Your browser doesn't support javascript.
loading
Show: 20 | 50 | 100
Results 1 - 20 de 29
Filter
1.
Arch. cardiol. Méx ; 90(1): 42-47, Jan.-Mar. 2020. tab, graf
Article in English | LILACS | ID: biblio-1131004

ABSTRACT

Abstract Background: Despite increase in survival of human immunodeficiency virus (HIV) patients due to highly active antiretroviral therapy, non-infectious complications are still prevalent such as presentation of lung vasculopathy, even in asymptomatic patients. Endothelial nitric oxide synthase (eNOS) is necessary to produce nitric oxide that causes pulmonary endothelial vasodilation. Participation of this protein in the pulmonary circulation in HIV patients has not been elucidated. This work studied the presence and expression of eNOS in pulmonary complex vascular lesions associated with HIV (PCVL/HIV). Methods: In lung tissues from patients who died from complications of HIV, we used immunohistochemistry and immune chemiluminescence (imageJ) to determine the different degrees of expression of eNOS in PCVL-HIV in comparison with non-PCVL/HIV. Reagents used were anti-eNOS and an automated system. All data are presented as mean and standard deviation. Differences were analyzed with Wilcoxon; p < 0.05 was accepted as statistically significant. Results: In 57 tissues, the histological evidence of pulmonary vasculopathy was showed as different types (proliferative, obliterative, and plexiform) and severe presentation of vasculopathy than non-PCVL/HIV. A statistically significant decrease of eNOS was observed in all PCVL/HIV tissue samples. Conclusion: eNOS has a relevant role in the pathogenesis of pulmonary vasculopathy in acquired immunodeficiency syndrome patients. It is necessary to determine in the future the participation of eNOS and other mechanisms involved in PCVL/HIV.


Resumen Antecedentes: A pesar del incremento en la sobrevivencia del paciente con virus de inmunodeficiencia humana (VIH) debido al uso del tratamiento antiretroviral altamente efectivo, las complicaciones no infecciosas siguen ocasionando vasculopatía pulmonar, aun en pacientes asintomáticos. La óxido nítrico sintetasa (ONSe) es necesaria para la producción de óxido nítrico la cual provoca vasodilatación pulmonar. La participación de esta proteína en la circulación pulmonar en los pacientes con VIH aún no se ha dilucidado. Este trabajo estudia la presencia y la expresión de ONSe en las lesiones vasculares pulmonares complejas asociadas al VIH (LVPC/VIH). Métodos: En tejidos pulmonares de pacientes que fallecieron por complicaciones del VIH, se utilizó inmunohistoquímica e inmunoquimioluminescencia (imageJ) para determinar los diferentes grados de expresión de la ONSe en LVPC/VIH. Los reactivos utilizados son anti-ONSe en sistema automatizado. Todos los datos son presentados en media y desviación estándar. Las diferencias son analizadas con la prueba de Wilcoxon; se aceptó como estadísticamente significativa una p < 0.05. Resultados: En 57 pacientes, la histología de la vasculopatía pulmonar mostró diferentes tipos (proliferativo, obliterativo y plexiforme) además de varias presentaciones de vasculopatía en tejidos no-LVPC/VIH. Se observó diferencia estadística en la disminución de ONSe en todos los tejidos LVPC/VIH. Conclusiones: La ONSe tiene un papel relevante en la patogénesis de la vasculopatía pulmonar en el VIH. Es necesario determinar en el futuro la participación de ONSe y otros mecanismos involucrados en LVPC/VIH.


Subject(s)
Humans , Male , Female , Adult , Middle Aged , Young Adult , Vascular Diseases/physiopathology , HIV Infections/complications , Nitric Oxide Synthase Type III/metabolism , Nitric Oxide/metabolism , Pulmonary Artery/physiopathology , Vascular Diseases/enzymology , Vascular Diseases/virology , Severity of Illness Index
3.
Rev. latinoam. enferm. (Online) ; 26: e3084, 2018. tab, graf
Article in English | LILACS, BDENF | ID: biblio-978615

ABSTRACT

Objective to compare two compression times of the radial artery after coronary angiography with customized compressive dressing regarding the occurrence of hemostasis and vascular complications. Method a randomized clinical study was carried out in patients undergoing elective transradial coronary angiography in two study groups: (G30), whose compressive dressing was maintained for 30 minutes, and (G60), whose compressive dressing was maintained for 60 minutes, both until the first evaluation of hemostasis. Variables related to patients, procedure, occurrence of hemostasis, and vascular complications were analyzed. Patency of the radial artery was assessed with Doppler vascular ultrasonography, immediately after removing the compressive dressing and 30 days after the procedure. Results the sample consisted of 152 patients in G30 and 151 in G60. Hemostasis was evidenced in the first evaluation in 76.3% of G30 patients and 84.2% of G60 patients (p = 0.063). There were 91 immediate complications, being 53 hematomas and 38 occlusions of the radial artery. We identified 18 late occlusions, 7 (5.5%) in G30 and 11 (8.2%) in G60. Conclusion the different compression times of the radial artery after coronary angiography did not significantly influence the occurrence of hemostasis and vascular complications. Brazilian Registry of Clinical Trials (Rebec): RBR-7VJYMJ.


