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1.
Actual. nutr ; 21(2): 43-49, Abril-Junio de 2020.
Article in Spanish | LILACS | ID: biblio-1282315

ABSTRACT

En las últimas décadas, los cambios en el estilo de vida pro-vocaron un incremento en la prevalencia del síndrome meta-bólico y que la enfermedad por hígado graso no alcohólico (nonalcoholic fatty liver disease, NAFLD sus siglas en inglés) se convierta en la enfermedad hepática crónica más fre-cuente en todo el mundo. Los componentes del síndrome metabólico no son sólo altamente prevalentes en pacientes con hígado graso no alcohólico, sino que a la vez aumentan el riesgo de desarrollarlo. Esta relación bidireccional ha sido claramente establecida. Asimismo se considera que NAFLD podría ser el componente hepático del síndrome metabólico. Aunque NAFLD se considera principalmente una enfermedad benigna, puede progresar a fibrosis hepática grave y carcino-ma hepatocelular (CHC), incluso se encontraría este último en hígados no cirróticos. El objetivo de esta revisión es determinar los procesos fisio-patológicos comunes a estas entidades, cuáles son las estra-tegias diagnósticas recomendadas y cuáles las intervenciones terapéuticas actualmente aprobadas.


Subject(s)
Humans , Male , Female , Carcinoma, Hepatocellular/etiology , Metabolic Syndrome/etiology , Non-alcoholic Fatty Liver Disease/complications , Liver Neoplasms/etiology , Fibrosis/etiology , Fibrosis/physiopathology , Fibrosis/therapy , Risk Factors , Carcinoma, Hepatocellular/physiopathology , Carcinoma, Hepatocellular/therapy , Carcinoma, Hepatocellular/diagnostic imaging , Metabolic Syndrome/diagnosis , Metabolic Syndrome/physiopathology , Metabolic Syndrome/therapy , Diabetes Mellitus/etiology , Diabetes Mellitus/physiopathology , Diabetes Mellitus/therapy , Non-alcoholic Fatty Liver Disease/diagnosis , Non-alcoholic Fatty Liver Disease/physiopathology , Non-alcoholic Fatty Liver Disease/therapy , Liver Neoplasms/physiopathology , Liver Neoplasms/therapy , Liver Neoplasms/diagnostic imaging
2.
Rev. chil. cardiol ; 38(1): 37-45, abr. 2019. tab, graf
Article in Spanish | LILACS | ID: biblio-1003636

ABSTRACT

Resumen: Introducción: Atletas altamente entrenados muestran cambios cardíacos estructurales como adaptación a la sobrecarga, producto del ejercicio repetitivo y extenuante. Se han evidenciado elevación de biomarcadores de remodelado y fibrosis miocárdica posterior al ejercicio intenso en atletas. Sin embargo, el comportamiento de estos biomarcadores según el nivel de entrenamiento previo no se ha evaluado. Objetivo: Investigar biomarcadores de fibrosis y función ventricular derecha en maratonistas con distinto nivel de entrenamiento previo. Métodos: Se incluyeron 36 maratonistas hombres, sanos, que completaron 42 km en la maratón de Santiago. Se dividieron según entrenamiento previo en dos grupos, Grupo 1 (G1): ≥100 km/semana y Grupo 2 (G2): <100 km/semana. Se realizó ecocardiografía transtorácica y se evaluaron niveles plasmáticos de galectina-3 y del propéptido amino terminal del procolágeno tipo III (PIIINP) en la semana previa a la carrera e inmediatamente posterior a ésta. Resultados: Posterior a la maratón, la función sistólica del ventrículo derecho disminuyó en el grupo G2 junto con un aumento significativo de los niveles plasmáticos de PIIIPNP (61±16 a 94±24 ng/mL, p=0,01). Estos cambios no se observaron en el grupo G1 (65 ± 11 a 90±29 ng/mL, p=0,10). Los niveles plasmáticos de galectina-3 aumentaron significativamente en ambos grupos posterior al ejercicio (6,8±2,2 a 19,7±4,9 ng/mL, p 0,012 y 6,0±1,1 a 19,4 ± 5,9 ng/mL, p 0,01) en los grupos G1 y G2, respectivamente). Conclusiones: Atletas con menor grado de entrenamiento, presentan posterior a una maratón un significativo aumento de productos de degradación del colágeno (PIIIPNP) asociado a disminución de la función del ventrículo derecho. Los niveles de galectina-3 plasmática aumentan significativamente en ambos grupos post-esfuerzo independiente del entrenamiento previo.


