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  1 / 2965 MEDLINE  
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[PMID]:28541008
[Au] Autor:Ahn WK; Park S; Kim HD
[Ad] Dirección:Division of Pediatric Neurology, Department of Pediatrics, Severance Children's Hospital, Yonsei University College of Medicine, Seoul, Korea.
[Ti] Título:Protein-Losing Enteropathy as a Complication of the Ketogenic Diet.
[So] Fuente:Yonsei Med J;58(4):891-893, 2017 Jul.
[Is] ISSN:1976-2437
[Cp] País de publicación:Korea (South)
[La] Idioma:eng
[Ab] Resumen:The ketogenic diet is an effective treatment for the patients with intractable epilepsy, however, the diet therapy can sometimes be discontinued by complications. Protein-losing enteropathy is a rarely reported serious complication of the ketogenic diet. We present a 16-month-old Down syndrome baby with protein-losing enteropathy during the ketogenic diet as a treatment for West syndrome. He suffered from diarrhea, general edema and hypoalbuminemia which were not controlled by conservative care for over 1 month. Esophagogastroduodenoscopy and stool alpha-1 antitrypsin indicated protein-losing enteropathy. Related symptoms were relieved after cessation of the ketogenic diet. Unexplained hypoalbuminemia combined with edema and diarrhea during ketogenic suggests the possibility of protein-losing enteropathy, and proper evaluation is recommended in order to expeditiously detect it and to act accordingly.
[Mh] Términos MeSH primario: Dieta Cetogénica/efectos adversos
Enteropatías Perdedoras de Proteínas/complicaciones
[Mh] Términos MeSH secundario: Duodeno/patología
Humanos
Lactante
Masculino
Membrana Mucosa/patología
Apoyo Nutricional
[Pt] Tipo de publicación:CASE REPORTS
[Em] Mes de ingreso:1710
[Cu] Fecha actualización por clase:171020
[Lr] Fecha última revisión:171020
[Sb] Subgrupo de revista:IM
[Da] Fecha de ingreso para procesamiento:170525
[St] Status:MEDLINE
[do] DOI:10.3349/ymj.2017.58.4.891


  2 / 2965 MEDLINE  
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[PMID]:29022673
[Au] Autor:Angeletti A; Marasà M; Cravedi P
[Ad] Dirección:University of Bologna, Bologna, Italy
[Ti] Título:CD55 Deficiency and Protein-Losing Enteropathy.
[So] Fuente:N Engl J Med;377(15):1499, 2017 10 12.
[Is] ISSN:1533-4406
[Cp] País de publicación:United States
[La] Idioma:eng
[Mh] Términos MeSH primario: Procedimiento de Fontan
Enteropatías Perdedoras de Proteínas
[Mh] Términos MeSH secundario: Humanos
[Pt] Tipo de publicación:LETTER; COMMENT
[Em] Mes de ingreso:1710
[Cu] Fecha actualización por clase:171018
[Lr] Fecha última revisión:171018
[Sb] Subgrupo de revista:AIM; IM
[Da] Fecha de ingreso para procesamiento:171012
[St] Status:MEDLINE
[do] DOI:10.1056/NEJMc1710011


  3 / 2965 MEDLINE  
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[PMID]:29020582
[Au] Autor:Kurolap A; Eshach-Adiv O; Baris HN
[Ad] Dirección:Technion-Israel Institute of Technology, Haifa, Israel.
[Ti] Título:CD55 Deficiency and Protein-Losing Enteropathy.
[So] Fuente:N Engl J Med;377(15):1500, 2017 10 12.
[Is] ISSN:1533-4406
[Cp] País de publicación:United States
[La] Idioma:eng
[Mh] Términos MeSH primario: Procedimiento de Fontan
Enteropatías Perdedoras de Proteínas
[Mh] Términos MeSH secundario: Humanos
[Pt] Tipo de publicación:LETTER; COMMENT
[Em] Mes de ingreso:1710
[Cu] Fecha actualización por clase:171018
[Lr] Fecha última revisión:171018
[Sb] Subgrupo de revista:AIM; IM
[Da] Fecha de ingreso para procesamiento:171011
[St] Status:MEDLINE
[do] DOI:10.1056/NEJMc1710011


  4 / 2965 MEDLINE  
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[PMID]:29020581
[Au] Autor:Ozen A; Comrie WA; Lenardo MJ
[Ad] Dirección:Marmara University, Istanbul, Turkey
[Ti] Título:CD55 Deficiency and Protein-Losing Enteropathy.
