this novel and fascinating area of vascular biology. In this article, we will review the evidence supporting a role for VWF in blood vessel formation, the link between VWF dysfunction and vascular malformations causing GI bleeding and how they may be causally related. Finally, we will discuss how these findings point to novel therapeutic approaches to bleeding refractory to VWF replacement therapy in VWD.
[Mh] Termos MeSH primário: Neovascularização Fisiológica
Fator de von Willebrand/metabolismo
[Mh] Termos MeSH secundário: Angiodisplasia/metabolismo
Animais
Coagulação Sanguínea
Plaquetas/metabolismo
Células Endoteliais/metabolismo
Hemorragia Gastrointestinal/sangue
Glicoproteínas/metabolismo
Hemorragia
Hemostasia
Seres Humanos
Megacariócitos/metabolismo
Camundongos
Neovascularização Patológica
Transdução de Sinais
Células-Tronco/metabolismo
Receptor 2 de Fatores de Crescimento do Endotélio Vascular/metabolismo
Doenças de von Willebrand/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Glycoproteins); 0 (von Willebrand Factor); EC 2.7.10.1 (Vascular Endothelial Growth Factor Receptor-2)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180222
[Lr] Data última revisão:
180222
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161026
[St] Status:MEDLINE
[do] DOI:10.1111/jth.13551


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[PMID]:28729354
[Au] Autor:Kang J; Hennessy-Strahs S; Kwiatkowski P; Bermudez CA; Acker MA; Atluri P; McConnell PI; Bartoli CR
[Ad] Endereço:From the MD/PhD Program, Vanderbilt University School of Medicine, Nashville, TN (J.K.); Division of Cardiovascular Surgery, Hospital of the University of Pennsylvania, Philadelphia (J.K., S.H.-S., C.A.B., M.A.A., P.A., C.R.B.); and The Ohio State University, Columbus (P.K., P.I.M.).
[Ti] Título:Continuous-Flow LVAD Support Causes a Distinct Form of Intestinal Angiodysplasia.
[So] Source:Circ Res;121(8):963-969, 2017 Sep 29.
[Is] ISSN:1524-4571
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:RATIONALE: The objective of this autopsy study was to determine whether gastrointestinal angiodysplasia develops during continuous-flow left ventricular assist device (LVAD) support. OBJECTIVE: LVAD support causes pathologic degradation of von Willebrand factor (vWF) and bleeding from gastrointestinal angiodysplasia at an alarming rate. It has been speculated that LVAD support itself may cause angiodysplasia. The relationship to abnormal vWF metabolism is unknown. We tested the hypothesis that abnormal gastrointestinal vascularity develops during continuous-flow LVAD support. METHODS AND RESULTS: Small bowel was obtained from deceased humans, cows, and sheep supported with a continuous-flow LVAD (n=9 LVAD, n=11 control). Transmural sections of jejunum were stained with fluorescein isothiocyanate-conjugated isolectin-B4 for endothelium to demarcate vascular structures and quantify intestinal vascularity. Paired plasma samples were obtained from humans before LVAD implantation and during LVAD support (n=41). vWF multimers and degradation fragments were quantified with agarose and polyacrylamide gel electrophoresis and immunoblotting. Abnormal vascular architecture was observed in the submucosa of the jejunum of human patients, cows, and sheep supported with a continuous-flow LVAD. Intestinal vascularity was significantly higher after LVAD support versus controls (5.2±1.0% versus 2.1±0.4%, =0.004). LVAD support caused significant degradation of high-molecular-weight vWF multimers (-9±1%, <0.0001) and accumulation of low-molecular-weight vWF multimers (+40±5%, <0.0001) and vWF degradation fragments (+53±6%, <0.0001). CONCLUSIONS: Abnormal intestinal vascular architecture and LVAD-associated vWF degradation were consistent findings in multiple species supported with a continuous-flow LVAD. These are the first direct evidence that LVAD support causes gastrointestinal angiodysplasia. Pathologic vWF metabolism may be a mechanistic link between LVAD support, abnormal angiogenesis, gastrointestinal angiodysplasia, and bleeding.
