[Marfan syndrome associated with aortic dissection, venous thromboembolism and hyperhomocysteinemia]. / Síndrome de Marfan con disección aórtica asociada a tromboembolismo venoso e hiperhomocisteinemia.

Marfan syndrome is an infrequent genetic disorder of connective tissue whose clinical manifestations mainly affect the cardiovascular, ocular and musculoskeletal systems. Serious cardiovascular manifestations are generally the cause of mortality of Marfan patients. Thromboembolic venous disease is intimately related to different risk factors: inherited, acquired, mixed or unknown; hyperhomocysteinemia is a moderate risk factor for venous thromboembolism. We present the case of a 47-year-old woman with Marfan syndrome associated to a painless type A aortic dissection, who simultaneously suffered venous thromboembolism of left upper and lower limbs with pulmonary embolism. Hyperhomocysteinemia was found through thrombofilia screening. The patient's condition has evolved favorably.

Síndrome de Marfan con disección aórtica asociada a tromboembolismo venoso e hiperhomocisteinemia / Marfan syndrome associated with aortic dissection, venous thromboembolism and hyperhomocysteinemia

El síndrome de Marfan es un desorden genético infrecuente, cuyas manifestaciones clínicas afectan a los sistemas cardiovascular, ocular y músculo esquelético, la gravedad de las manifestaciones cardiovasculares son generalmente responsables de la mortalidad de estos pacientes. La enfermedad tromboembólica venosa está íntimamente relacionada con diversos factores de riesgo, congénitos, adquiridos, mixtos o desconocidos. La hiperhomocisteinemia es un factor de riesgo moderado para tromboembolismo venoso. Presentamos el caso de una mujer de 47 años de edad con síndrome de Marfan asociado a disección aórtica tipo A indolora, que simultáneamente padeció trombosis venosa de miembros inferior y superior izquierdos con embolia de pulmón. Al realizar el cribado de trombofilia se constató hiperhomocisteinemia. Con la terapéutica instituida evolucionó favorablemente.

Marfan syndrome is an infrequent genetic disorder of connective tissue whose clinical manifestations mainly affect the cardiovascular, ocular and musculoskeletal systems. Serious cardiovascular manifestations are generally the cause of mortality of Marfan patients. Thromboembolic venous disease is intimately related to different risk factors: inherited, acquired, mixed or unknown; hyperhomocysteinemia is a moderate risk factor for venous thromboembolism. We present the case of a 47-year-old woman with Marfan syndrome associated to a painless type A aortic dissection, who simultaneously suffered venous thromboembolism of left upper and lower limbs with pulmonary embolism. Hyperhomocysteinemia was found through thrombofilia screening. The patient's condition has evolved favorably.

[Determination of blood markers and inflammation in subjects with impaired glucose tolerance]. / Determinación de marcadores séricos de trombosis e inflamación en sujetos con intolerancia a la glucosa: evidencia de un estado protrombótico.

OBJECTIVE: This study was designed to explore the presence of a prothrombotic state, fibrinolytic dysfunction and inflammation in impaired glucose tolerance subjects, by evaluating serum markers of thrombosis, fibrinolysis and inflammation. METHODS: In 48 consecutive adults, 25 patients with impaired glucose tolerance (nine men and 16 women, 50.0 ± 9.2 years) were compared with 23 control subjects (six men and 17 women, 48.0 ± 11 years). The markers of thrombotic activation used were D-dimer and fibrinogen. Fibrinolysis dysfunction was evaluated with plasminogen activator inhibitor 1 (PAI-1) and the inflammatory marker studied was hs-C reactive protein (hs-CRP). RESULTS: The markers of thrombotic state were significantly higher in patients with impaired glucose tolerance (IGT) than in controls: D dimer (489.6 ± 277.3 vs. 345.8 ± 158.9 ng/mL) (p< 0.01) and fibrinogen (317.7 ± 32.1 vs. 266.7 ± 25.4 mg/dL) (p < 0.0001). Fibrinolytic marker PAI-1 also differed significantly between the two study groups (66.4 ± 30.7 vs. 35.5 ± 31.0 ng/mL) (p < 0.006). However, hs-CRP, as inflammation marker, (0.45 ± 0.62 mg/dL vs. 0.38 ± 0.47) did not differ significantly between the two study groups (<0.28). CONCLUSION: This result suggests the presence of a prothrombotic state with fibrinolytic dysfunction in subjects with impaired glucose tolerance.