[So] Fuente:N Engl J Med;377(15):1499-1500, 2017 10 12.
[Is] ISSN:1533-4406
[Cp] País de publicación:United States
[La] Idioma:eng
[Mh] Términos MeSH primario: Procedimiento de Fontan
Enteropatías Perdedoras de Proteínas
[Mh] Términos MeSH secundario: Humanos
[Pt] Tipo de publicación:LETTER; COMMENT
[Em] Mes de ingreso:1710
[Cu] Fecha actualización por clase:171018
[Lr] Fecha última revisión:171018
[Sb] Subgrupo de revista:AIM; IM
[Da] Fecha de ingreso para procesamiento:171011
[St] Status:MEDLINE
[do] DOI:10.1056/NEJMc1710011


  5 / 2965 MEDLINE  
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[PMID]:28657829
[Au] Autor:Ozen A; Comrie WA; Ardy RC; Domínguez Conde C; Dalgic B; Beser ÖF; Morawski AR; Karakoc-Aydiner E; Tutar E; Baris S; Ozcay F; Serwas NK; Zhang Y; Matthews HF; Pittaluga S; Folio LR; Unlusoy Aksu A; McElwee JJ; Krolo A; Kiykim A; Baris Z; Gulsan M; Ogulur I; Snapper SB; Houwen RHJ; Leavis HL; Ertem D; Kain R; Sari S; Erkan T; Su HC; Boztug K; Lenardo MJ
[Ad] Dirección:From the Section of Molecular Development of the Immune System, Laboratory of Immunology (A.O., W.A.C., A.R.M., H.F.M., M.J.L.), the Clinical Genomics Program (A.O., W.A.C., A.R.M., Y.Z., H.F.M., H.C.S., M.J.L.), and the Human Immunological Diseases Section, Laboratory of Host Defenses (Y.Z., H.C.S.
[Ti] Título:CD55 Deficiency, Early-Onset Protein-Losing Enteropathy, and Thrombosis.
[So] Fuente:N Engl J Med;377(1):52-61, 2017 07 06.
[Is] ISSN:1533-4406
[Cp] País de publicación:United States
[La] Idioma:eng
[Ab] Resumen:BACKGROUND: Studies of monogenic gastrointestinal diseases have revealed molecular pathways critical to gut homeostasis and enabled the development of targeted therapies. METHODS: We studied 11 patients with abdominal pain and diarrhea caused by early-onset protein-losing enteropathy with primary intestinal lymphangiectasia, edema due to hypoproteinemia, malabsorption, and less frequently, bowel inflammation, recurrent infections, and angiopathic thromboembolic disease; the disorder followed an autosomal recessive pattern of inheritance. Whole-exome sequencing was performed to identify gene variants. We evaluated the function of CD55 in patients' cells, which we confirmed by means of exogenous induction of expression of CD55. RESULTS: We identified homozygous loss-of-function mutations in the gene encoding CD55 (decay-accelerating factor), which lead to loss of protein expression. Patients' T lymphocytes showed increased complement activation causing surface deposition of complement and the generation of soluble C5a. Costimulatory function and cytokine modulation by CD55 were defective. Genetic reconstitution of CD55 or treatment with a complement-inhibitory therapeutic antibody reversed abnormal complement activation. CONCLUSIONS: CD55 deficiency with hyperactivation of complement, angiopathic thrombosis, and protein-losing enteropathy (the CHAPLE syndrome) is caused by abnormal complement activation due to biallelic loss-of-function mutations in CD55. (Funded by the National Institute of Allergy and Infectious Diseases and others.).