[Mh] Termos MeSH primário: Angiodisplasia/etiologia
Coração Auxiliar/efeitos adversos
Doenças do Jejuno/etiologia
Jejuno/irrigação sanguínea
Implante de Prótese/efeitos adversos
Implante de Prótese/instrumentação
Função Ventricular Esquerda
[Mh] Termos MeSH secundário: Adulto
Idoso
Angiodisplasia/metabolismo
Angiodisplasia/patologia
Animais
Autopsia
Bovinos
Modelos Animais de Doenças
Hemorragia Gastrointestinal/etiologia
Seres Humanos
Doenças do Jejuno/metabolismo
Doenças do Jejuno/patologia
Jejuno/metabolismo
Jejuno/patologia
Meia-Idade
Peso Molecular
Desenho de Prótese
Proteólise
Carneiro Doméstico
Fator de von Willebrand/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (von Willebrand Factor)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171010
[Lr] Data última revisão:
171010
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170722
[St] Status:MEDLINE
[do] DOI:10.1161/CIRCRESAHA.117.310848


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[PMID]:28709802
[Au] Autor:Magri G; Comerma L; Pybus M; Sintes J; Lligé D; Segura-Garzón D; Bascones S; Yeste A; Grasset EK; Gutzeit C; Uzzan M; Ramanujam M; van Zelm MC; Albero-González R; Vazquez I; Iglesias M; Serrano S; Márquez L; Mercade E; Mehandru S; Cerutti A
[Ad] Endereço:Program for Inflammatory and Cardiovascular Disorders, Institut Hospital del Mar d'Investigacions Mèdiques (IMIM), Barcelona 08003, Spain. Electronic address: gmagri@imim.es.
[Ti] Título:Human Secretory IgM Emerges from Plasma Cells Clonally Related to Gut Memory B Cells and Targets Highly Diverse Commensals.
[So] Source:Immunity;47(1):118-134.e8, 2017 Jul 18.
[Is] ISSN:1097-4180
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Secretory immunoglobulin A (SIgA) enhances host-microbiota symbiosis, whereas SIgM remains poorly understood. We found that gut IgM plasma cells (PCs) were more abundant in humans than mice and clonally related to a large repertoire of memory IgM B cells disseminated throughout the intestine but rare in systemic lymphoid organs. In addition to sharing a gut-specific gene signature with memory IgA B cells, memory IgM B cells were related to some IgA clonotypes and switched to IgA in response to T cell-independent or T cell-dependent signals. These signals induced abundant IgM which, together with SIgM from clonally affiliated PCs, recognized mucus-embedded commensals. Bacteria recognized by human SIgM were dually coated by SIgA and showed increased richness and diversity compared to IgA-only-coated or uncoated bacteria. Thus, SIgM may emerge from pre-existing memory rather than newly activated naive IgM B cells and could help SIgA to anchor highly diverse commensal communities to mucus.
[Mh] Termos MeSH primário: Angiodisplasia/imunologia
Linfócitos B/imunologia
Neoplasias do Colo/imunologia
Pólipos do Colo/imunologia
Imunoglobulina M/metabolismo
Intestinos/imunologia
Plasmócitos/imunologia
[Mh] Termos MeSH secundário: Adulto
Idoso
Idoso de 80 Anos ou mais
Animais
Células Clonais
Feminino
Microbioma Gastrointestinal/imunologia
Seres Humanos
Imunidade nas Mucosas
Imunoglobulina A/metabolismo
Switching de Imunoglobulina
Memória Imunológica
Intestinos/microbiologia
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Meia-Idade
Simbiose
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Immunoglobulin A); 0 (Immunoglobulin M)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170925
[Lr] Data última revisão:
170925
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170716
[St] Status:MEDLINE


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[PMID]:28552982
[Au] Autor:Grooteman KV; Matheeuwsen M; van Geenen EJM; Drenth JPH
[Ad] Endereço:Department of Gastroenterology and Hepatology, Radboud University Medical Center, Nijmegen, The Netherlands.