Abstracts: Introduction: Highly trained athletes show structural cardiac changes as adaptation to overload. Rise in remodeling biomarkers and myocardial fibrosis after intense exercise in athletes has been evidenced; however, the behavior of these biomarkers according to pre-competition training level has not been evaluated. Objective: To evaluate fibrosis biomarkers levels and right ventricle function in marathon runners according to their previous training level, in the period prior to a marathon race and immediately after it. Methods: Thirty-six healthy male marathon runners were included. Subjects were grouped according to their previous training level: Group 1 (G1): ≥100 km/week and Group 2 (G2): <100 km/week. Transthoracic echocardiography along with plasmatic levels of galectin-3 and amino terminal propeptide of type III procollagen (PIIINP) were measured one week previous and immediately after the marathon. Results: Post-effort right ventricle systolic function decreased in G2, together with a significant elevation of PIIIPNP (61±16 to 94±24 ng/mL, p=0.01). These changes were not observed in G1 (from 65±11 to 90±29 ng/mL, p=0.10). Plasma galectin-3 increased significantly in both groups immediately post-exercise (6.8±2.2 to 19.7±4.9 ng/mL, p=0.012, and 6.0±1.1 to 19.4±5.9 ng/mL, p=0.01, in G1 and G2. respectively). Conclusion: Less trained athletes evidenced higher post marathon levels of PIIIPNP which is associated with a decreased global right ventricle function. Plasma galectin-3 levels increased significantly after intense exertion regardless of the intensity of previous training.


Subject(s)
Humans , Male , Adult , Middle Aged , Running/physiology , Fibrosis/blood , Biomarkers/blood , Ventricular Function, Right , Heart Injuries/blood , Peptide Fragments/blood , Fibrosis/physiopathology , Exercise/physiology , Single-Blind Method , Chile , Prospective Studies , Longitudinal Studies , Ventricular Function, Left , Procollagen/blood , Galectin 3/blood , Athletes
3.
Arq. bras. cardiol ; 110(2): 124-131, Feb. 2018. tab, graf
Article in English | LILACS | ID: biblio-888018

ABSTRACT

Abstract Background: Previous data has shown that patients in the indeterminate form of Chagas disease may present myocardial fibrosis as shown on through magnetic resonance imaging (MRI). However, there is little information available regarding the degree of severity of myocardial fibrosis in these individuals. This variable has the potential to predict the evolution of Chagas' disease into its cardiac form. Objectives: To describe the frequency and extent of myocardial fibrosis evaluated using an MRI in patients in the indeterminate form, and to compare it with other forms of the disease. Methods: Patients were admitted one after another. Their clinical history was collected and they were submitted to laboratory exams and an MRI. Results: Sixty-one patients with Chagas' disease, with an average age of 58 ± 9 years old, 17 patients in the indeterminate form, 16 in the cardiac form without left ventricular (LV) dysfunction and 28 in the cardiac form with LV dysfunction were studied. P <0.05 was considered to be statistically significant. Late enhancement was detected in 37 patients (64%). Myocardial fibrosis was identified in 6 individuals in indeterminate form (41%; 95% CI 23-66) in a proportion similar to that observed in cardiac form without LV dysfunction (44%); p = 1.0. Among the individuals with fibrosis, the total area of the affected myocardium was 4.1% (IIQ: 2.1 - 10.7) in the indeterminate form versus 2.3% (IIQ: 1-5) in the cardiac form without LV (p = 0.18). The left ventricular fraction ejection in subjects in the indeterminate form was similar to that of the individuals in the cardiac form without ventricular dysfunction (p = 0.09). Conclusion: The presence of fibrosis in the indeterminate form of Chagas' disease has a frequency and extension similar to that of in the cardiac form without dysfunction, suggesting that the former is part of a subclinical disease spectrum, rather than lacking cardiac involvement.


Resumo Fundamento: Dados prévios têm demonstrado que pacientes na forma indeterminada podem apresentar fibrose miocárdica à ressonância magnética (RM). No entanto, são poucas as informações disponíveis quanto ao grau de fibrose miocárdica apresentada por esses indivíduos, o que guardaria relação com o potencial dessa variável na predição de evolução para a forma cardíaca da doença de Chagas. Objetivos: Descrever a frequência e extensão da fibrose miocárdica avaliada por RM em pacientes da forma indeterminada, comparando com as outras formas da doença. Métodos: Pacientes consecutivamente admitidos tiveram história clínica colhida e foram submetidos à realização de exames laboratoriais e RM. Resultados: Foram estudados 61 pacientes portadores da doença de Chagas, com média de idade de 58 ± 9 anos, sendo 17 pacientes na forma indeterminada, 16 na forma cardíaca sem disfunção do ventrículo esquerdo (VE) e 28 na forma com disfunção do VE. Foi considerado estatisticamente significante p < 0,05. Realce tardio foi detectado em 37 pacientes (64%). Foi identificada fibrose miocárdica em 6 indivíduos na forma indeterminada (41%; IC95% 23 - 66), proporção semelhante à observada na forma cardíaca sem disfunção do VE (44%); p = 1,0. Entre os indivíduos com fibrose, a área total do miocárdio acometida foi de 4,1% (IIQ: 2,1 - 10,7) na forma indeterminada versus 2,3% (IIQ: 1 - 5) na forma cardíaca sem disfunção do VE (p = 0,18). A fração de ejeção do ventrículo esquerdo nos indivíduos na forma indeterminada foi semelhante aos portadores da forma cardíaca sem disfunção ventricular (p = 0,09). Conclusão: A presença de fibrose na forma indeterminada da doença de Chagas tem frequência e extensão semelhante à forma cardíaca sem disfunção, o que sugere que a primeira faz parte de um espectro de doença subclínica, em vez da ausência de acometimento cardíaco.