[Mh] Términos MeSH primario: Antígenos CD55/genética
Activación de Complemento/genética
Proteínas del Sistema Complemento/metabolismo
Mutación
Enteropatías Perdedoras de Proteínas/genética
Trombosis/genética
[Mh] Términos MeSH secundario: Antígenos CD55/sangre
Niño
Preescolar
Activación de Complemento/efectos de drogas
Inactivadores del Complemento/farmacología
Femenino
Homocigoto
Humanos
Inmunoglobulina A/sangre
Lactante
Intestino Delgado/patología
Masculino
Linaje
Enteropatías Perdedoras de Proteínas/complicaciones
Estadísticas no Paramétricas
Síndrome
Linfocitos T/metabolismo
[Pt] Tipo de publicación:JOURNAL ARTICLE
[Nm] Nombre de substancia:
0 (Antigens, CD55); 0 (Complement Inactivating Agents); 0 (Immunoglobulin A); 9007-36-7 (Complement System Proteins)
[Em] Mes de ingreso:1707
[Cu] Fecha actualización por clase:171018
[Lr] Fecha última revisión:171018
[Sb] Subgrupo de revista:AIM; IM
[Da] Fecha de ingreso para procesamiento:170628
[St] Status:MEDLINE
[do] DOI:10.1056/NEJMoa1615887


  6 / 2965 MEDLINE  
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[PMID]:28060125
[Au] Autor:Simpson EA; Jaring MRF; Andronikou S
[Ad] Dirección:*Department of Paediatric Radiology, Bristol Royal Hospital for Children, University Hospitals Bristol NHS Foundation Trust †CRIC Bristol, University of Bristol, Bristol, UK.
[Ti] Título:Massive Mesenteric Lymphadenopathy Causing Protein-losing Enteropathy in Gaucher Disease.
[So] Fuente:J Pediatr Hematol Oncol;39(5):e300-e301, 2017 Jul.
[Is] ISSN:1536-3678
[Cp] País de publicación:United States
[La] Idioma:eng
[Ab] Resumen:Protein-losing enteropathy due to massive mesenteric lymphadenopathy is a rare complication of Gaucher disease which is generally refractory to treatment with enzyme replacement and substrate reduction therapies. It is postulated that lymph nodes may act as a "sanctuary site" into which these treatments cannot penetrate. We present the case of a male child with Gaucher disease who developed massive mesenteric lymph nodes despite otherwise successful treatment with enzyme replacement therapy, and subsequently developed protein-losing enteropathy. The sonographic and magnetic resonance appearances of this complication are shown. Large volume lymphadenopathy inevitably provokes concern about the possibility of malignancy, but in a patient with Gaucher disease-particularly with significant ascites and clinical features of protein-losing enteropathy-this rare complication should be considered.
[Mh] Términos MeSH primario: Enfermedad de Gaucher/complicaciones
Ganglios Linfáticos/diagnóstico por imagen
Linfadenopatía/complicaciones
Enteropatías Perdedoras de Proteínas/etiología
[Mh] Términos MeSH secundario: Terapia de Reemplazo Enzimático
Humanos
Lactante
Ganglios Linfáticos/patología
Linfadenopatía/diagnóstico por imagen
Imagen por Resonancia Magnética
Masculino
Mesenterio/diagnóstico por imagen
Mesenterio/patología
Ultrasonografía
[Pt] Tipo de publicación:CASE REPORTS; JOURNAL ARTICLE; RETRACTED PUBLICATION
[Em] Mes de ingreso:1709
[Cu] Fecha actualización por clase:171017
[Lr] Fecha última revisión:171017
[Sb] Subgrupo de revista:IM
[Da] Fecha de ingreso para procesamiento:170106
[St] Status:MEDLINE
[do] DOI:10.1097/MPH.0000000000000763


  7 / 2965 MEDLINE  
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[PMID]:28210768
[Au] Autor:Menon S; Chennapragada M; Ugaki S; Sholler GF; Ayer J; Winlaw DS
[Ad] Dirección:The Heart Centre for Children, The Children's Hospital at Westmead, Sydney, NSW, Australia.
[Ti] Título:The Lymphatic Circulation in Adaptations to the Fontan Circulation.
