ABSTRACT
El deterioro paradójico durante el tratamiento tuberculostático se define por la exacerbación de los síntomas clínicos o el empeoramiento radiológico de las lesiones tuberculosas preexistentes o la aparición de otras nuevas. Este fenómeno es relativamente frecuente; se observa entre el 6 y el 30% de los pacientes que reciben tratamiento tuberculostático. La patogenia no está clara; se acepta generalmente como una respuesta inmunológica anormal a las proteínas liberadas de los bacilos tuberculosos destruidos. Las manifestaciones clínicas y radiológicas pueden localizarse en el sistema nervioso central, pulmones, pleura, ganglios linfáticos y piel. El diagnóstico frecuentemente es dificultoso y sin embargo el curso suele ser favorable. Posiblemente el tratamiento con glucocorticoides puede ser beneficioso en el curso de este fenómeno. En este artículo pretendemos revisar la definición, la patogenia, las manifestaciones clínicas y el tratamiento de esta afección (AU)
The exacerbation of clinical symptoms or radiological worsening of pre-existing tuberculous lesions or the development of new lesions defines paradoxical deterioration during antituberculosis therapy. This phenomenon is relatively frequent: it is observed between 6 and 30% of patients receiving antituberculous therapy. The pathogenesis is not completely clear and it is generally regarded as an abnormal immune response to the proteins released from dead bacilli. Clinical and radiological manifestations may locate in the central nervous system, lungs, pleura, lymph nodes and skin. The diagnosis is frequently difficult and outcome is most often spontaneously favourable. It is possible that the addition of corticosteroid therapy could be beneficial on the outcome of this phenomenon. In this paper we try to review the definition, pathogenesis, clinical manifestations and treatment of this pathology (AU)
Subject(s)
Humans , Antitubercular Agents/adverse effects , Immunocompetence , Tuberculosis/complications , Tuberculosis/drug therapy , Signs and Symptoms , Adrenal Cortex Hormones/adverse effectsABSTRACT
The exacerbation of clinical symptoms or radiological worsening of pre-existing tuberculous lesions or the development of new lesions defines paradoxical deterioration during antituberculosis therapy. This phenomenon is relatively frequent: it is observed between 6 and 30% of patients receiving antituberculous therapy. The pathogenesis is not completely clear and it is generally regarded as an abnormal immune response to the proteins released from dead bacilli. Clinical and radiological manifestations may locate in the central nervous system, lungs, pleura, lymph nodes and skin. The diagnosis is frequently difficult and outcome is most often spontaneously favourable. It is possible that the addition of corticosteroid therapy could be beneficial on the outcome of this phenomenon. In this paper we try to review the definition, pathogenesis, clinical manifestations and treatment of this pathology.
Subject(s)
Antitubercular Agents/adverse effects , Immunocompetence , Tuberculosis/complications , Tuberculosis/drug therapy , HumansABSTRACT
No disponible
Subject(s)
Female , Aged , Humans , Demyelinating Diseases/etiology , Tuberculosis, Lymph Node/physiopathology , Mycobacterium tuberculosis/pathogenicityABSTRACT
Myoglobinuric acute renal failure has three pathogenic mechanisms: tubular obstruction, renal vasoconstriction, and oxidative stress. The latter is generated through the iron released from the group hemo of the myoglobin. Iron induces the formation of high-activity oxygen free radicals that increase oxidative stress and provoke lipid peroxidation and cellular death. This oxidative stress can be measured in several ways, both total or partially with the total antioxidant status or the intermediate enzymes. On the other hand, N-acetylcysteine is a demonstrated substance with antioxidant properties. The aim of the present work was to assess the effect of N-acetylcysteine on the oxidative stress in the glycerol-induced acute renal failure in rats model. We observed that the animals treated with N-acetylcysteine showed an improvement in the antioxidant activity given by an increase in the total antioxidant status and glutathione reductase levels in serum. This improvement was greater when treatment was administered before the induction of rhabdomyolysis. Nevertheless, the observed increase in antioxidant status was only statistically significant for glutathione reductase but not for total antioxidant status. Our results support an important role for N-acetylcysteine in the treatment of this form of acute renal failure, although we think that oxidative stress is not the main pathogenic mechanism of the tubular necrosis induced by rhabdomyolysis, tubular obstruction and renal vasoconstriction being still more important.