Subject(s)
Humans , Male , Female , Adolescent , Adult , Middle Aged , Aged , Young Adult , Fibrosis/diagnostic imaging , Magnetic Resonance Imaging/methods , Cardiomyopathies/diagnostic imaging , Fibrosis/physiopathology , Ventricular Dysfunction, Left/physiopathology , Ventricular Dysfunction, Left/diagnostic imaging , Cardiomyopathies/physiopathology
5.
São Paulo; s.n; 2014. [164] p. ilus, tab, graf.
Thesis in Portuguese | LILACS | ID: lil-730869

ABSTRACT

As doenças cardiovasculares são a maior causa de morte no mundo e entre essas doenças, a hipertrofia cardíaca (HC) tem se destacado especialmente por ser um fator de risco de insuficiência cardíaca. A HC é um fenômeno que acompanha a hipertensão arterial e no qual se observa aumento de proteínas estruturais e contráteis dos cardiomiócitos, havendo muitas vezes concomitantemente aumento do colágeno intersticial. Fatores independentes da pressão arterial também podem contribuir para o desenvolvimento da hipertrofia cardíaca. Dentre estes fatores, a sobrecarga de sal na dieta tem se destacado. Diversos estudos comprovam o efeito hipertrófico do sal. Em modelos animais onde se estudou sobrecarga de sal, não foi detectado aumento da atividade de renina plasmática, sugerindo que o sistema renina-angiotensina aldosterona (SRA) circulante pode não estar envolvido no desenvolvimento da hipertrofia cardíaca. Apesar de alguns estudos tentarem elucidar o papel do sal no desenvolvimento da hipertrofia ventricular esquerda, os mecanismos pelo qual o sal atua ainda não estão totalmente esclarecidos. Neste contexto, o objetivo do presente estudo é observar os fenômenos que ocorrem no ventrículo esquerdo em resposta a sobrecarga de sal na dieta na tentativa de elucidar sua fisiopatologia. Para tanto, ratos Wistar machos foram divididos em cinco grupos de acordo com a dieta (normossódica 1,26% e hipersódica 8% de NaCl) e com o tratamento (losartan, cloridrato de hidralazina ou N-acetilcisteína). Foi avaliada a evolução ponderal, pressão arterial caudal, medida do diâmetro transverso do cardiomiócito, fibrose intersticial, expressão gênica e proteica dos componentes do SRA, dosagem de aldosterona sérica e cardíaca, dosagem de TBARS cardíaco, concentração de angiotensina II e estado conformacional dos receptores AT1 e AT2. Os principais resultados observados foram: o aumento do consumo de ração (com elevada concentração de NaCl) do grupo HS+NAC e consequente aumento na...


Cardiovascular diseases are the leading cause of death worldwide and among these diseases, the cardiac hypertrophy (CH) has been highlighted, especially as an important risk factor for developing heart failure. The CH is a phenomenon that accompanies hypertension and in which there is increased structural and contractile proteins in cardiomyocytes, with often concomitant increase of interstitial collagen. Blood pressure independent risk factors can also contribute to the development of cardiac hypertrophy. Among these factors, the high salt intake has been outstanding. Several studies confirm the hypertrophic effect of salt. In animal models submitted to salt overload, no increase in plasma renin activity was observed, suggesting that the renin-angiotensin (RAS) circulating system may not be involved in the development of cardiac hypertrophy. Although some studies attempting to elucidate the role of salt in the development of left ventricular hypertrophy, the mechanisms by which salt acts are not yet fully understood. In this context, the objective of this study is to observe the phenomena occurring in the left ventricle in response to dietary salt overload in an attempt to elucidate its pathophysiology.Male Wistar rats were divided into five groups according to their diet (1.26% and 8% NaCl) and treatment (losartan, hydralazine or N-acetylcysteine). We evaluated the body weight, tail-cuff blood pressure, the transverse diameter of the cardiomyocyte, interstitial fibrosis, gene and protein expression of RAAS components, serum and cardiac aldosterone dosage, cardiac TBARS, angiotensin II concentration and binding of conformation-specific anti-AT1 and anti-AT2 antibodies. The main results were: increased food intake (with high NaCl content) in the HS + NAC group and consequent increase in blood pressure and body weight; developing blood pressure-independent CH in the HS + HZ group partial or total prevention of such hypertrophy by treatment with losartan and...