[So] Fuente:Pediatr Cardiol;38(5):886-892, 2017 Jun.
[Is] ISSN:1432-1971
[Cp] País de publicación:United States
[La] Idioma:eng
[Ab] Resumen:Failing Fontan continues to be major problem for patients on the univentricular pathway. Failing Fontan is often complicated by chylothorax, plastic bronchitis and protein loosing enteropathy. The role of lymphatic circulation in Fontan circulation is still being researched. Newer imaging modalities give insight into the role of abnormal dilatation and retrograde flow in lymphatic channels post Fontan. Interventional strategies targeting abnormal lymphatic channels, provides an alternative management strategy for patients with failing Fontan. This review focuses on the role of lymphatic system in adaptations to Fontan circulation.
[Mh] Términos MeSH primario: Procedimiento de Fontan/efectos adversos
Cardiopatías Congénitas/cirugía
Enfermedades Linfáticas/fisiopatología
Sistema Linfático/fisiopatología
[Mh] Términos MeSH secundario: Adaptación Fisiológica
Circulación Sanguínea/fisiología
Bronquitis/etiología
Dilatación Patológica
Humanos
Enfermedades Linfáticas/diagnóstico
Enfermedades Linfáticas/etiología
Enfermedades Linfáticas/terapia
Vasos Linfáticos/fisiopatología
Enteropatías Perdedoras de Proteínas/etiología
[Pt] Tipo de publicación:JOURNAL ARTICLE; REVIEW
[Em] Mes de ingreso:1710
[Cu] Fecha actualización por clase:171005
[Lr] Fecha última revisión:171005
[Sb] Subgrupo de revista:IM
[Da] Fecha de ingreso para procesamiento:170217
[St] Status:MEDLINE
[do] DOI:10.1007/s00246-017-1576-y


  8 / 2965 MEDLINE  
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[PMID]:28338158
[Au] Autor:Gong K; Guo S; Wang K
[Ad] Dirección:Department of General Surgery, The First People's Hospital of Yunnan Province, Kunming 650032, China.
[Ti] Título:[Diagnosis and treatment of duodenal injury and fistula].
[So] Fuente:Zhonghua Wei Chang Wai Ke Za Zhi;20(3):266-269, 2017 Mar 25.
[Is] ISSN:1671-0274
[Cp] País de publicación:China
[La] Idioma:chi
[Ab] Resumen:Duodenal injury is a serious abdominal organ injury. Duodenal fistula is one of the most serious complications in gastrointestinal surgery, which is concerned for its critical status, difficulty in treatment and high mortality. Thoracic and abdominal compound closed injury and a small part of open injury are common causes of duodenal injury. Iatrogenic or traumatic injury, malnutrition, cancer, tuberculosis, Crohn's disease etc. are common causes of duodenal fistula, however, there has been still lacking of ideal diagnosis and treatment by now. The primary treatment strategy of duodenal fistula is to determine the cause of disease and its key point is prevention, including perioperative parenteral and enteral nutrition support, improvement of hypoproteinemia actively, avoidance of stump ischemia by excessive separate duodenum intraoperatively, performance of appropriate duodenum stump suture to ensure the stump blood supply, and avoidance of postoperative input loop obstruction, postoperative stump bleeding or hematoma etc. Once duodenal fistula occurs, a simple and reasonable operation can be selected and performed after fluid prohibition, parenteral and enteral nutrition, acid suppression, enzyme inhibition, anti-infective treatment and maintaining water salt electrolyte and acid-base balance. Double tube method, duodenal decompression and peritoneal drainage can reduce duodenal fistula-related complications, and then reduce the mortality, which can save the lives of patients.