Subject(s)
Acetylcysteine/pharmacology , Acute Kidney Injury/drug therapy , Acute Kidney Injury/pathology , Oxidative Stress/drug effects , Analysis of Variance , Animals , Disease Models, Animal , Female , Glycerol , Kidney Function Tests , Male , Oxidative Stress/physiology , Probability , Random Allocation , Rats , Rats, Sprague-Dawley , Reference Values , Sensitivity and SpecificityABSTRACT
BACKGROUND: Accurate estimation of the Total Antioxidant Status (TAS) in the myoglobinuric acute renal failure (ARF) is necessary because its pathogenesis is believed to be mediated, at least in part, by the development of oxidative stress resulting from the generation of oxygen free radicals and reduced antioxidant defense system. The purpose of this study is to examine the TAS 24 and 72 h after glycerol injection in a model of myoglobinuric-ARF. EXPERIMENTAL DESIGN: The study was conduced in 28 Sprague-Dawley rats. In group 1 (n = 7) rats were placed into individual metabolic cages and deprived of water during 24 h. afterwards an intramuscular injection of glycerol was administrated (50% vol/vol in sterile saline) 10 mg/100 g of body weight and 24 h later blood samples were collected for biochemical measurements (urea, creatinine, creatine-kinase, and TAS levels). In group 2 (n = 7), rats followed the same conditions than group 1 ones but blood samples were collected 72 h after glycerol injection. In groups 3 (n = 7) and 4 (n = 7) rats didn't receive glycerol injection, and blood samples were collected within 24 and 72 h respectively after they were placed into metabolic cages. RESULTS: In groups 1 and 2 we observed a renal function decrease, with higher serum levels of urea and creatinine in group 2 (urea levels: 269 +/- 16 mg/dL vs. 586 +/- 147 mg/dL; p < 0.001. Creatinine levels: 2.8 +/- 0.2 mg/dL vs. 5.8 +/- 0.7 mg/dL; p < 0.001). TAS levels in groups 2, 3, and 4 were similar, but in group 1 was significantly lower (group 1: 0.81 +/- 0.2 mmol/L; group 2: 1.3 +/- 0.1 mmol/L; group 3: 1.2 +/- 0.3 mmol/L, and group 4: 1.2 +/- 0.2 mmol/L; p < 0.005). CONCLUSION: In the model of glycerol induced myoglobinuric-ARF we observed a decrease of serum TAS level within 24 h with spontaneous recuperation 72 h after.
Subject(s)
Acute Kidney Injury/metabolism , Antioxidants/metabolism , Acute Kidney Injury/physiopathology , Animals , Biomarkers/blood , Creatine Kinase/blood , Creatinine/blood , Disease Models, Animal , Diuresis/physiology , Kidney Function Tests , Random Allocation , Rats , Rats, Sprague-Dawley , Statistics as Topic , Urea/blood , Urination/physiologyABSTRACT
Oxygen metabolites play an important role in renal injury during myoglobinuric acute renal failure (ARF). This study was designed to determine the protective influence of N-acetylcysteine (NAC), a hydroxyl radical scavenger, and treatment in an experimental model of myoglobinuric-ARF induced by intramuscular injection of hypertonic glycerol in rats. The rats were randomly distributed into five groups: Group 0 (n = 10), was assigned to receive 2mL saline (0,9%) intraperitoneally (ip); Group 1 (n = 10), NAC ip in a dose of 0 mg/100 g of body weight 30 min before the intramuscular (im) injection of 50% glycerol (10 mg/kg); Group 2 (n = 10), received saline 0,9% ip in a equivalent volume of NAC in Group I before the im injection of glycerol; Group 3 (n = 10), received NAC ip in a dose of 10 mg/100 g after im injection of glycerol; Group 4 (n = 10), saline 0,9% ip in a equivalent volume of NAC of the Group 3 after im administration of glycerol. After 24 h rats were sacrificed and kidney morphology and renal function were determined. A severe renal failure was produced by glycerol injection in the Groups 1, 2, 3, and 4, with significant tubular proximal necrosis and cast formation, and creatinine and urea concentrations were elevated in these groups without significant differences among groups, but Group 0 where the values were significantly lower. The results of this study suggests that ip administration of NAC in rats before or after glycerol injection do not confer protection against impairment of renal function under these conditions in this model of myoglobinuric-ARF.