Objetivo comparar dois tempos de compressão da artéria radial pós-cinecoronariografia com curativo compressivo customizado, quanto à ocorrência de hemostasia e de complicações vasculares. Método estudo clínico randomizado realizado em pacientes submetidos a cinecoronariografia eletiva pelo acesso transradial, alocados em dois grupos de estudo: G30, cujo curativo compressivo foi mantido por 30 minutos, e G60, no qual o curativo foi mantido por 60 minutos, ambos até a primeira avaliação de hemostasia. Foram avaliadas variáveis relativas aos pacientes, procedimento, ocorrência de hemostasia e complicações vasculares. A patência da artéria radial foi avaliada com ultrassonografia vascular com Doppler, imediatamente após a retirada da compressão e após 30 dias do procedimento. Resultados a amostra foi composta de 152 pacientes no G30 e 151 no G60. A hemostasia foi evidenciada na primeira avaliação em 76,3% dos pacientes do G30 e em 84,2% do G60 (p=0,063). Ocorreram 91 complicações imediatas, sendo 53 hematomas e 38 oclusões da artéria radial. Foram identificadas 18 oclusões tardias, sendo 7 (5,5%) no G30 e 11 (8,2%) no G60. Conclusão os diferentes tempos de compressão da artéria radial, após cinecoronariografia, não influenciaram significativamente a ocorrência de hemostasia e complicações vasculares. Registro Brasileiro de Ensaios Clínicos (Rebec): RBR-7VJYMJ.


Objetivo comparar dos tiempos de compresión de la arteria radial, después de cinecoronariografía con curativo compresivo personalizado, referido a la ocurrencia de hemostasia y de complicaciones vasculares. Método estudio clínico aleatorizado realizado en pacientes sometidos a cinecoronariografía electiva por acceso transradial, asignados en dos grupos de estudio: (G30) cuyo curativo compresivo fue mantenido por 30 minutos y (G60) en el cual el curativo fue mantenido por 60 minutos; ambos hasta la primera evaluación de hemostasia. Fueron evaluadas variables relativas a: pacientes, procedimiento, ocurrencia de hemostasia y complicaciones vasculares. La capacidad de mantener desobstruida la arteria radial fue evaluada con ultrasonografia vascular con Doppler, inmediatamente después de la retirada de la compresión y después de 30 días del procedimiento. Resultados la muestra estuvo compuesta por 152 pacientes en el G30 y 151 en el G60. La hemostasia fue evidenciada en la primera evaluación en 76,3% de los pacientes del G30 y en 84,2% del G60 (p=0,063). Ocurrieron 91 complicaciones inmediatas, siendo 53 hematomas y 38 oclusiones de la arteria radial. Fueron identificadas 18 oclusiones tardías, siendo 7(5,5%%) en el G30 y 11(8,2%) en el G60. Conclusión los diferentes tiempos de compresión de la arteria radial después de cinecoronariografía no influenciaron significativamente la ocurrencia de hemostasia y complicaciones vasculares. Registro Brasileño de Ensayos Clínicos (Rebec): RBR-7VJYMJ.


Subject(s)
Humans , Male , Female , Vascular Diseases/physiopathology , Radial Artery/physiopathology , Percutaneous Coronary Intervention/adverse effects , Regional Blood Flow/physiology , Peripheral Vascular Diseases
5.
Int. braz. j. urol ; 41(3): 547-551, May-June 2015. tab
Article in English | LILACS | ID: lil-755874

ABSTRACT

ABSTRACTObjectives:

Pseudoexfoliation syndrome (PES) is a common age-related fibrillopathy related to accumulation of pseudoexfoliation material (PEM) in certain places in the body, especially blood vessels. Erectile dysfunction (ED) is another condition related to vascular pathology and in this study it is aimed to identify the relationship between ED and PES.

Materials and Methods:

Data of 92 patients were investigated. There were 34 patients in the PES group and 58 patients in the control group. Presence of diabetes, hypertension, smoking history, BMI, and serum levels of lipids and testosterone were recorded. The groups were compared for ED rates and severity. Also logistic regression analysis was performed to identify independent risk factors for development of ED.

Results:

Mean age of the population was 67.3. No significant difference was observed between the two groups regarding the presece of DM, HT, smoking, BMI and laboratory measurements. ED rate was significantly higher in the PES group (70.6% vs 48.3%, p=0.002). Also, severe ED rate was higher in the PES group (p=0.002). PES was detected as an independent risk factors for the development of ED.

Conclusion:

ED is a possible consequence of PES. ED rate and severity is found to be higher in the PES group and PES is detected as an independent risk factor for development of ED. Patients with PES should be informed about development of ED and further prospective trials with objective measurements of penile blood flow should be conducted to verify the erectile status and penile blood fow in PES patients.

.