Subject(s)
Animals , Male , Rats , Acetylcysteine , Arterial Pressure , Cardiomegaly/physiopathology , Fibrosis/physiopathology , Hydralazine , Losartan , Models, Animal , Rats, Wistar , Renin-Angiotensin System , Sodium Chloride, Dietary
6.
Clinics ; 68(4): 441-448, abr. 2013. tab, graf
Article in English | LILACS | ID: lil-674238

ABSTRACT

OBJECTIVES: Chronic paracoccidioidomycosis can diffusely affect the lungs. Even after antifungal therapy, patients may present with residual respiratory abnormalities due to fungus-induced lung fibrosis. METHODS: A cross-sectional analysis of 50 consecutive inactive, chronic paracoccidioidomycosis patients was performed using high resolution computed tomography, pulmonary function tests, ergospirometry, the six-minute walk test and health-related quality of life questionnaires. RESULTS: Radiological abnormalities were present in 98% of cases, the most frequent of which were architectural distortion (90%), reticulate and septal thickening (88%), centrilobular and paraseptal emphysema (84%) and parenchymal bands (74%). Patients typically presented with a mild obstructive disorder and a mild reduction in diffusion capacity with preserved exercise capacity, including VO2max and six-minute walking distance. Patient evaluation with the Saint-George Respiratory Questionnaire showed low impairment in the health-related quality of life, and the Medical Research Council questionnaire indicated a low dyspnea index. There were, however, patients with significant oxygen desaturation upon exercise that was associated with respiratory distress compared with the non-desaturated patients. The initial counterimmunoelectrophoresis of these patients was higher and lung emphysema was more prominent; however, there were no differences in the interstitial fibrotic tomographic abnormalities, tobacco exposure, functional responses, exercise capacity or quality of life. CONCLUSIONS: Inactive, chronic paracoccidioidomycosis patients show persistent and disseminated radiological abnormalities by high resolution computed tomography, short impairments in pulmonary function and low impacts on aerobic capacity and quality of life. However, there was a subset of individuals whose functional impairment was more severe. These patients present with higher initial ...


Subject(s)
Adult , Aged , Female , Humans , Male , Middle Aged , Lung/physiopathology , Paracoccidioidomycosis/physiopathology , Cross-Sectional Studies , Epidemiologic Methods , Fibrosis/microbiology , Fibrosis/pathology , Fibrosis/physiopathology , Lung/microbiology , Lung/pathology , Oxygen Consumption/physiology , Paracoccidioidomycosis/pathology , Quality of Life , Respiratory Function Tests , Smoking/adverse effects , Time Factors , Tomography, X-Ray Computed
7.
Rev. cuba. oftalmol ; 24(1): 183-187, ene.-jun. 2011.
Article in Spanish | LILACS | ID: lil-615626

ABSTRACT

El síndrome de fibrosis congénita es definido como un grupo de desórdenes congénitos raros caracterizado por la restricción de los músculos extraoculares y el reemplazo de los músculos por el tejido fibroso. Muchos autores utilizan la clasificación en la que se manifiesta en cinco tipos diferentes. El caso que se presenta corresponde a un niño quien desde el nacimiento está imposibilitado de elevar su ojo izquierdo. Al examen oftalmológico resultó positivo una ptosis palpebral en su ojo izquierdo, enoftalmo, limitación de la abducción, elevación en supraabducción y depresión. La agudeza visual en ambos ojos era de la unidad. El diagnóstico confirmado por genética fue de una fibrosis unilateral congénita con enoftalmo y ptosis. A pesar de tratarse de un desorden genético poco común, tiene formas esporádicas más raras aún. De ahí la importancia de presentar este caso, poco frecuente en nuestra práctica médica diaria


The syndrome of congenital fibrosis is defined like a group of rare congenital disorders characterized by restriction of extraocular muscles and replacement of fibrous tissue muscles. Many authors use the classification in which it is manifested in five different types. Present case is a child who from its birth can not to raise its left eye. The ophthalmic examination was positive to palpebral ptosis in this eye, enophthalmos, limitation of abduction, raise in supra-abduction and depression. The visual acuity in both eyes was of the unit. The diagnosis confirmed by genetics was that of a congenital unilateral fibrosis with enophthalmos and ptosis. Despite it is uncommon genetic disorder, it has more rare sporadic ways yet. Presentation of this uncommon case in our daily medical practice is very significant


Subject(s)
Humans , Male , Child, Preschool , Eye Abnormalities/diagnosis , Blepharoptosis/congenital , Enophthalmos/congenital , Fibrosis/physiopathology , Case Reports
8.
Braz. j. med. biol. res ; 42(1): 29-37, Jan. 2009. ilus, tab
Article in English | LILACS | ID: lil-505413