[Mh] Términos MeSH primario: Procedimientos Quirúrgicos del Sistema Digestivo/efectos adversos
Procedimientos Quirúrgicos del Sistema Digestivo/métodos
Enfermedades Duodenales/prevención & control
Enfermedades Duodenales/terapia
Duodeno/lesiones
Duodeno/cirugía
Fístula Intestinal/prevención & control
Fístula Intestinal/terapia
[Mh] Términos MeSH secundario: Traumatismos Abdominales/complicaciones
Antiinfecciosos/uso terapéutico
Descompresión Quirúrgica
Drenaje
Enfermedades Duodenales/diagnóstico
Enfermedades Duodenales/etiología
Duodeno/irrigación sanguínea
Nutrición Enteral
Humanos
Hipoproteinemia/terapia
Fístula Intestinal/diagnóstico
Fístula Intestinal/etiología
Isquemia/prevención & control
Apoyo Nutricional
Nutrición Parenteral
Complicaciones Posoperatorias/prevención & control
Complicaciones Posoperatorias/terapia
Técnicas de Sutura
Traumatismos Torácicos/complicaciones
[Pt] Tipo de publicación:JOURNAL ARTICLE
[Nm] Nombre de substancia:
0 (Anti-Infective Agents)
[Em] Mes de ingreso:1709
[Cu] Fecha actualización por clase:170922
[Lr] Fecha última revisión:170922
[Sb] Subgrupo de revista:IM
[Da] Fecha de ingreso para procesamiento:170324
[St] Status:MEDLINE


  9 / 2965 MEDLINE  
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[PMID]:28390394
[Au] Autor:Allenspach K; Rizzo J; Jergens AE; Chang YM
[Ad] Dirección:Department of Clinical Sciences and Services, University of London, North Mymms, Hertfordshire, UK. allek@iastate.edu.
[Ti] Título:Hypovitaminosis D is associated with negative outcome in dogs with protein losing enteropathy: a retrospective study of 43 cases.
[So] Fuente:BMC Vet Res;13(1):96, 2017 Apr 08.
[Is] ISSN:1746-6148
[Cp] País de publicación:England
[La] Idioma:eng
[Ab] Resumen:BACKGROUND: Hypovitaminosis D has previously been shown to be prevalent amongst dogs with protein losing enteropathy (PLE). The hypothesis of this study was that Low 25-hydroxyvitamin D (25(OH) D) serum concentrations could be a risk factor for negative outcome in dogs with PLE. Forty-three dogs diagnosed with PLE (2005-2014) and which serum Vitamin D serum concentrations were collected and archived at -80 Degrees C were analyzed. Post-diagnostic communication with referring veterinarians was made to determine outcome of PLE dogss: Dogs which died due to PLE within 4 months after diagnosis (negative outcome group, n = 22) and dogs alive or which died due to another disease at the end point of the study (1 year after diagnosis, good outcome group, n = 21). Serum samples taken at the time of diagnosis were analysed for ionized calcium (iCa) concentrations and serum 25(OH) D concentration. RESULTS: Clinical (CCECAI) scores, age at PLE diagnosis, and iCa concentrations were not significantly different between dog groups. A significantly greater (p < 0.001) number of PLE dogs treated with hydrolyzed or elimination diet alone showed good outcome as compared to the PLE negative outcome group. Median serum 25(OH) D concentration was significantly (p = 0.017) lower in dogs with negative outcome versus PLE dogs with good outcome. Using logistic regression analysis, 25(OH) D serum concentration was shown to be a statistically significant factor for outcome determination. Cox regression analysis yielded a hazard ratio of 0.974 (95% CI 0.949, 0.999) per each one nmol/l increase in serum 25(OH) D concentration. CONCLUSIONS: Low serum 25(OH) D concentration in PLE dogs was significantly associated with poor outcome. Further studies are required to investigate the clinical efficacy of Vitamin D (cholecalciferol) as a potential therapeutic agent for dogs with PLE.