Subject(s)
Aged , Humans , Male , Middle Aged , Endothelium, Vascular , Erectile Dysfunction/etiology , Exfoliation Syndrome/complications , Vascular Diseases/complications , Age Factors , Body Mass Index , Cholesterol/blood , Diabetes Complications , Epidemiologic Methods , Endothelium, Vascular/physiopathology , Erectile Dysfunction/physiopathology , Exfoliation Syndrome/physiopathology , Hypertension/complications , Penis/blood supply , Risk Factors , Smoking/adverse effects , Triglycerides/blood , Vascular Diseases/physiopathology
6.
Arq. bras. cardiol ; 104(2): 159-168, 02/2015. tab, graf
Article in English | LILACS | ID: lil-741144

ABSTRACT

Background: Cardiac magnetic resonance imaging provides detailed anatomical information on infarction. However, few studies have investigated the association of these data with mortality after acute myocardial infarction. Objective: To study the association between data regarding infarct size and anatomy, as obtained from cardiac magnetic resonance imaging after acute myocardial infarction, and long-term mortality. Methods: A total of 1959 reports of “infarct size” were identified in 7119 cardiac magnetic resonance imaging studies, of which 420 had clinical and laboratory confirmation of previous myocardial infarction. The variables studied were the classic risk factors – left ventricular ejection fraction, categorized ventricular function, and location of acute myocardial infarction. Infarct size and acute myocardial infarction extent and transmurality were analyzed alone and together, using the variable named “MET-AMI”. The statistical analysis was carried out using the elastic net regularization, with the Cox model and survival trees. Results: The mean age was 62.3 ± 12 years, and 77.3% were males. During the mean follow-up of 6.4 ± 2.9 years, there were 76 deaths (18.1%). Serum creatinine, diabetes mellitus and previous myocardial infarction were independently associated with mortality. Age was the main explanatory factor. The cardiac magnetic resonance imaging variables independently associated with mortality were transmurality of acute myocardial infarction (p = 0.047), ventricular dysfunction (p = 0.0005) and infarcted size (p = 0.0005); the latter was the main explanatory variable for ischemic heart disease death. The MET-AMI variable was the most strongly associated with risk of ischemic heart disease death (HR: 16.04; 95%CI: 2.64-97.5; p = 0.003). Conclusion: The anatomical data of infarction, obtained from cardiac magnetic resonance imaging after acute myocardial infarction, were independently ...


Fundamento: A ressonância magnética cardíaca fornece informações anatômicas detalhadas do infarto, porém poucos estudos investigaram a associação desses dados com mortalidade pós-infarto agudo do miocárdio. Objetivo: Verificar a associação entre os dados de anatomia e magnitude do infarto, obtidos da ressonância magnética cardíaca pós-infarto agudo do miocárdio, e mortalidade em longo prazo. Métodos: Foram identificados 1.959 laudos com “massa infartada” em 7.119 exames de ressonância magnética cardíaca, dos quais 420 possuíam documentação clínica e laboratorial de infarto agudo do miocárdio prévio. As variáveis estudadas foram os fatores de risco clássicos, fração de ejeção do ventrículo esquerdo, função ventricular categorizada e localização do infarto agudo do miocárdio. Massa infartada, extensão e transmuralidade do infarto agudo do miocárdio foram analisadas de maneira isolada e conjuntamente, pela variável denominada “MET-IAM”. A análise estatística foi feita pelo elastic net regularization, pelo modelo de Cox e por árvores de sobrevida. Resultados: A idade média foi 62,3 ± 12 anos, sendo 77,3% de homens. Durante o seguimento de 6,4 ± 2,9 anos, foram identificados 76 óbitos (18,1%). Creatinina sérica, diabetes melito e infarto agudo do miocárdio prévio demonstraram associação independente com mortalidade. A idade foi o principal fator explicativo. As variáveis da ressonância magnética cardíaca que se associaram de forma independente com a mortalidade foram: transmuralidade do infarto agudo do miocárdio (p = 0,047), disfunção ventricular (p = 0,0005) e massa infartada (p = 0,0005) − sendo essa última a principal variável explicativa para morte por doença isquêmica cardíaca. A variável MET-IAM exibiu a maior associação de risco para morte por doença isquêmica cardíaca (HR: 16,04; IC95%: 2,64-97,5; p = 0,003). Conclusão: Os dados anatômicos do infarto obtidos da ressonância magnética cardíaca pós-infarto ...


Subject(s)
Aged , Aged, 80 and over , Female , Humans , Male , Middle Aged , Magnetic Resonance Imaging/methods , Myocardial Infarction/diagnosis , Myocardial Infarction/mortality , Cause of Death , Endpoint Determination , Epidemiologic Methods , Myocardial Infarction/physiopathology , Severity of Illness Index , Time Factors , Vascular Diseases/mortality , Vascular Diseases/physiopathology , Ventricular Dysfunction, Left/physiopathology , Ventricular Function, Left/physiology
7.
Korean Journal of Radiology ; : 942-946, 2015.
Article in English | WPRIM | ID: wpr-50479

ABSTRACT

Pulmonary vein (PV) stenosis is a complication of ablation therapy for arrhythmias. We report two cases with chronic lung parenchymal abnormalities showing no improvement and waxing and waning features, which were initially diagnosed as nonspecific pneumonias, and finally confirmed as PV stenosis. When a patient presents for nonspecific respiratory symptoms without evidence of infection after ablation therapy and image findings show chronic and repetitive parenchymal abnormalities confined in localized portion, the possibility of PV stenosis should be considered.