[Ti] Título:Decreased health-related quality of life in angiodysplasia patients: A cross-sectional cohort.
[So] Source:PLoS One;12(5):e0177522, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Gastrointestinal angiodysplasias may cause anemia. Quality of life (QoL) is a valid patient reported outcome and improvement of QoL represents an important treatment goal. There is a paucity of data on the effect of angiodysplasias on QoL. Therefore, we aim to evaluate QoL and fatigue in angiodysplasia patients. We performed a cross-sectional patient-reported outcome study. We included patients with endoscopy proven angiodysplasias and measured QoL with Short Form-36 and level of fatigue using Multi Fatigue Inventory-20. We distinguished three subgroups of patients according to disease severity: 1) with treatment for angiodysplasias, 2) without treatment for angiodysplasias and 3) without recent hospital visits. The primary outcome was the physical component summary (PCS) score on the SF-36. Multivariate regression analysis were performed to correct for differences at baseline. A total of 144 patients completed the questionnaires (response rate = 62%; mean age 68 years; 65% men). Angiodysplasia patients have a significant lower PCS compared to the age-matched general population (respectively 41.0 vs. 43.3, p = 0.01). Disease severity is independently associated with a negative outcome on QoL (ß -4.6, 95% CI -7.8--1.3). Similarly patients score lower on multiple QoL subdomains, i.e. role limitations due to physical health problems (40.8 vs. 44.0, p<0.01), general health (39.7 vs. 47.3, p<0.01). Angiodysplasia patients are more fatigued compared to the general population (male 56.1 vs. 48.5, p<0.01, female 59.2 vs. 51.5, p = 0.01). In conclusion, angiodysplasias are independently associated with clinically significant impairments in multiple domains of health-related QoL, especially in measures of functional limitation.
[Mh] Termos MeSH primário: Angiodisplasia/fisiopatologia
Qualidade de Vida
[Mh] Termos MeSH secundário: Idoso
Estudos de Coortes
Estudos Transversais
Fadiga
Feminino
Seres Humanos
Masculino
Meia-Idade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170921
[Lr] Data última revisão:
170921
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170530
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0177522


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[PMID]:28406792
[Au] Autor:Lamoria S; De A; Sharma V
[Ad] Endereço:Assistant Professor in the Department of Medicine at the Post Graduate Institute of Medical Education and Research and a Gastroenterologist at Dr Ram Manohar Lohia Hospital in Delhi, India. doctorlamoria@yahoo.com.
[Ti] Título:Image Diagnosis: Unusual Cause of Gastrointestinal Bleeding in a Young Man: Isolated Gastric Angiodysplasias.
[So] Source:Perm J;21, 2017.
[Is] ISSN:1552-5775
[Cp] País de publicação:United States
[La] Idioma:eng
[Mh] Termos MeSH primário: Angiodisplasia/diagnóstico
Hemorragia Gastrointestinal/diagnóstico
Gastropatias/diagnóstico
[Mh] Termos MeSH secundário: Adulto
Angiodisplasia/complicações
Hemorragia Gastrointestinal/etiologia
Seres Humanos
Masculino
Gastropatias/complicações
Adulto Jovem
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170913
[Lr] Data última revisão:
170913
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170414
[St] Status:MEDLINE
[do] DOI:10.7812/TPP/16-094


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[PMID]:28395783
[Au] Autor:Beg S; Ragunath K
[Ad] Endereço:NIHR Nottingham Digestive Diseases Biomedical Research Unit, Department of Gastroenterology, Queen Medical Centre, Nottingham, United Kingdom. Electronic address: sabina.beg@nhs.net.
[Ti] Título:Review on gastrointestinal angiodysplasia throughout the gastrointestinal tract.
[So] Source:Best Pract Res Clin Gastroenterol;31(1):119-125, 2017 Feb.