Determinación de marcadores séricos de trombosis e inflamación en sujetos con intolerancia a la glucosa: evidencia de un estado protrombótico / Determination of blood markers and inflammation in subjects with impaired glucose tolerance

Objetivo: Este estudio fue diseñado para explorar la presencia de un estado protrombótico, disfunción fibrinolítica e inflamación en sujetos con intolerancia a la glucosa, mediante la evaluación de los marcadores séricos de trombosis, fibrinólisis e inflamación. Métodos: Se estudiaron 48 individuos consecutivos, 25 intolerantes a la glucosa: (nueve hombres y 16 mujeres, 50.0 ±9.2 años) y 23 sujetos control (seis hombres y 17 mujeres, 48.0 ±11 años). Se compararon entre ambos grupos los niveles de dímero-D y fibrinógeno como marcadores de trombosis, el PAI-1 como marcador de fibrinólisis y la proteína C reactiva ultrasensible (PCR-us) como marcador de inflamación. Resultados: En los sujetos intolerantes a la glucosa respecto al grupo control, se observaron diferencias significativas en los marcadores de trombosis: fibrinógeno 317.7 ± 32.1 vs. 266.7 ± 25.4 mg/dL (p<0.0001), dímero-D 489.6 ± 277.3 vs. 345.8 ± 158.9 ng/mL (p<0.01) y en el marcador de fibrinólisis PAI-1 66.4 ± 30.7 vs. 35.5 ± 31.0 ng/mL (p<0.006). En el marcador de inflamación, PCR-us no se observó diferencia significativa, respecto al grupo control 0.45 ± 0.6 vs. 0.38 ± 0.4 mg/dL (p<0.28). Conclusiones: Estos resultados sugieren la presencia de un estado protrombótico con disfunción del sistema fibrinolítico, en sujetos intolerantes a la glucosa.

Objective: This study was designed to explore the presence of a prothrombotic state, fibrinolytic dysfunction and infammation in impaired glucose tolerance subjects, by evaluating serum markers of thrombosis, fibrinolysis and infammation. Methods: In 48 consecutive adults, 25 patients with impaired glucose tolerance (nine men and 16 women, 50.0 ±9.2 years) were compared with 23 control subjects (six men and 17 women, 48.0 ±11 years). The markers of thrombotic activation used were D-dimer and fibrinogen. Fibrinolysis dysfuntion was evaluated with plasminogen activator inhibitor 1 (PAI-1) and the infammatory marker studied was hs-C reactive protein (hs-CRP). Results: The markers of thrombotic state were significantly higher in patients with impaired glucose tolerance (IGT) than in controls: D dimer (489.6 ± 277.3 vs. 345.8 ± 158.9 ng/mL) (p < 0.01) and fibrinogen (317.7 ±32.1 vs. 266.7 ±25.4 mg/dL) (p < 0.0001). Fibrinolytic marker PAI-1 also differed significantly between the two study groups (66.4 ± 30.7 vs. 35.5 ± 31.0 ng/ mL) (p < 0.006). However, hs-CRP, as infammation marker, (0.45 ± 0.62 mg/dL vs. 0.38 ± 0.47) did not differ significantly between the two study groups (<0.28). Conclusion: This result suggests the presence of a prothrombotic state with fibrinolytic dysfunction in subjects with impaired glucose tolerance.

Inflammatory and prothrombotic activation with conserved endothelial function in patients with chronic, asymptomatic Chagas disease.