Subject(s)
Female , Humans , Male , Middle Aged , Atrial Fibrillation/surgery , Catheter Ablation/adverse effects , Constriction, Pathologic/diagnosis , Diagnostic Errors , Lung/surgery , Pneumonia/diagnosis , Pulmonary Infarction/pathology , Pulmonary Veins/physiopathology , Tomography, X-Ray Computed/adverse effects , Vascular Diseases/physiopathology
8.
Article in English | IMSEAR | ID: sea-156524

ABSTRACT

Hyperactivation of proliferative and growth promoting pathways underlies the progression of vessel remodeling, leading to vascular dysfunction. An upregulation of early growth response protein 1 (Egr-1), a zinc finger transcription factor has been observed in several models of vascular diseases. In the vasculature, Egr-1 expression can be induced by multiple hormonal, metabolic and external stimuli, such as growth factors, cytokines, reactive oxygen species, hyperglycaemia and stretch-induced stress. The structure of the Egr-1 promoter allows both its auto-regulation and its binding with several regulatory transcription cofactors like the serum response factor and the cAMP response element binding protein. Pharmacological and genetic studies have revealed the involvement of several signaling pathways that contribute to the expression of Egr-1. Among them, the mitogen-activated protein kinase pathway has emerged as a predominant signaling cascade that regulates Egr-1 transcription in response to various stimuli. Moreover, targeted deletion of Egr-1 by DNAzymes, antisense oligonucleotides or RNA interference has also helped in defining the importance of Egr-1 in the pathophysiology of vascular diseases. Neointimal formation and expression of genes directly linked with proinflammatory processes have been demonstrated to be enhanced by Egr-1 expression and activity. This review provides an overview on the signaling components implicated in Egr-1 expression and discusses its potential involvement in vascular pathophysiology.


Subject(s)
Animals , Cytokines/immunology , Early Growth Response Protein 1/immunology , Humans , Models, Cardiovascular , Models, Immunological , Phosphotransferases/immunology , Signal Transduction/immunology , Vascular Diseases/immunology , Vascular Diseases/physiopathology , /immunology
9.
J. bras. med ; 101(4): 13-18, jul.-ago. 2013. ilus
Article in Portuguese | LILACS | ID: lil-699659

ABSTRACT

O fenômeno de Raynaud (FRy) caracteriza-se por episódios reversíveis de vasoespasmos de extremidades, que ocorrem usualmente após estresse ou exposição ao frio. O FRy pode ser primário ou secundário a uma série de condições, principalmente a doenças do espectro da esclerose sistêmica (ES). Na ES, o FRy costuma ser mais grave, e lesões isquêmicas de extremidades são frequentes. Nos últimos anos, avanços no estudo da fisiopatologia do FRy e da doença vascular na ES propiciaram o surgimento de novas opções terapêuticas para esta manifestação. Os bloqueadores de canal de cálcio devem ser utilizados como tratamento de primeira escolha para o FRy. Novas drogas, como os inibidores da fosfodiesterase V e os prostanoides, podem ser utilizados em pacientes com FRy grave, e a bosentana (antagonista do receptor da endotelina-1) é indicada para a prevenção de úlceras digitais recorrentes.


Raynaud's phenomenon (RP) is characterized by episodic vasospasm of the extremities, usually in response to stress or cold exposure. It can be primary or secondary to several conditions, especially systemic sclerosis-related diseases. In systemic sclerosis (SSc), RP is usually more severe and digital ischemic lesions are a frequent problem. In recent years, advances in the understanding of the pathophysiology of RP and of SSc vasculopathy led to the development of new therapeutic options for this condition. Calcium-channel blockers are the first choice for the treatment of RP. New drugs including phosphodiesterase type V inhibitors and prostanoids can be used for severe RP, and bosentan (endothelin-1 receptor antagonist) for prevention of recurrent digital ulcers.


Subject(s)
Humans , Male , Female , Raynaud Disease/physiopathology , Raynaud Disease/drug therapy , Scleroderma, Systemic/physiopathology , Scleroderma, Systemic/drug therapy , Microscopic Angioscopy/methods , Autoantibodies , Calcium Channel Blockers/therapeutic use , Vascular Diseases/physiopathology , /therapeutic use , Receptors, Endothelin/antagonists & inhibitors , Skin Ulcer/prevention & control , Skin Ulcer/drug therapy , Vasodilator Agents/therapeutic use
11.
Arch. venez. pueric. pediatr ; 70(4): 130-135, oct.-dic. 2007. tab, graf
Article in Spanish | LILACS | ID: lil-589300