[Is] ISSN:1532-1916
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Gastrointestinal angiodysplasia are rare but clinically important vascular aberrations found within the gastrointestinal mucosa and submucosa. Their clinical impact varies from being an asymptomatic incidental finding, to causing life threatening bleeding. In this review we critically appraise the key findings from the current literature on the pathology, clinical presentation and management of these lesions.
[Mh] Termos MeSH primário: Angiodisplasia
Gastroenteropatias
Hemorragia Gastrointestinal/etiologia
[Mh] Termos MeSH secundário: Idoso
Seres Humanos
Masculino
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170503
[Lr] Data última revisão:
170503
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170412
[St] Status:MEDLINE


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[PMID]:28198025
[Au] Autor:Bosch X; Montori E; Guerra-García M; Costa-Rodríguez J; Quintanilla MH; Tolosa-Chapasian PE; Moreno P; Guasch N; López-Soto A
[Ad] Endereço:Quick Diagnosis Unit, Adult Day Care Center, Hospital Clínic, University of Barcelona, Barcelona, Spain.
[Ti] Título:Haemoglobin responses to transfusion in severe iron deficiency anaemia: potential impact of gastrointestinal disorders.
[So] Source:Vox Sang;112(3):257-267, 2017 Apr.
[Is] ISSN:1423-0410
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND AND OBJECTIVES: Red blood cell (RBC) transfusion may be justified in iron deficiency anaemia (IDA) when an increase in oxygen delivery is needed, as sometimes occurs in subjects with haemoglobin <8·0 mg/dL, serious comorbidities or at risk of cardiovascular instability. Earlier investigations showed that some patients with severe IDA requiring transfusion had lower than expected post-transfusion haemoglobin levels with poorer clinical outcomes than other patients. After hypothesizing that haemoglobin responses to transfusion were different and that the underlying gastrointestinal (GI) disorders causing IDA could be a confounder explaining this association, these responses were analysed in a prospective cohort of IDA adults referred for outpatient GI investigation. MATERIALS AND METHODS: Transfused patients with proven IDA, baseline haemoglobin at referral <9·0 g/dL and no extraintestinal bleeding were eligible. To assess a homogeneous population, only GI disorders known to cause occult bleeding were considered. Haemoglobin increments per 100 mL of RBCs were investigated. RESULTS: In total, 2818 patients were enrolled over 10·5 years. On multivariable regression, diffuse angiodysplasias and GI cancer independently predicted for reduced increments in post-transfusion haemoglobin [adjusted regression coefficients: -0·082 (95% confidence interval, -0·093 to -0·072) and -0·073 (95% confidence interval, -0·081 to -0·066), respectively, P < 0·001 in both]. Haemoglobin responses in the remaining bleeding disorders were adequate and agreed with the principle that one RBC unit increases the haemoglobin an average of 1 g/dL. CONCLUSION: The potential differential impact of GI disorders on changes in haemoglobin levels after RBC transfusion could be useful for transfusing physicians, especially for diagnostic purposes.
[Mh] Termos MeSH primário: Anemia Ferropriva/terapia
Transfusão de Eritrócitos
Gastroenteropatias/complicações
[Mh] Termos MeSH secundário: Adulto
Idoso
Anemia Ferropriva/sangue
Anemia Ferropriva/etiologia
Angiodisplasia/complicações
Angiodisplasia/patologia
Transfusão de Eritrócitos/efeitos adversos
Feminino
Gastroenteropatias/patologia
Hemoglobinas/análise
Seres Humanos
Masculino
Meia-Idade
Análise Multivariada
Estudos Prospectivos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Hemoglobins)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170502
[Lr] Data última revisão:
170502
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170216
[St] Status:MEDLINE
[do] DOI:10.1111/vox.12491


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[PMID]:28065528
[Au] Autor:Bosch X; Montori E; Guerra-García M; Costa-Rodríguez J; Quintanilla MH; Tolosa-Chapasian PE; Moreno P; Guasch N; López-Soto A
[Ad] Endereço:Quick Diagnosis Unit, Adult Day Care Center, Clinical Institute of Medicine and Dermatology (ICMiD), Hospital Clínic, Institutd'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), University of Barcelona, Barcelona, Spain; Department of Internal Medicine, Clinical Institute of Medicine and Derm
[Ti] Título:A comprehensive evaluation of the gastrointestinal tract in iron-deficiency anemia with predefined hemoglobin below 9mg/dL: A prospective cohort study.