UNLABELLED: Previously, our group showed a prothrombotic state in asymptomatic patients with chronic Chagas disease. The current paper studies the inflammatory status and endothelial function in these patients. METHODS: In 40 patients and 40 healthy volunteers, we evaluated prothrombotic state, blood parasitemia (molecular biology: polymerized chain reaction [PCR]-amplification), tissue factor pathway inhibitor antibodies (aTFPI), interleukin 6 (IL-6), and vascular cell adhesion molecule-1 (VCAM-1). Endothelial function was determined by reactive hyperemia (pulse plethysmography). RESULTS: In patients, prothrombin fragment 1 + 2, d-dimer, PAI-1, and fibrinogen were higher. Amplification of 121/122 primers (Trypanosoma cruzi) was positive in 45% of the patients. Patients presented higher values of aTFPI- immunoglobulin G (IgG; P < .05), aTFPI-IgM (P < .001), IL-6 (P = .004), and VCAM-1 (P = .00001). In both groups, endothelial function was preserved. CONCLUSIONS: We found that asymptomatic patients with chronic Chagas disease presented a prothrombotic/inflammatory status. The fact that endothelial function is still preserved suggests that prothrombosis and inflammation are primarily implicated in the beginning of cardiovascular damage.

Probables mecanismos involucrados en la etiopatogenia del estado protrombótico en la enfermedad de Chagas crónica. ¿Activación inflamatoria con función endotelial conservada? / Possible mechanisms involved in the pathogenesis of prothrombotic state Chronic Chagas disease. Inflammatory activation with preserved endothelial function?

Introducción: En el estadio indeterminado de la enfermedad de Chagas crónica, se comprobó un estado protrombótico asociado con factores de riesgo trombofílicos. La etiopatogenia de la enfermedad de Chagas es multifactorial sin que ninguno de los mecanismos involucrados explique por sí mismo el inicio y progresión de las lesiones. Objetivo: Evaluar probables mecanismos involucrados en la etiopatogenia del estado protrombótico en el estadio indeterminado de la enfermedad de Chagas crónica. Material y Métodos: Desde marzo de 2004 hasta diciembre de 2006 se evaluaron 40 pacientes chagásicos crónicos, 14 varones y 26 mujeres, (33.5 ± 4.9 años); en clase funcional I, de la clasificación clínica de la miocardiopatía chagásica crónica, comparándolos con un muestreo accidental de 40 voluntarios sanos, 19 varones y 21 mujeres (28.8 ± 6.3 años). Se evaluó la presencia del parásito por técnica de amplificación de las cadenas de polimerasa (PCR) y se determinó anticuerpo inhibidor de la vía extrínseca de la coagulación (aTFPI) por un método de ELISA optimizado, con valor de corte para aTFPI IgG >18 Uml-1 y para aTFPI IgM >15 Uml-1. Valores altos de aTFPI (IgG e IgM) se consideraron los >50 Uml-1. Se tomaron también muestras de sangre para la determinación por ELISA de dos marcadores de inflamación; Interleuquina 6 (IL-6) y de la molécula de adhesión a célula vascular (VCAM-1). La función endotelial se evaluó por pletismografía de onda de pulso digital para determinar hiperemia reactiva, la que discrimina sujetos con y sin disfunción endotelial. Resultados: En los pacientes chagásicos estudiados se detectó presencia del parásito por la técnica de amplificación de PCR utilizada en el 45 por ciento (n=18) de los casos. Los pacientes chagásicos presentaron valores de aTFPI mayores que los controles, con una p<0.05 para aTFPI IgG y p<0.001 para aTFPI IgM; superando en muy pocos casos los valores de corte establecidos para el método...

[Diagnosis, management and treatment of chronic Chagas' heart disease in areas where Trypanosoma cruzi infection is not endemic]. / Diagnóstico, manejo y tratamiento de la cardiopatía chagásica crónica en áreas donde la infección por Trypanosoma cruzi no es endémica.