ABSTRACT

Evidencia reciente confirma que la enfermedad cardiovascular se inicia en la infancia, y la dislipidemia es uno de los principales factores de riesgo asociados. La detección precoz de la hipercolesterolemia en niños con factores de riesgo, previene la morbimortalidad cardiovascular en el adulto. Se propone un esquema de detección y manejo de la dislipidemia, basado en la experiencia de grupos de expertos, así como medidas dietéticas y terapéuticas a seguir. Se debe hacer hincapié en cambios de estilo de vida a largo plazo, recomendando hábitos alimentarios saludables y ejercicio ya que la obesidad es la causa mas frecuente de dislipidemia en el niño. Existen varias alternativas farmacológicas, y en su uso y selección se debe evaluar el riesgo en forma individual, tomando en cuenta la edad, los niveles séricos de lípidos, la magnitud y el número de eventos cardiovasculares en familiares y los posibles efectos secundarios. Actualmente las estatinas están tomando un papel importante en el tratamiento de la hipercolesterolemia familiar en niños sin embargo se requieren más estudios a fin de establecer su seguridad en este grupo de edad. En vista que la hipercolesterolemia es un factor de riesgo modificable y determinante en la enfermedad cardiovascular, todas las intervenciones que se puedan hacer en la niñez, ofrecen una oportunidad de prevención.


Recent evidence corroborate that cardiovascular disease begins in childhood and that hyperlipidemia is one of the main associated risk factors. Early screening of hypercholesterolemia in high risk children should be performed in order to prevent cardiovascular morbidity and mortality in adulthood. An approach for detection and management of hypercholesterolemia is proposed with dietary and therapeutic strategies based on the experience of expert groups. Since obesity is the most common cause of hyperlipidemia in children, special emphasis should be made in long lasting lifestyle changes. Treatment always must include dietary modifications and exercise. Several pharmacologic alternatives are available, and when deciding its use, the child's risk must be individually analyzed, considering age, type and degree of dyslipidemia, and possible adverse effects. Since hypercholesterolemia is a modifiable and determinant risk in cardiovascular disease, all interventions done in childhood offer the opportunity of cardiovascular disease prevention in adulthood.


Subject(s)
Humans , Male , Female , Child , Adolescent , Arteriosclerosis/pathology , Dyslipidemias/metabolism , Dyslipidemias/pathology , Dyslipidemias/therapy , Cardiovascular Diseases/etiology , Hypercholesterolemia/therapy , Vascular Diseases/physiopathology , Obesity/prevention & control , Pediatrics
12.
J. bras. pneumol ; 33(2): 213-221, mar.-abr. 2007. tab
Article in Portuguese | LILACS | ID: lil-459293

ABSTRACT

Diabetes melito relacionado à fibrose cística (DMFC) é a principal complicação extrapulmonar da fibrose cística. Atualmente, ele afeta 15-30 por cento dos adultos com fibrose cística e sua prevalência tende a aumentar com o aumento da expectativa de vida desses pacientes. Esse trabalho tem por objetivo rever a fisiopatologia, morbidade, manifestações clínicas, diagnóstico e tratamento do DMFC. Uma pesquisa bibliográfica utilizou os bancos de dados Medline e Literatura Latino-Americana e do Caribe em Ciências da Saúde, selecionando artigos publicados nos últimos vinte anos. A insulinopenia secundária à destruição de células beta pancreáticas é o principal mecanismo causal, embora a resistência insulínica também possa estar presente. O DMFC apresenta características do diabetes melito tipo 1 e tipo 2 e tem início, em média, aos 20 anos de idade. Ele pode cursar com hiperglicemia em jejum, pós-prandial ou intermitente. As alterações do metabolismo glicêmico agravam o estado nutricional, aumentam a morbidade, diminuem a sobrevida e pioram a função pulmonar. As complicações microvasculares estão presentes, porém raramente observam-se as macrovasculares. A triagem para o DMFC deve ser anual, a partir dos 10 anos de idade, através do teste de tolerância oral à glicose e, em qualquer faixa etária, se houver perda ponderal inexplicada ou sintomatologia de diabetes. Pacientes hospitalizados também devem ser investigados e receber terapia insulínica se a hiperglicemia em jejum persistir além de 48 h. A insulina é o tratamento de escolha para o diabetes com hiperglicemia em jejum. Não existe consenso quanto ao tratamento do diabetes intermitente ou sem hiperglicemia de jejum. Não há orientações de restrições alimentares. O acompanhamento deve ser multidisciplinar.


Cystic fibrosis-related diabetes (CFRD) is the principal extra-pulmonary complication of cystic fibrosis, occurring in 15-30 percent of adult cystic fibrosis patients. The number of cystic fibrosis patients who develop diabetes is increasing in parallel with increases in life expectancy. The aim of this study was to review the physiopathology, clinical presentation, diagnosis and treatment of CFRD. A bibliographic search of the Medline and Latin American and Caribbean Health Sciences Literature databases was made. Articles were selected from among those published in the last twenty years. Insulin deficiency, caused by reduced beta-cell mass, is the main etiologic mechanism, although insulin resistance also plays a role. Presenting features of type 1 and type 2 diabetes, CFRD typically affects individuals of approximately 20 years of age. It can also be accompanied by fasting, non-fasting or intermittent hyperglycemia. Glucose intolerance is associated with worsening of nutritional status, increased morbidity, decreased survival and reduced pulmonary function. Microvascular complications are always present, although macrovascular complications are rarely seen. An oral glucose tolerance test is recommended annually for patients e" 10 years of age and for any patients presenting unexplained weight loss or symptoms of diabetes. Patients hospitalized with severe diseases should also be screened. If fasting hyperglycemia persists for more than 48 h, insulin therapy is recommended. Insulin administration remains the treatment of choice for diabetes and fasting hyperglycemia. Calories should not be restricted, and patients with CFRD should be managed by a multidisciplinary team.