[Mh] Términos MeSH primario: Enfermedades de los Perros/sangre
Enteropatías Perdedoras de Proteínas/veterinaria
Deficiencia de Vitamina D/veterinaria
[Mh] Términos MeSH secundario: Animales
Calcio/sangre
Dieta/veterinaria
Enfermedades de los Perros/mortalidad
Perros
Femenino
Masculino
Enteropatías Perdedoras de Proteínas/sangre
Enteropatías Perdedoras de Proteínas/mortalidad
Estudios Retrospectivos
Vitamina D/análogos & derivados
Vitamina D/sangre
Deficiencia de Vitamina D/sangre
[Pt] Tipo de publicación:JOURNAL ARTICLE
[Nm] Nombre de substancia:
1406-16-2 (Vitamin D); 64719-49-9 (25-hydroxyvitamin D); SY7Q814VUP (Calcium)
[Em] Mes de ingreso:1709
[Cu] Fecha actualización por clase:170919
[Lr] Fecha última revisión:170919
[Sb] Subgrupo de revista:IM
[Da] Fecha de ingreso para procesamiento:170409
[St] Status:MEDLINE
[do] DOI:10.1186/s12917-017-1022-7


  10 / 2965 MEDLINE  
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[PMID]:28534240
[Au] Autor:Unseld B; Stiller B; Borth-Bruhns T; du Bois F; Kroll J; Grohmann J; Fleck T
[Ad] Dirección:Department of Congenital Heart Disease and Pediatric Cardiology, University Heart Centre Freiburg, Mathildenstrasse 1, 79106, Freiburg, Germany.
[Ti] Título:An Early Glenn Operation May be Associated with the Later Occurrence of Protein-Losing Enteropathy in Fontan Patients : Association of Early Glenn and Failing Fontan.
[So] Fuente:Pediatr Cardiol;38(6):1155-1161, 2017 Aug.
[Is] ISSN:1432-1971
[Cp] País de publicación:United States
[La] Idioma:eng
[Ab] Resumen:Protein-losing enteropathy (PLE) and plastic bronchitis (PB) are major causes of long-term mortality after Fontan operation. The objective of this study was to determine early clinical risk factors before the onset of PLE and PB. In a cohort study, 106 Fontan patients between 2005 and 2013 were examined. A median of 5.3 (1.5-8.5) years later, follow-up questionnaires were used to group the patients in a PLE or PB group (n = 14) and a non-PLE/PB group (n = 92). Prevalence of PLE was 9.4% (n = 10) and of PB 3.8% (n = 4). At follow-up, five patients (4.7%) died of PLE or PB. Median age at death was 6.2 years (IQR 10.5, 95% CI 5.3-23.4). We observed no significant group differences in gender distribution (p = 0.73), ventricular morphology (p = 0.87), surgical technique (p = 0.64), conduit fenestration (p = 0.34), age at Fontan operation (p = 0.54), and need for diuretics (p = 0.56). Hypoplastic left heart syndrome was more frequent in the PLE/PB group 50 vs. 22.8% (p = 0.03) OR 3.4 (95% CI 1.1-10.8). The modified Glenn procedure was performed at a median age of 4 months (IQR 4.0) in the PLE/PB group versus 8 months (IQR 8.0) in the non-PLE/PB group (p = 0.01). The early Glenn procedure and hypoplastic left heart syndrome may be associated with the development of PLE and PB.
[Mh] Términos MeSH primario: Procedimiento de Fontan/efectos adversos
Cardiopatías Congénitas/cirugía
Enteropatías Perdedoras de Proteínas/etiología
[Mh] Términos MeSH secundario: Bronquitis/etiología
Niño
Preescolar
Femenino
Procedimiento de Fontan/rehabilitación
Cardiopatías Congénitas/rehabilitación
Humanos
Síndrome del Corazón Izquierdo Hipoplásico/rehabilitación
Síndrome del Corazón Izquierdo Hipoplásico/cirugía
Lactante
Masculino
Estudios Retrospectivos
Factores de Riesgo
Encuestas y Cuestionarios
Factores de Tiempo
Procedimientos Quirúrgicos Vasculares/efectos adversos
Procedimientos Quirúrgicos Vasculares/rehabilitación
[Pt] Tipo de publicación:JOURNAL ARTICLE
[Em] Mes de ingreso:1709
[Cu] Fecha actualización por clase:170914
[Lr] Fecha última revisión:170914
[Sb] Subgrupo de revista:IM
[Da] Fecha de ingreso para procesamiento:170523
[St] Status:MEDLINE
[do] DOI:10.1007/s00246-017-1632-7



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