ABSTRACT

Two major stress-activated protein kinases are the p38 mitogen-activated protein kinase (MAPK) and the c-Jun amino terminal kinase (JNK). p38 and JNK are widely expressed in different cell types in various tissues and can be activated by a diverse range of stimuli. Signaling through p38 and JNK is critical for embryonic development. In adult kidney, p38 and JNK signaling is evident in a restricted pattern suggesting a normal physiological role. Marked activation of both p38 and JNK pathways occurs in human renal disease, including glomerulonephritis, diabetic nephropathy and acute renal failure. Administration of small molecule inhibitors of p38 and JNK has been shown to provide protection from renal injury in different types of experimental kidney disease through inhibition of renal inflammation, fibrosis, and apoptosis. In particular, a role for JNK signaling has been identified in macrophage activation resulting in up-regulation of pro-inflammatory mediators and the induction of renal injury. The ability to provide renal protection by blocking either p38 or JNK indicates a lack of redundancy for these two signaling pathways despite their activation by common stimuli. Therefore, the stress-activated protein kinases, p38 and JNK, are promising candidates for therapeutic intervention in human renal diseases.


Subject(s)
Animals , Humans , Rats , JNK Mitogen-Activated Protein Kinases/metabolism , Kidney Diseases/physiopathology , Kidney/physiopathology , Signal Transduction/physiology , /metabolism , Apoptosis/physiology , Fibrosis/metabolism , Fibrosis/pathology , Fibrosis/physiopathology , Inflammation/metabolism , Inflammation/pathology , Inflammation/physiopathology , JNK Mitogen-Activated Protein Kinases/antagonists & inhibitors , Kidney Diseases/metabolism , Kidney Diseases/pathology , Kidney/metabolism , Kidney/pathology , /antagonists & inhibitors
9.
Acta gastroenterol. latinoam ; 36(4): 211-217, dic. 2006. ilus
Article in Spanish | LILACS | ID: lil-459135

ABSTRACT

Apoptosis es un término griego que significa “caída de las hojas viejas de los árboles en otoño”. Esta palabra describe el proceso por el cual células indeseables, dañadas o senescentes son eliminadas de los organismos multicelulares. La muerte cellular patológica en el hígado fue siempre referida como necrosis, pero procesos fisiopatológicos en este órgano pueden conducir a injuria celular tanto por apoptosis como por necrosis. Apoptosis difiere de necrosis porque la primera es controlada activamente y la membrana celular es mantenida, evitando la extravasación de material intracelular con la consecuente respuesta inflamatoria. El proceso de apoptosis puede ocurrir por dos mecanismos: el de receptor de muerte (DR) o extrínseco o por el mecanismo mitochondrial llamado también intrínseco. Las células hepaticas expresan diferentes receptores de muerte: Fas, TNF-R1, TRAIL-R1 y TRAIL-R2. Las células estelares expresan Fas y TRAIL cuando están activadas y transformadas fenotípicamente en miofibroblastos, y éstas también sufren apoptosis durante la resolución de la injuria hepática. Los colangiocitos parecen ser células tipo II (en éstas el mecanismo de apoptosis mitochondrial parece ser esencial). Apoptosis mediada por estos receptors juega un rol importante en una variedad de procesos biológicos tales como el daño tisular, protección contra microorganismos patógenos, y su papel central en la injuria hepática y posterior progresión a la fibrosis ha sido bien establecido en diferentes enfermedades hepáticas. Un factor importante en apoptosis cellular es que puede ocurrir en ausencia de elevación sérica de transaminasas hepáticas como ocurre en la necrosis celular. Este artículo es una revisión de este proceso.


Apoptosis is a Greek term that means "the fall of the old leaves of the autumn trees". This term describes the process by which undesirable, damaged or old cells are eliminated from the multicellular organisms. Pathologic cell death in the liver has traditionally been referred to as necrosis, but pathophysiologic process in the liver can lead to cell injury and death by apoptosis as well by necrosis. The first differs from the second, because it is actively controlled and the membrane integrity is maintained, avoiding extravasations of intracellular mate rial and inflammatory response. Apoptosis can occur by two mechanisms: death receptor (DR) or extrinsic mechanism and mitochondrial or intrinsic mechanism. Liver cells express different death receptors: hepatocytes express Fas, TNF-R1, TRAIL-R1, TRAIL-R2; Stellate Cell (HCS) express Fas and TRAIL when is activated into myofibroblast-like phenotype and undergo apoptosis during resolution of liver injury in vivo. Cholangiocytes seem to be type II cells (in which the mitochondrial mechanism to apoptotic is essential) regarding signaling of Fas endothelial cells from rat livers express Fas, and their activation may lead to apoptosis of endothelial cells from hepatic sinusoids. Apoptosis mediated by these receptors have a major role in a variety of biological processes as tissue injury, protection against pathogenic microorganisms, and the role on hepatic injury and posterior progression to fibrosis has been well established in different hepatic diseases. Apoptosis may occur in the absence of significant transaminase elevations as happen in cellular necrosis. This paper is a review of this process.