Subject(s)
Adolescent , Adult , Female , Humans , Male , Cystic Fibrosis/complications , Diabetes Mellitus/etiology , Age Factors , Cystic Fibrosis/diagnosis , Cystic Fibrosis/physiopathology , Cystic Fibrosis/therapy , Glucose Tolerance Test , Glucose Intolerance/etiology , Glucose Intolerance/physiopathology , Hyperglycemia/etiology , Hyperglycemia/physiopathology , Insulin Resistance , Insulin , Insulin/therapeutic use , Nutritional Status , Respiratory Tract Infections/etiology , Respiratory Tract Infections/physiopathology , Time Factors , Vascular Diseases/etiology , Vascular Diseases/physiopathology
13.
São Paulo; s.n; 2004. [60] p. ilus, tab, graf.
Thesis in Portuguese | LILACS | ID: lil-397902

ABSTRACT

A hiperfosfatemia (HP) contribui para a patogênese da doença cardiovascular e da osteodistrofia renal. Avaliamos o efeito da HP na histologia cardiovascular, na função renal e no tecido ósseo em uremia experimental. Ratos Wistar foram submetidos a PTx e Nx com reposição contínua de paratormônio ou eram sham operados. Apenas o conteúdo de fósforo era diferente nas dietas. O peso do coração corrigido para o peso do animal e a creatinina foram maior no grupo PTx+Nx+HP que nos demais grupos. A histologia não evidenciou calcificação vascular ou fibrose. / Hyperphosphatemia (HP) contributes to cardiovascular disease and renal osteodystrophy. We evaluated the effect of HP on cardiovascular system, renal function and bone in experimental uremia. Wistar rats were submitted to PTx and Nx with rat parathormone replacement, or were sham-operated. Only phosphorus content differentiated diets. Heart weight normalized to body weight and creatinine levels were higher in PTx+Nx+HP rats than in any other group. We detected no cardiovascular calcification or fibrosis...


Subject(s)
Animals , Male , Rats , Cardiomegaly/physiopathology , Phosphorus Metabolism Disorders/physiopathology , Vascular Diseases/physiopathology , Vascular Diseases/complications , Nephrectomy , Chronic Kidney Disease-Mineral and Bone Disorder/complications , Chronic Kidney Disease-Mineral and Bone Disorder/physiopathology , Parathyroidectomy , Rats, Wistar
14.
Southeast Asian J Trop Med Public Health ; 2003 Jun; 34(2): 361-4
Article in English | IMSEAR | ID: sea-35503

ABSTRACT

The diagnosis of patients with fever of unknown origin (FUO) is often problematic because the range of possible differential diagnoses is broad. We report on a case in which a patient presented with FUO and was subsequently found to have both a collagen vascular disease and an intercurrent infection. Treatment for the collagen vascular disease with corticosteroids exacerbated the intercurrent infection. The problems in the diagnosis and management of such cases are discussed.


Subject(s)
Adolescent , Collagen Diseases/physiopathology , Diagnosis, Differential , Fever of Unknown Origin/diagnosis , Humans , Lupus Erythematosus, Systemic/diagnosis , Male , Tuberculosis/diagnosis , Vascular Diseases/physiopathology
15.
Article in English | IMSEAR | ID: sea-125183

ABSTRACT

Various autonomic dysfunctions (AD) are known to occur in cirrhosis of the liver. The haemodynamic abnormalities of cirrhosis have been correlated with AD and have prognostic implications. The relevance of AD in extrahepatic portal vein obstruction (EHPVO) is not well established. We evaluated AD and cardiac indices in 30 patients, 19 male and 11 female and compared the results with those of 10 controls. The mean age of the patients and controls was 23.77 +/- 1.33 and 20.5 +/- 2.51 years, respectively. Five standard autonomic function tests were done in all the patients. Cardiac output (CO) was measured by echocardiography. Anthropometric measurements were done to determine the cardiac index (CI = Cardiac output/Body surface area) and indicized peripheral vascular resistance (iPVR) was calculated using the formula: mean arterial pressure (MAP) x 80/CI. Each autonomic function test was given a score and the results were interpreted as normal, early or definite, according to the score. AD was recorded as normal in 5, early in 11 and definite in 14 patients. None of the controls had any abnormality in autonomic function. There was a significant difference in the baseline heart rate of controls and patients (76 +/- 2.55 v. 98.9 +/- 2.96 beats/min). There was no difference in the MAP (92.65 +/- 1.71 v. 81.7 +/- 1.99 mmHg), CI (2.99 +/- 0.15 v. 3.23 +/- 0.08), iPVR (2533.59 +/- 124 v. 2176 + 104). CI, iPVR and MAP were also calculated separately in patients in the normal (N), early (E) and definite (D) AD groups. Their respective values were as follows CI: N 3.44 +/- 0.19, E 3.44 +/- 0.19, D 3.23 +/- 0.6; iPVR: N 2150 +/- 75.4, E 2140 +/- 180, D 2372 +/- 142; MAP: N 86 +/- 3.01, E 85.8 +/- 3.59, D 90.79 +/- 3.09. Results are expressed as mean +/- SE. Unlike in cirrhotics, cardiovascular haemodynamics are not altered in patients with EHPVO, even in the presence of AD.