[So] Source:Dig Liver Dis;49(4):417-426, 2017 Apr.
[Is] ISSN:1878-3562
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Anemia is defined as hemoglobin below the cutoff of normal in studies examining the gastrointestinal (GI) tract in iron-deficiency anemia (IDA). Although the risk of GI cancer (GIC) increases as hemoglobin decreases, guidelines do not usually recommend hemoglobin thresholds for IDA investigation. METHODS: To elucidate whether underlying GI disorders explain the different hemoglobin values and clinical outcomes observed initially in IDA patients referred for GI workup, we prospectively investigated the diagnostic yield of a thorough GI examination in consecutive IDA adults with predefined hemoglobin <9g/dL and no extraintestinal bleeding. RESULTS: 4552 patients were enrolled over 10 years. 96% of 4038 GI lesions were consistent with occult bleeding disorders and 4% with non-bleeding disorders. Predominant bleeding disorders included upper GI ulcerative/erosive lesions (51%), GIC (15%), and angiodysplasias (12%). Diffuse angiodysplasias (45% of angiodysplasias) and GIC showed the lowest hemoglobin values (6.3 [1.5] and 6.4 [1.3]g/dL, respectively). While the spread (diffuse vs. localized) and number (<3 vs. ≥3) of angiodysplasias correlated with the degree of anemia, hemoglobin values were lower in GIC with vs. without ulcerated/friable lesions (6.0 [1.1] vs. 7.0 [1.2]g/dL, P<0.001). CONCLUSION: Not only GIC but also diffuse angiodysplasias caused the most severe anemia in IDA with predefined hemoglobin values <9g/dL.
[Mh] Termos MeSH primário: Anemia Ferropriva/epidemiologia
Angiodisplasia/complicações
Angiodisplasia/diagnóstico
Gastroenteropatias/complicações
Gastroenteropatias/diagnóstico
Hemoglobinas/análise
[Mh] Termos MeSH secundário: Idoso
Idoso de 80 Anos ou mais
Anemia Ferropriva/etiologia
Endoscopia do Sistema Digestório
Feminino
Seguimentos
Hemorragia Gastrointestinal/etiologia
Trato Gastrointestinal/patologia
Seres Humanos
Masculino
Meia-Idade
Sangue Oculto
Estudos Prospectivos
Espanha
[Pt] Tipo de publicação:JOURNAL ARTICLE; MULTICENTER STUDY
[Nm] Nome de substância:
0 (Hemoglobins)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171003
[Lr] Data última revisão:
171003
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170110
[St] Status:MEDLINE


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[PMID]:28065527
[Au] Autor:Efthymakis K; Milano A; Laterza F; Serio M; Neri M
[Ad] Endereço:Department of Medicine and Ageing Sciences and Center for Excellence on Ageing and Translational Medicine (CeSI-MeT), "G. D'Annunzio" University and Foundation, Chieti, Italy.
[Ti] Título:Iron deficiency anemia despite effective gluten-free diet in celiac disease: Diagnostic role of small bowel capsule endoscopy.
[So] Source:Dig Liver Dis;49(4):412-416, 2017 Apr.