Subject(s)
Humans , Animals , Apoptosis/physiology , Hepatocytes/pathology , Liver Diseases/pathology , Liver Diseases/physiopathology , Disease Progression , Fibrosis/pathology , Fibrosis/physiopathology , Receptors, TNF-Related Apoptosis-Inducing Ligand/physiology , Receptors, Tumor Necrosis Factor/physiology
10.
Article in Portuguese | LILACS | ID: lil-439353

ABSTRACT

Objetivo: A maioria dos episódios de Encefalopatia Hepática (EH) em pacientes com doença hepática crônica possui algum evento clínico precipitante reconhecido. A proposta deste estudo foi determinar as manifestações clínicas e os fatores desencadeantes de EH em pacientes com cirrose. Métodos: Cirróticos admitidos na emergência do Hospital de Clínicas de Porto Alegre por episódio de EH (n=20) foram avaliados quanto à presença de fatores precipitantes tais como infecção (incluindo peritonite bacteriana), hemorragia gastrointestinal, constipação, dieta rica em proteína, azotemia, hipocalemia, uso de drogas psicoativas, desidratação, desenvolvimento de hepatoma e outros. Todos os pacientes foram acompanhados até alta hospitalar ou óbito. Resultados: Todos os pacientes tiveram pelo menos um fator desencadeante de EH. O principal fator contribuinte para o desenvolvimento de EH foi infecção (60 por cento), como infecção urinária (35 por cento), infecção respiratória (20 por cento) e Peritonite Bacteriana Espontânea (15 por cento). Conclusão: A medida terapêutica mais importante na EH é identificar os fatores precipitantes e corrigi-los prontamente. O estudo mostra que estes eventos são muito comuns e o diagnóstico precoce de infecção é importante nestes casos


Subject(s)
Humans , Male , Female , Hepatic Encephalopathy/physiopathology , Hepatic Encephalopathy/therapy , Hepatic Encephalopathy , Fibrosis , Fibrosis/physiopathology
11.
Asian Pac J Allergy Immunol ; 2001 Dec; 19(4): 275-82
Article in English | IMSEAR | ID: sea-37074

ABSTRACT

Immunohistochemical, flow cytometric and ELISA studies were performed to examine the expression of endoglin (CD105, a TGF beta receptor) on dermal endothelial cells, peripheral blood monocytes and free and bound serum levels in patients with systemic sclerosis as compared with appropriate controls. Endoglin was found to be significantly upregulated on dermal blood vessels in patients with scleroderma (and in patients with inflammatory skin disorders) as compared to healthy skin (p < 0.05). In contrast, there was no significant difference in endoglin expression on circulating blood monocytes between scleroderma patients and patients with a rheumatic disoder or healthy control subjects; however, endoglin expression was upregulated on monocytes in inflammatory joint fluid from patients with rheumatoid arthritis. Endoglin expression on monocytes was also influenced by isolation techniques and during whole blood culture. No differences were found in circulating free or bound endoglin levels between scleroderma patients and healthy controls. In conclusion, endoglin expression on dermal endothelial cells was significantly enhanced in scleroderma but levels on circulating monocytes and in the serum were within normal limits. The functional significance of this upregulation is uncertain but may reflect endothelial activation in scleroderma.


Subject(s)
Aged , Aged, 80 and over , Antigens, CD , Cells, Cultured , Dermis/cytology , Endothelium/metabolism , Enzyme-Linked Immunosorbent Assay , Female , Fibrosis/physiopathology , Flow Cytometry , Humans , Immunohistochemistry , Male , Middle Aged , Monocytes/metabolism , Receptors, Cell Surface , Receptors, Transforming Growth Factor beta/blood , Scleroderma, Systemic/physiopathology , Telangiectasis/physiopathology , Vascular Cell Adhesion Molecule-1/blood
12.
Rev. chil. cir ; 51(4): 347-50, ago. 1999. ilus
Article in Spanish | LILACS | ID: lil-245512

ABSTRACT

Uno de nuestros enfermos presentó ictericia en el postoperatorio y la ERCP demostró un clip en el colédoco. Esto motivó la búsqueda en la literatura si existía un tiempo, después de producido el accidente, en el cual se podía retirar el clip o ligadura, sin que existiera daño o reacción importante del colédoco. Al no encontrarlo, diseñamos un modelo experimental el cual desarrollamos en nuestro laboratorio de cirugía e investigación experimental. El objetivo de esta investigación fue determinar la cuantía y el momento en que se producen las alteraciones anatómicas (principalmente la fibrosis), que van a llevar, eventualmente, a una estenosis futura (aunque el clip se haya retirado). Se planifica una serie de 10 perros que se operaron bajo anestesia general, en forma consecutiva, a los cuales se les coloca un clip en el colédoco, el que fue retirado en días sucesivos (del 1 al 10). El colédoco fue extirpado y la muestra analizada en anatomía patológica posteriormente. Se observó una fibrosis leve a moderada, con inflamación rica en linfocitos y células plasmáticas. El sitio del clip presentó necrosis focal de tipo isquémica. Estos hallazgos pueden constituir una línea interesante de investigación en el estudio de los mecanismos que llevan a la estenosis de la vía biliar, y definir el momento en que se producen alteraciones probablemente irreversibles en el colédoco