Subject(s)
Adolescent , Adult , Autonomic Nervous System/physiopathology , Case-Control Studies , Child , Female , Hemodynamics , Humans , Male , Portal Vein , Vascular Diseases/physiopathology
16.
An. Acad. Nac. Med ; 162(2): 74-76, jul./dez.2002.
Article in Portuguese | LILACS | ID: lil-391118

ABSTRACT

Os hemangiomas e/ou tumores vasculares são anomalias congênitas que surgem em consequência de uma interrupção durante a fase de formação de capilares. O objetivo deste trabalho é fazer o diagnóstico correto dos diferentes tipos de hemangiomas, indicando o tratamento mais adequado. Para facilitar seu estudo, os hemangiomas foram classificados em benignos e malignos. A faixa etária das crianças estudadas ficou estabelecida entre recém-nascidas e adolescentes. Para os hemangiomas graves cirúrgicos e os hemangiomas malignos, o tratamento com laser a CO² ainda é o mais utilizado entre nós. Nos casos de hemangioma plano (nevus), o laser KTP está apresentando atualmente resultados excelentes


Subject(s)
Humans , Infant, Newborn , Infant , Child, Preschool , Child , Adolescent , Vascular Diseases/diagnosis , Vascular Diseases/physiopathology , Hemangiosarcoma , Port-Wine Stain
17.
Rev. med. Tucumán ; 5(3): 115-40, jul.-sept. 1999.
Article in Spanish | LILACS | ID: lil-263434

ABSTRACT

En este artículo se resume brevemente el rol de la inflamación en la patogénesis y la fisiopatología de los síndromes coronarios agudos y los avances recientes del conocimiento sobre los factores responsables de la inestabilidad. Se examina la evidencia que sostiene la aseveración de que la inflamación de la placa ateroesclerótica puede jugar un rol clave en la patogénesis de la angina inestable y también los mecanismos a través de los cuales la activación de las células inflamatorias en la placa ateroesclerótica pueden conducir a una oclusión transitoria o permanente. El proceso de aterogénesis ha sido considerado fundamentalmente como la acumulación de lípidos dentro de la pared arterial; sin embargo es mucho más que eso. Las lesiones ateroescleróticas pueden describirse como correspondientes a una enfermedad inflamatoria. De hecho, la más precoz de las lesiones, la llamada estría grasa, es una lesión puramente inflamatoria, constituída sólo por macrófagos derivados de monocitos y linfocitos T. Se discute el uso de marcadores bioquímicos para la identificación y estratificación precoz de riesgo. La evaluación temprana del riesgo es esencial para la aplicación del tratamiento apropiado y el manejo futuro de pacientes con síndromes coronarios agudos. La proteína C reactiva, un reactante de fase aguda, es un marcador sensible de inflamación, y es un buen candidato para conocer el riesgo de futuros eventos cardiovasculares. La interacción adhesiva es un prerequisito para el normal funcionamiento de todos los componentes del sistema cardiovascular, sin embargo también está involucrada en la patogénesis de la enfermedad cardiovascular. Existe creciente evidencia de que las moléculas de adhesión (integrinas, selectinas y la superfamilia de las inmunoglobulinas) juegan un importante rol en la patología cardiovascular. Datos experimentales y epidemiológicos sugieren que la disyunción endotelial, luego de una infección o una inflamación, puede ser un factor de riesgo transitorio para enfermedad cardiovascular, que podría promover una respuesta vascular anormal. La disrupción, fisura o ruptura de placa, complican el curso de la ateroesclerosis coronaria. El riesgo de disrupción de una placa depende más de su composición que del tamaño de la placa y de la severidad de la estenosis...