Subject(s)
Acetylcysteine/therapeutic use , Acute Kidney Injury/prevention & control , Free Radical Scavengers/therapeutic use , Myoglobinuria/prevention & control , Acetylcysteine/administration & dosage , Acute Kidney Injury/chemically induced , Acute Kidney Injury/pathology , Animals , Cryoprotective Agents/adverse effects , Disease Models, Animal , Free Radical Scavengers/administration & dosage , Glycerol/adverse effects , Hypertonic Solutions/adverse effects , Injections, Intraperitoneal , Kidney/drug effects , Kidney/pathology , Kidney/physiopathology , Myoglobinuria/chemically induced , Myoglobinuria/pathology , Rats , Rats, Sprague-Dawley , Severity of Illness Index , Time FactorsABSTRACT
BACKGROUND: Diabetic cardiomyopathy (DMC) is a complication of diabetes mellitus (DM)that is more frequently observed in those patients with microalbuminuria. Left ventricular diastolic dysfunction (LVDD) in patients with diabetes, in absence of another etiology that justifies it, is an early marker of DMC. We carried out a prospective study on young diabetic type 1 patients with microalbuminuria, aimed at knowing the effect of captopril on LVDD. PATIENTS AND METHOD: We included 30 patients (18 males and 12 females) diagnosed with type 1 DM,aged 40 years old, who had been recently found to have microalbuminuria and thus they were candidates to receive captopril. We excluded patients having factors different from DM that could modify the diastolic function. All patients underwent a complete biochemical and echocardiographic study before starting the treatment with captopril and six months later. A diagnosis of LVDD was made when at least one of the following parameters was present in the echocardiographic study: isovolumetric relaxing time (IRT) >100 ms, deceleration time (DT) > 220 ms or early filling rate peak/late filling rate peak ratio (E/A) < 1. According to the results of the second echocardiogram, patients were classified in two groups: improved group (when there was at least a 10% improvement of initial LVDD altered parameters) and non-improved group. A control group of 28 type 1 diabetic patients without microalbuminuria who were not given captopril was included (group C). RESULTS: The initial echocardiographic study yielded 11 patients having a normal diastolic function (group FDN) and 19 patients having LVDD (group FDA). After 6 moths of captopril treatment, an improvement of the ratio E/A was observed in the group FDN: from 1.58 (0.36)in the beginning to 1,68 (0.29) six moths later (p < 0.05),and in the group FDA: from 1.09 (0.24) to 1.24 (0.28) (p <0.05). In the group FDA, an improvement of IRT was found: from 110 (16) ms to 99.9 (9.6) ms (p < 0.01). Moreover, in the group FDA, LVDD improved after sixth months in 15 (78.9%) patients but not in 4 (21,6%). This LVDD improvement was associated with a decrease of the diastolic blood pressure (DBP) and the systolic blood pressure (SBP) at the end of the study. A logistic regression analysis showed an independent association between the reduction of the mean SBP and the improvement of LVDD. CONCLUSION: Our results suggest that captopril can improve LVDD in young patients with type 1 diabetes and microalbuminuria, possibly due to a decrease of blood pressure.
Subject(s)
Albuminuria/complications , Angiotensin-Converting Enzyme Inhibitors/therapeutic use , Captopril/therapeutic use , Diabetes Mellitus, Type 1/complications , Ventricular Dysfunction, Left/drug therapy , Adult , Diastole/drug effects , Female , Humans , Male , Prospective Studies , Ventricular Dysfunction, Left/etiology , Ventricular Dysfunction, Left/physiopathologyABSTRACT
FUNDAMENTO: La miocardiopatía diabética (MD) es una complicación de la diabetes mellitus (DM) que se observa principalmente en presencia de microalbuminuria. La disfunción diastólica del ventrículo izquierdo (DDVI), en ausencia de otra causa que la justifique, se considera la fase temprana de esta alteración cardíaca. Con el propósito de analizar el efecto del captopril sobre la DDVI en estos pacientes, realizamos un estudio prospectivo en jóvenes con diabetes tipo 1 y microalbuminuria de reciente diagnóstico. PACIENTES Y MÉTODO: Se incluyó 30 pacientes (18 varones y 12 mujeres) diagnosticados de DM tipo 1, de edad 40 años, en quienes la microalbuminuria se había detectado recientemente, por lo que eran candidatos a recibir captopril. Excluimos a aquellos que pudieran tener otro factor diferente de la DM que pudiera modificar la función diastólica. Los