[Is] ISSN:1878-3562
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:BACKGROUND & AIM: Iron deficiency anemia (IDA) is associated with celiac disease (CD). Although gluten-free diet (GFD) is an efficient treatment for CD, IDA remains an occasional finding during follow-up and correlates to inadequate gluten exclusion. Little is known regarding persistent IDA despite effective GFD. We aimed to evaluate the role of small bowel capsule endoscopy (SBCE) in this setting. METHODS: We prospectively included consecutive patients undergoing GFD for ≥24 months with persistent concomitant IDA. Patients were assessed serologically and, if negative, underwent endoscopic evaluation. RESULTS: Twenty-six patients underwent esophago-gastro-duodenoscopy (EGD), colonoscopy and SBCE. Altogether, 11 patients resulted positive. EGD showed mucosal lesions in 7: erosive gastritis (n=3), erosive duodenitis (n=1), active CD (n=3). Colonoscopy showed hemorrhoids in 2. SBCE was positive in 6 cases: erosive jejunitis (n=3, 1 eventually diagnosed as refractory CD, 2 as Crohn's disease), angiodysplasias (n=2), lymphangectasia (n=1). Some overlap was observed between procedures, since in 4 subjects EGD and SBCE produced significant findings. However, in 3 cases SBCE documented severe disease, not found at EGD. Hypoalbuminemia was significantly associated with a positive SBCE outcome (p<0.01). CONCLUSION: SBCE yielded significant findings in 23% of celiacs with persistent IDA despite adequate GFD. These were associated to hypoalbuminemia, indicating their occurrence at more severe stages of the disease.
[Mh] Termos MeSH primário: Anemia Ferropriva/epidemiologia
Endoscopia por Cápsula
Doença Celíaca/complicações
Doença Celíaca/dietoterapia
Intestino Delgado/patologia
[Mh] Termos MeSH secundário: Adolescente
Adulto
Angiodisplasia/diagnóstico
Dieta Livre de Glúten
Enterite/diagnóstico
Feminino
Gastrite/diagnóstico
Hemorragia Gastrointestinal/diagnóstico
Seres Humanos
Itália
Masculino
Meia-Idade
Estudos Prospectivos
[Pt] Tipo de publicação:EVALUATION STUDIES; JOURNAL ARTICLE
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171003
[Lr] Data última revisão:
171003
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170110
[St] Status:MEDLINE


  10 / 827 MEDLINE  
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[PMID]:28003433
[Au] Autor:Ishimaru T; Ishida J; Kim JD; Mizukami H; Hara K; Hashimoto M; Yagami KI; Sugiyama F; Fukamizu A
[Ad] Endereço:Graduate School of Life and Environmental Sciences, University of Tsukuba, 1-1-1 Tennodai, Tsukuba, Ibaraki 305-8572, Japan.
[Ti] Título:Angiodysplasia in embryo lacking protein arginine methyltransferase 1 in vascular endothelial cells.
[So] Source:J Biochem;161(3):255-258, 2017 Mar 01.
[Is] ISSN:1756-2651
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Protein arginine methyltransferase 1 (PRMT1) is involved in multiple cellular functions including proliferation and differentiation. Although PRMT1 is expressed in vascular endothelial cells (ECs), which are responsible for angiogenesis during embryonic development, its role has remained elusive. In this study, we generated endothelial-specific prmt1-knockout (Prmt1-ECKO) mice, and found that they died before embryonic day 15. The superficial temporal arteries in these embryos were poorly perfused with blood, and whole-mount 3D imaging revealed dilated and segmentalized luminal structures in Prmt1-ECKO fetuses in comparison with those of controls. Our findings provide evidence that PRMT1 is important for embryonic vascular formation.
[Mh] Termos MeSH primário: Angiodisplasia/metabolismo
Células Endoteliais/metabolismo
Proteína-Arginina N-Metiltransferases/metabolismo
[Mh] Termos MeSH secundário: Animais
Camundongos
Camundongos Knockout
Camundongos Transgênicos
Proteína-Arginina N-Metiltransferases/química
Proteína-Arginina N-Metiltransferases/deficiência
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
EC 2.1.1.319 (Prmt1 protein, mouse); EC 2.1.1.319 (Protein-Arginine N-Methyltransferases)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170515
[Lr] Data última revisão:
170515
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161223
[St] Status:MEDLINE
[do] DOI:10.1093/jb/mvw095



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