Subject(s)
Humans , Vascular Diseases/physiopathology , Coronary Thrombosis/therapy , Atherosclerosis/complications , Atherosclerosis/physiopathology , Angina, Unstable/etiology , Cholesterol, LDL/pharmacokinetics , Inflammation , Biomarkers , Disease Progression , Protein C , Smoking , Trans-Activators/immunology , Risk Factors , Coronary Disease/etiology , Coronary Disease/therapy , Creatine Kinase , Fibrinogen/pharmacokinetics
18.
Rev. Inst. Nac. Enfermedades Respir ; 11(4): 318-21, oct.-dic. 1998.
Article in Spanish | LILACS | ID: lil-240946

ABSTRACT

El Síndrome hepatopulmonar (SHP) es una entidad clínica reconocida por vez primera en 1884 por Flückiger, sin embargo fue hasta 1977 cuando Kennedy y Knudson la consideraron como un síndrome, el cual se caracteriza por una tríada conformada por insuficiencia hepática, vasodilatación pulmonar e hipoxemia. Entre las causas de esta entidad clínica se encuentra la insuficeincia hepatica, ya sea aguda o crónica. El factor relajante del endotelio es aparentemente la principal causa de las alteraciones vasculares pulmonares. La sintomatología es la producida por la insuficiencia hepática per se como ascitis, ictericia, eritema palmar, varices esofágicas, hemorragia del tubo digestivo, y por el componente pulmonar como son, ortodeoxia, hipocratismo digital y cianosis. Los mecanismos de hipoxemia en el SHP son alteraciones de la ventilación perfusión, cortos circuitos y trastornos de la difusión. El diagnóstico se realiza con base en diferentes estudios, como son la radiografía de tórax, el gammagrama perfusorio, la ecocardiografía contrastada bidimensional y la angiografía. Hasta el momento, no hay un tratamiento conocido que sea totalmente efectivo, no obstante el trasplante hepático ha sido considerado como la mejor opción, aunque otros como la embolización y terapia farmacológica pueden ser utilizados


Subject(s)
Humans , Liver Cirrhosis/complications , Endothelium, Vascular/physiopathology , Hypoxia/etiology , Lung Diseases/etiology , Lung Diseases/physiopathology , Vascular Diseases/diagnosis , Vascular Diseases/drug therapy , Vascular Diseases/etiology , Vascular Diseases/physiopathology , Vasodilation
19.
Medicina (B.Aires) ; 58(4): 367-73, 1998. tab
Article in Spanish | LILACS | ID: lil-217516

ABSTRACT

El óxido nítrico (NO.) es producido por la oxidación de la arginina a citrulina, una reacción catalizada por las enzimas óxido nítrico sintasas (NOS). Se acepta que esa reacción es la única capaz de producir NO en los sistemas biológicos, en condiciones normales o patológicas. El NO regula diferentes funciones en células y tejidos de mamíferos, tales como: (a) el control de la presión sanguínea; (b) la relajación del tono del músculo liso arterial; (c) la agregación y adhesión plaquetaria; (d) la neurotransmisión; (e) la función neuro-endócrina. El NO. también participa en la destrucción de microorganismos patógenos y de células tumorales por leucocitos y macrófagos. La producción de anión superóxido (O2-) y NO. ha sido asociada al desarrollo de muchas patologías, pero recientemente se ha comprobado que la interacción de esas moléculas genera el ión peroxintrito (ONOO-), lo que constituye un importante mecanismo fisiopatológico pues, como oxidante, el ONOO- ataca un gran número de blancos biológicos. Por su influencia sobre la producción de ONOO-, el balance entre la producción de NO y O2- es crítico en la etiología de procesos como hipertensión, ateroesclerosis, enfermedades neurodegenerativas, infecciones virales, daño por isquemia-reperfusión y cáncer.


Subject(s)
Humans , Neoplasms/physiopathology , Neurodegenerative Diseases/physiopathology , Nitrates/physiology , Nitric Oxide/physiology , Oxidants/physiology , Oxidative Stress/physiology , Reactive Oxygen Species/physiology , Vascular Diseases/physiopathology , Virus Diseases/physiopathology , Antioxidants/pharmacology , Liver Transplantation/physiology , Reperfusion Injury/physiopathology
20.
Clín. méd. H.C.C ; 2(3): 188-91, sept.-dic. 1997.
Article in Spanish | LILACS | ID: lil-275692

ABSTRACT

La enfermedad vascular pulmonar (EVP) que ocurre en nuestros pacientes con enfermedad broncopulmonar obstructiva crónica (EBPOC) es una complicación común y seria. Se ha estimado que el 50 por ciento de los pacientes mayores de los 50 años y que poseen una EBPOC presentan hipertensión pulmonar y, por ende EVP. La tasa de sobrevida de estos pacientes se asemeja bastante a la tasa que presentan los pacientes con cáncer de pulmón inoperable. Esta enfermedad (EVP) disminuye aún más la captación de O² por el pulmón. También produce una disminución de la calidad de vida del paciente² y como los síntomas que produce la EVPson silentes o se asemejan mucho a los que produce la EBPOC es común que el médico no se percate de que está ocurriendo. En este artículo discutimos la clínica, la fisiopatología y los nuevos métodos de tratamiento de esta complicación que con frecuencia acompaña a la enfermedad pulmonar


Subject(s)
Humans , Animals , Female , Lung Diseases, Obstructive/complications , Lung Diseases, Obstructive/diagnosis , Lung Diseases, Obstructive/physiopathology , Vascular Diseases/diagnosis , Vascular Diseases/physiopathology , Vascular Diseases/therapy
SELECTION OF CITATIONS
SEARCH DETAIL