Chagas' disease, or American trypanosomiasis, is a parasitic zoonosis found only in the Americas. Under natural conditions, Trypanosoma cruzi is transmitted by insects belonging to different species of Triatoma. However, several routes of transmission that do not involve insect vectors have also been described, such as transmission via blood products or transplantation of infected organs, and vertical transmission. At present, the number of people infected with Chagas' disease worldwide is estimated to be about 10-12 million. The process of urbanization in Latin America and migratory population movements from endemic countries have led to the disease being diagnosed in non-endemic areas. It is estimated that 20-30% of individuals infected with T. cruzi will develop symptomatic heart disease at some point during their lives. The specific differential characteristics of chronic chagasic cardiopathy, lack of knowledge of the disease among many healthcare workers, and the fact that arrhythmia or sudden death is frequently the first manifestation of disease all make it essential that diagnostic and therapeutic protocols for the disease are developed and disseminated. The aim should be to improve patient care by increasing understanding of the condition by physicians and other healthcare professionals who may be involved in its detection and treatment.

[Pheochromocytoma associated with von Recklinghausen neurofibromatosis]. / Feocromocitoma asociado a neurofibromatosis de von Recklinghausen.

A pheochromocytoma is an adrenal gland tumor that secretes epinephrine and norepinephrine hormones, and is responsible for regulating heart rate and blood pressure, among other functions. The condition can occur alone or in combination with other disorders, and genetic and environmental factors play a key role. Neurofibromatosis-1 (NF-1) an inherited "autosomal dominant" disorder is one of the most common genetic disorders, characterized by formation of neurofibromas (tumors involving nerve tissue) in the skin, subcutaneous tissue, cranial and spinal root nerves. NF1 generally is diagnosed by physical examination. There is no cure for NF1, but there are ways to treat some of its effects. Neurofibromatosis arterial hypertension caused by pheochromocytoma is extremely rare, less frecuent than 1% in childrens less than 10 years old, and young adults. We present a case of an extremely infrequent association between neurofibromatosis and a pheochromocytoma in a young woman with a newly diagnosed hypertension. We discuss the underlying pathophysiological mechanisms and clinical implications.

Feocromocitoma asociado a neurofibromatosis de von Recklinghausen / Pheochromocytoma associated with von Recklinghausen neurofibromatosis

El feocromocitoma es un tumor glandular adrenal secretor de hormonas epinefrina y norepinefrina, responsables de regular la frecuencia cardíaca y la presión arterial, entre otras funciones. Este tumor puede ocurrir solo o en combinación con otros desórdenes; los factores genéticos y ambientales juegan un rol clave en su aparición. La neurofibromatosis tipo 1 (NF-1) es un desorden genético frecuente que se hereda en forma autosómica dominante, caracterizado por la formación de neurofibromas (tumores que involucran los nervios tisulares) en piel, tejido subcutáneo, nervios craneales y espinales. La NF-1 se diagnostica generalmente con el examen físico. No existe un tratamiento curativo para la NF-1, pero hay modos de tratar algunas de sus complicaciones. La hipertensión arterial en la neurofibromatosis causada por un feocromocitoma es extremadamente rara con una incidencia de menos del 1% en menores de 10 años y en adultos jóvenes. Presentamos el caso clínico de una mujer joven con hipertensión de reciente diagnóstico, con la infrecuente asociación de neurofibromatosis y feocromocitoma. Discutimos los mecanismos fisiopatológicos subyacentes y sus implicancias clínicas.

A pheochromo cytoma is an adrenal gland tumor that secretes epinephrine and norepinephrine hormones, and is responsible for regulating heart rate and blood pressure, among other functions. The condition can occur alone or in combination with other disorders, and genetic and environmental factors play a key role. Neurofibromatosis- 1 (NF-1) an inherited "autosomal dominant" disorder is one of the most common genetic disorders, characterized by formation of neurofibromas (tumors involving nerve tissue) in the skin, subcutaneous tissue, cranial and spinal root nerves. NF1 generally is diagnosed by physical examination. There is no cure for NF1, but there are ways to treat some of its effects. Neurofibromatosis arterial hypertension caused by pheochromocytoma is extremely rare, less frecuent than 1% in childrens less than 10 years old, and young adults. We present a case of an extremely infrequent association between neurofibromatosis and a pheochromocytoma in a young woman with a newly diagnosed hypertension. We discuss the underlying pathophysiological mechanisms and clinical implications.