Subject(s)
Animals , Dogs , Biliary Atresia/physiopathology , Cholecystectomy, Laparoscopic/adverse effects , Fibrosis/physiopathology , Common Bile Duct/physiopathology , Surgical Instruments/adverse effects
13.
Rev. argent. radiol ; 63(1): 49-54, ene.-mar. 1999. ilus
Article in Spanish | LILACS | ID: lil-240617

ABSTRACT

A fin de revisar y divulgar los hallazgos clínicos, imagenológicos y anatomopatológicos de cuatro pacientes con fibromatosis colli (FC) y realizar una puesta al día de esta interesante patología, se revisaron los hallazgos ecográficos y se categorizaron dentro de las 2 formas descriptas en la literatura: Tipo I, hipoecoico homogéneo y Tipo II, parcheado, analizando además la incidencia de antecedentes considerados como factores de riesgo. La ecografía demostró ser un método sumamente útil en el manejo de pacientes con FC, no sólo para su diagnóstico sino también para su seguimiento, demostrando altísima sensibilidad y especificidad. El diagnóstico ecográfico precoz de FC evita la necesidad de recurrir a métodos más complejos y costosos, que pueden requerir sedación, contraste, radiación o procedimientos intervencionistas


Subject(s)
Humans , Male , Female , Infant, Newborn , Fibroma , Fibrosis/physiopathology , Neck Muscles/pathology , Torticollis/congenital , Fibroma/diagnosis , Fibroma/physiopathology , Neck Muscles , Neoplasms, Muscle Tissue , Neoplasms, Muscle Tissue/diagnosis , Tomography, X-Ray Computed
14.
Arq. bras. oftalmol ; 57(5): 322-8, out. 1994. ilus
Article in Portuguese | LILACS | ID: lil-150608

ABSTRACT

Descrevemos um caso raro de fibrose sub-retiniana progressiva subsequente à coroidite multifocal, associado a uma severa e dramática neurite óptica resistente à prednisona, à droga citotóxica e finalmente à ciclosporina. A literatura foi revista e discutida


Subject(s)
Humans , Female , Adult , Choroiditis/etiology , Fibrosis/physiopathology , Optic Neuritis/physiopathology , Retina/pathology , Choroiditis/diagnosis
15.
Pesqui. méd. (Porto Alegre) ; 27(2): 25-30, 1993.
Article in Portuguese | LILACS | ID: lil-161044

ABSTRACT

Este trabalho revisa as alteraçöes hemodinâmicas e renais mais comumente observadas no paciente cirrótico. Do ponto de vista hemodinâmico, demonstra haver um estado circulatório hipercinético caracterizado por elevaçäo do débito cardíaco, diminuiçäo da pressäo arterial média e da resistência vascular sistêmica, bem como um aumento do volume plasmático total e ativaçäo dos sistemas neurohumorias. No rim constata haver vasoconstriçäo renal, diminuiçäo do fluxo sanguíneo renal, da taxa de filtraçäo glomerular e aumento na reabsorçäo de sódio e água.


Subject(s)
Humans , Fibrosis/physiopathology , Hemodynamics , Kidney/physiopathology
16.
Rev. Hosp. Säo Paulo Esc. Paul. Med ; 4(1/4): 1-18, Dec. 1992. tab
Article in Portuguese | LILACS | ID: lil-141158

ABSTRACT

Foram analisadas 119 esplenoportografias, de 100 pacientes com suspeita clínica e laboratorial de hipertensäo portal (H.P.); o exame foi repetido em tempos diferentes 19 vezes. Dos 100 pacientes, 9 eram normais, e serviram como termo de comparaçäo. Do total, 57 eram esquistossomóticos da forma hepatoesplênica, 19 cirróticos, 6 tinham hipertensäo portal por bloqueio extra-hepático, 11 tinham a síndrome de Cruveilhier-Baungarten, e 8 foram submetidos a anastomoses porto-cava. Na análise do material verificamos que as veias esplênicas e porta apresentavam nos cirróticos e esquistossomóticos comprimento e diâmetros maiores de que nos indivíduos normais. Os diâmetros das veias porta e esplênicas eram maiores nos esquistossomóticos do que nos cirróticos. Já os comprimentos näo diferiram nos 2 grupos. A circulaçäo porta intra-hepâtica, nos cirróticos, é excessiva com distribuiçäo irregular, com distorçöes e estreitamentos. Já nos esquistossomóticos ela é abundante, com discretas distorçöes e sem amputaçöes. Com frequência observamos extravasamento de contraste em torno dos ramos dicotômicos de 1ª a 4ª ordem com sinal de Bogliolo. A circulaçäo colorretal é de observaçäo frequente em cirróticos como em esquistossomóticos, enquanto a congestäo portal também näo se refere nos 2 grupos. Na H.P. por bloqueio extra-hepático, a congestäo portal é sempre intensa, com circulaçäo colateral de direçäo centrípeta em relaçäo ao hilo hepático. Já na síndrome de Cruveilhier-Baumgarten ela é moderada. O estudo de funçäo hepática é mais alterado nos cirráticos. A esplenomanometria mostrou níveis elevados tanto em cirróticos como em esquistossomóticos, näo apresentando diferenças estatisticamente significantes nos 2 grupos, nem naqueles com circulaçäo colateral ou nos com e sem antecedentes de hemorragia digestiva ou ascite. Os doentes com congestäo portal menos intensa tiveram níveis pressóricos menos elevado do que aqueles com congestäo portal mais intensa. A esplenoportografia e a esplenomanometria, constituem exames subsidiários, de maior importância, para a avaliaçäo da permeabilidade e eficácia das anastomoses portocava artificiais. Para a avaliaçäo das varizes esofagogástricas, o RX e a esofagoscopia säo mais eficazes do que a esplenoportografia. A associaçäo dos 3 métodos aumentou esta eficácia de 84,9 por cento para 97,5 por cento. O resultado foi o mesmo quando analisamos em separado o grupo com e sem antecedente hemorrágico ou de ascite