pacientes fueron sometidos a un estudio bioquímico y ecocardiográfico antes de iniciar el tratamiento con captopril y 6 meses después. Se consideró que existía DDVI cuando en el ecocardiograma inicial se observaba al menos una de las siguientes consideraciones: tiempo de relajación isovolumétrica (TRIV) > 100 ms, tiempo de desaceleración (TD) > 220 ms o índice entre el pico de llenado rápido y el pico de llenado lento (E/A) < 1. Según el resultado del segundo ecocardiograma, los pacientes se clasificaron en dos grupos: grupo mejoría (si los parámetros de DDVI alterados inicialmente mejoraban al menos en un 10 por ciento el valor alterado al inicio) y grupo no mejoría (si no mejoraban). Se utilizó un grupo control formado por 28 pacientes con diabetes tipo 1 sin microalbuminuria, que no recibieron captopril (grupo C). RESULTADOS: En el ecocardiograma inicial, encontramos que 11 pacientes tenían una función diastólica normal (grupo FDN) y 19 pacientes tenían DDVI (grupo FDA). En el ecocardiograma realizado a los 6 meses de tratamiento con captopril el índice E/A mejoró en ambos grupos pasando en el grupo FDN de 1,58 (0,36) al inicio a 1,68 (0,29) al final del estudio (p < 0,05) y en el grupo FDA de 1,09 (0,24) a 1,24 (0,28) (p < 0,05). En el grupo FDA el TRI mejoró al pasar de 110 (16) ms a 99,9 (9,6) ms (p < 0,01). De los 19 pacientes del grupo FDA la DDVI mejoró al final del estudio en 15 (78,9 por ciento) y no lo hizo en 4 (21,1 por ciento); esta mejoría se asoció con una reducción de la presión arterial sistólica (PAS) y diastólica (PAD) al final del estudio, así como de la media de PAS y de la PAD a lo largo del estudio. El análisis de regresión logística demostró una asociación independiente entre la reducción de la PAS media y la mejoría de la DDVI. CONCLUSIÓN: El captopril puede mejorar la DDVI en los jóvenes con diabetes tipo 1 y microalbuminuria, posiblemente como consecuencia de una reducción de la presión arterial (AU)
Subject(s)
Middle Aged , Adolescent , Adult , Aged , Aged, 80 and over , Male , Female , Humans , Spain , Pneumonia, Bacterial , Community-Acquired Infections , Ventricular Dysfunction, Left , Prospective Studies , Angiotensin-Converting Enzyme Inhibitors , Anti-Bacterial Agents , Captopril , Diastole , Albuminuria , Diabetes Mellitus, Type 1ABSTRACT
No disponible
Subject(s)
Middle Aged , Male , Female , Humans , Sarcoidosis , Ofloxacin , Anti-Infective Agents, Urinary , Sweet Syndrome , TendinopathyABSTRACT
No disponible
Subject(s)
Male , Female , Humans , Risk Factors , Oxidative Stress , Myocardium , Prognosis , Autopsy , Cross-Sectional Studies , Diabetes Mellitus , Coronary Disease , Echocardiography , Hypertension , Electrocardiography , Heart , Cardiac Catheterization , Cardiomyopathies , Cardiomyopathy, DilatedABSTRACT
Objetivo. El objetivo de nuestro estudio fue evaluar la función diastólica del ventrículo izquierdo por estudio ecocardiográfico en jóvenes (< 40 años) asintomáticos con diabetes mellitus tipo 1 sin síntomas cardiovasculares, y analizar los factores asociados a disfunción diastólica del ventrículo izquierdo (DDVI) en estos pacientes. Pacientes y métodos. Fueron estudiados 35 diabéticos tipo 1 (edad media de 27,8 ñ 7,5 años) sin síntomas cardiovasculares y 54 controles sanos (edad media de 26,1 ñ 4,1 años). Se realizó una anamnesis, exploración física, analítica general y estudio eco-Doppler. Resultados. El DDVI estuvo presente en 13 (37,1 por ciento) de los pacientes diabéticos y en ninguno de los pacientes control. En el grupo de diabéticos encontramos un índice entre la velocidad de llenado precoz y llenado tardío (auricular) significativamente menor que en el grupo control (1,1 ñ 0,3 frente a 1,5 ñ 0,2; p < 0,01) y un tiempo de relajación isovolumétrico mayor que en el grupo control (104 ñ 11 frente a 79 ñ 11; p < 0,01). Los diabéticos con DDVI tenían una mayor edad, en su mayoría eran varones, tenían un peor control glucémico, más alteración del metabolismo lipídico y mayores concentraciones de microalbuminuria que aquellos sin DDVI. Conclusión. La DDVI es frecuente en diabéticos jóvenes sin síntomas cardiovasculares. Estos estudios sugieren que la presencia en estos pacientes de una mayor edad, sexo masculino, pobre control glucémico, metabolismo lipídico alterado y microalbuminuria puede asociarse a una DDVI que, en ausencia de enfermedad cardiovascular, podría ser una alteración preclínica potencialmente relacionada con el subsiguiente desarrollo de miocardiopatía diabética (AU)