Internal mammary artery grafts reactivity in hypertensive patients: role of stretching in extraendothelial nitric oxide.

BACKGROUND: The internal mammary artery (IMA) used in bypass coronary surgery remains efficient for a longer time than other grafts, such as saphenous veins; however, its biological characteristics are incompletely defined. OBJECTIVE: To compare in IMA grafts from hypertensive (HT) and normotensive (NT) patients the presence of endothelium and their functionability, the response to passive stretching and basal tone, the reactivity to exogenous vasoconstrictors, the role of stretching in NO release, and the possible extraendothelial NO source. METHODS AND RESULTS: IMA rings contractility, presence of endothelium, and nitrite release were studied. An endothelial dysfunction associated with hypertension was found. IMA rings from HT had an impaired response to passive stretching, resulting in a decreased relaxation. All IMA grafts had an increased basal tone demonstrated by relaxation to SNP; however, a lesser response was found in HT. Interestingly, it was demonstrated that NO release was present in IMA grafts, despite an endothelial dysfunction and that stretching increased NO release. This effect was inhibited by Ca2+ -free media, L-NAME and a specific neuronal NO synthase (nNOS) inhibitor. Furthermore, the demonstration of the presence of nNOS in smooth muscle cells by immunohistochemistry supports a role of extraendothelial NO. CONCLUSION: We demonstrate the impact of hypertension in IMA grafts producing increased endothelial dysfunction, reduced response to passive stretching, increased basal tone, and impaired responsiveness to exogenous vasoconstrictors and NO release. A specific role of stretching in extraendothelial NO release was demonstrated, which may have an important role in the outcome of IMA grafts due to the protective actions of NO, even in the absence of the endothelium.

[Diagnosis, management and treatment of chronic Chagas' heart disease in areas where Trypanosoma cruzi infection is not endemic]. / Diagnóstico, manejo y tratamiento de la cardiopatía chagásica crónica en áreas donde la infección por Trypanosoma cruzi no es endémica.

Chagas' disease, or American trypanosomiasis, is a parasitic zoonosis found only in the Americas. Under natural conditions, Trypanosoma cruzi is transmitted by insects belonging to different species of Triatoma. However, several routes of transmission that do not involve insect vectors have also been described, such as transmission via blood products or transplantation of infected organs, and vertical transmission. At present, the number of people infected with Chagas' disease worldwide is estimated to be about 10-12 million. The process of urbanization in Latin America and migratory population movements from endemic countries have led to the disease being diagnosed in non-endemic areas. It is estimated that 20-30% of individuals infected with T. cruzi will develop symptomatic heart disease at some point during their lives. The specific differential characteristics of chronic chagasic cardiopathy, lack of knowledge of the disease among many healthcare workers, and the fact that arrhythmia or sudden death is frequently the first manifestation of disease all make it essential that diagnostic and therapeutic protocols for the disease are developed and disseminated. The aim should be to improve patient care by increasing understanding of the condition by physicians and other healthcare professionals who may be involved in its detection and treatment.

Diagnostic role of new Doppler index in assessment of renal artery stenosis.