Subject(s)
Child , Adolescent , Adult , Middle Aged , Humans , Male , Female , Fibrosis/physiopathology , Hypertension, Portal/diagnosis , Schistosomiasis mansoni/physiopathology , Esophageal and Gastric Varices/diagnosis , Esophagoscopy , Liver/physiopathology , Hypertension, Portal , Portal Vein/pathology , Portography , Syndrome , Esophageal and Gastric Varices , Splenic Vein/pathology
18.
Diagnóstico (Perú) ; 28(3/4): 61-6, sept.-oct. 1991. tab
Article in Spanish | LILACS, LIPECS | ID: lil-118998

ABSTRACT

En el presente estudio se revisaron las historias clínicas y los hallazgos histológicos de la piel de 12 pacientes con el diagnóstico de Esclerosis Sistémica Progresiva (ESP), los que fueron atendidos en los Servicios de Medicina y Dermatología del Hospital Víctor Lazarte Echegaray, IPSS, Trujillo, Perú, en el período comprendido de Enero de 1975 a Diciembre de 1989, con el fin de evaluar sus manifestaciones clínicas, histopatológicas y su clasificación según la forma de presentación. Los hallazgos más importantes son que la mayor frecuencia fue vista en mujeres mayores de 30 años. El tiempo promedio de enfermedad fue de 1 año en los pacientes con Esclerodermia difusa y 10 años en los de tipo CREST. El número grande de casos correspondió a la Esclerodermia limitada (CREST). Los síntomas iniciales más reportados fueron Fenómeno de Raynaud, artralgias/artritis, y dedos hinchados. Las manifestaciones cutáneas predominantes fue exclerodermia con esclerodactilia y cara esclerótica, telangiectasias, cambios pigmentarios, úlceras e infartos en la punta de los dedos de las manos. El compromiso visceral observado afectó en orden de frecuencia al esófago, pulmones corazón y riñones. Los rasgos histológicos en la piel fueron característicos de la fase temprana de la ESP en la mitad de los pacientes y tardía en los restantes. Según la forma clínica, los pacientes se agruparon en Esclerosis sistémica limitada (CREST) y Esclerosis sistémica difusa


Subject(s)
Humans , Adult , Middle Aged , Male , Female , Scleroderma, Systemic/diagnosis , Connective Tissue/pathology , Peru , Arthritis/etiology , Scleroderma, Systemic/pathology , Fibrosis/physiopathology
19.
Rev. med. PUCRS ; 2(2): 62-8, jan.-mar. 1990. ilus
Article in Portuguese | LILACS | ID: lil-161068

ABSTRACT

Uma revisäo a respeito dos mecanismos de defesa imunológicos relacionados a infecçöes bacterianas em pacientes cirróticos é apresentada. É discutido o papel fisiológico desempenhado pelo fígado de pessoas normais e os eventos fisiológicos referentes a susceptibilidade às infecçöes bacterianas em pacientes com doença hepática, principalmente na cirrose. As alteraçöes nos mecanismos humorais (anticorpos, complemento, opsonizaçäo, atividade quimiotática), celulares (atividade dos polimorfonucleares), anatômicos ("shunts" protosistêmicos) e fisiológicas (decorrentes da hipertensäo portal), que ocorrem no portador de cirrose e predispöe os mesmos às infecçöes bacterianas säo explicadas.


Subject(s)
Humans , Antibodies/immunology , Liver Cirrhosis/immunology , Bacterial Infections/immunology , Fibrosis/complications , Fibrosis/physiopathology , Disease Susceptibility , Liver/physiology , Bacterial Infections/etiology , Bacterial Infections/physiopathology
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