BACKGROUND: Renal artery stenosis (RAS) is one of the main causes of secondary systemic arterial hypertension. Several non-invasive diagnostic methods for RAS have been used in hypertensive patients, such as color Doppler ultrasound (US). The aim of this study was to assess the sensitivity and specificity of a new renal Doppler US direct-method parameter: the renal-renal ratio (RRR), and compare with the sensitivity and specificity of direct-method conventional parameters: renal peak systolic velocity (RPSV) and renal aortic ratio (RAR), for the diagnosis of severe RAS. METHODS: Our study group included 34 patients with severe arterial hypertension (21 males and 13 females), mean age 54 (+/- 8.92) years old consecutively evaluated by renal color Doppler ultrasound (US) for significant RAS diagnosis. All of them underwent digital subtraction arteriography (DSA). RAS was significant if a diameter reduction > 50% was found. The parameters measured were: RPSV, RAR and RRR. The RRR was defined as the ratio between RPSV at the proximal or mid segment of the renal artery and RPSV measured at the distal segment of the renal artery. The sensitivity and specificity cutoff for the new RRR was calculated and compared with the sensitivity and specificity of RPSV and RAR. RESULTS: The accuracy of the direct method parameters for significant RAS were: RPSV >200 cm/s with 97% sensitivity, 72% specificity, 81% positive predictive value and 95% negative predictive value; RAR >3 with 77% sensitivity, 90% specificity, 90% positive predictive value and 76% negative predictive value. The optimal sensitivity and specificity cutoff for the new RRR was >2.7 with 97% sensitivity (p < 0.004) and 96% specificity (p < 0.02), with 97% positive predictive value and 97% negative predictive value. CONCLUSION: The new RRR has improved specificity compared with the direct method conventional parameters (RPSV >200cm/s and RAR >3). Both RRR and RPSV show better sensitivity than RAR for the RAS diagnosis.

[Prothrombotic state in early stages of chronic Chagas' disease. Its association with thrombotic risk factors]. / Estado protrombótico en estadios tempranos de la enfermedad de Chagas crónica. Su asociación con factores de riesgo trombótico.

OBJECTIVE: The aim of this study was to explore the presence of prothrombotic state in early stages of chronic Chagas' disease with serum markers of thrombosis and fibrinolysis, and to investigate it's association with thrombotic risk factors for venous thromboembolic disease. PATIENTS AND METHODS: Forty two patients with chronic Chagas' disease were compared with 21 healthy volunteers. Thrombotic markers used were fragment 1 + 2, ATM complex, fibrinogen/fibrin degradation products, D-dimer and beta-thromboglobulin. Fibrinolysis was evaluated with euglobulin lysis time, tissue plasminogen activator and it's inhibitor levels. A thrombophilic screening was performed. Antithrombin and protein C were determined by functional methods, as well as free fraction of protein S, resistance to activated protein C, factor V Leiden R506Q mutation, prothrombin G20210A mutation, homocysteine and antiphospholipid antibodies: lupus and anticardiolipin antibodies isoforms IgG and IgM. RESULTS: In chronic Chagas' disease patients, statistically significant differences were observed in thrombotic markers: fragment 1 + 2 (p < 0.0001), ATM complex (p < 0.0001), fibrinogen/fibrin degradation products (p < 0.05) and D-dimer (p < 0.05). beta-thromboglobulin did not reach statistically significant difference (p = 0.06). Statistically significant differences (p < 0.0001) were found only in euglobulin lysis time, a non specific fibrinolytic marker. Specific fibrinolytic markers tissue plasminogen activator and it's inhibitor, however, did not show statistically significant differences among studied groups. CONCLUSIONS: Eighty six percent of patients had positive thrombophilic screening for at least one thrombophilic risk factor. Thrombophilic risk factors were inherited in 39% and acquired in 83% of the patients.

Estado protrombótico en estadios tempranos de la enfermedad de Chagas crónica: Su asociación con factores de riesgo trombótico / Prothrombotic state in early stages of chronic Chagas' disease: Its association with thrombotic risk factors

Propósito del estudio: Investigar con marcadores de trombosis (trombóticos y fibrinolíticos), si existe estado protrombótico en estadios precoces de la enfermedad de Chagas crónica, y su asociación con factores de riesgo trombótico para enfermedad tromboembólica venosa. Métodos: Se compararon 42 chagásicos crónicos con 21 voluntarios sanos. Los marcadores de trombosis fueron: fragmento 1+2, complejo ATM, productos de degradación del fibrinógeno/fibrina, dímero D y β-tromboglobulina. Se evaluó la fibrinólisis con el tiempo de lisis de euglobulinas, y con determinaciones del activador tisular del plasminógeno y de su inhibidor. La trombofilia se evaluó con antitrombina, proteína C, fracción libre de la proteína S, resistencia a la proteína C activada, mutación R506Q del factor V Leiden, mutación de la protrombina G20210A, homocisteína y anticuerpos antifosfolipídicos: (lúpico y anticardiolipinas isoformas IgG e IgM) Resultados: En los marcadores de trombosis hubo diferencias estadísticamente significativas entre chagásicos crónicos y controles en las variables fragmento 1 + 2 (p < 0.0001), complejo ATM (p < 0.0001), productos de degradación del fibrinógeno/fibrina (p < 0.05) y dímero D (p < 0.05), pero no en la U-tromboglobulina (p = 0.06). En las variables fibrinolíticas, la diferencia fue estadísticamente significativa en el tiempo de lisis de euglobulinas (p < 0.0001), pero no en los valores del activador tisular del plasminógeno ni de su inhibidor. En la evaluación de trombofilia se obtuvieron resultados positivos para al menos 1 factor de riesgo trombofílico en 86% de los pacientes. Los anticuerpos anticardiolipinas estuvieron presentes en el 69% de los casos (p < 0.05). Los factores de riesgo trombofílicos fueron congénitos en el 39% de los casos y adquiridos en el 83%. Conclusiones: Aunque no hubo diferencias estadísticamente significativas en los marcadores de fibrinólisis, la diferencia estadísticamente significativa en los marcadores de trombosis constata la presencia de estado protrombótico en estadios precoces de la enfermedad de Chagas crónica, asociado de manera estadísticamente significativa con factores de riesgo trombofílico en el 86% de los casos (p < 0.0001), destacándose la frecuencia de anticuerpos antifosfolipídicos especialmente anticardiolipinas (69%) como factores de riesgo trombofílico adquirido.

Objective: The aim of this study was to explore the presence of prothrombotic state in early stages of chronic Chagas' disease with serum markers of thrombosis and fibrinolysis, and to investigate it's association with thrombotic risk factors for venous thromboembolic disease. Patients and methods: Forty two patients with chronic Chagas' disease were compared with 21 healthy volunteers. Thrombotic markers used were fragment 1 + 2, ATM complex, fibrinogen/fibrin degradation products, D-dimer and β-thromboglobulin. Fibrinolysis was evaluated with euglobulin lysis time, tissue plasminogen activator and it's inhibitor levels. A thrombophilic screening was performed. Antithrombin and protein C were determined by functional methods, as well as free fraction of protein S, resistance to activated protein C, factor V Leiden R506Q mutation, prothrombin G20210A mutation, homocysteine and antiphospholipid antibodies: lupus and anticardiolipin antibodies isoforms IgG and IgM. Results: In chronic Chagas' disease patients, statistically significant differences were observed in thrombotic markers: fragment 1 + 2 (p < 0.0001), ATM complex (p < 0.0001), fibrinogen/fibrin degradation products (p < 0.05) and D-dimer (p < 0.05). β-thromboglobulin did not reach statistically significant difference (p = 0.06). Statistically significant differences (p < 0.0001) were found only in euglobulin lysis time, a non specific fibrinolytic marker. Specific fibrinolytic markers tissue plasminogen activator and it's inhibitor, however, did not show statistically significant differences among studied groups. Conclusions: Eighty six percent of patients had positive thrombophilic screening for at least one thrombophilic risk factor. Thrombophilic risk factors were inherited in 39% and acquired in 83% of the patients.

[The prothrombotic state in early stages of chronic chagas' disease]. / Estado protrombótico en estadios tempranos de la enfermedad de Chagas crónica.

OBJECTIVE: This study was designed to explore the presence of a prothrombotic state in the early stages of chronic Chagas' disease by evaluating serum markers of thrombosis and fibrinolysis. PATIENTS AND METHOD: Forty-two patients with chronic Chagas' disease (12 men and 30 women, 32.5 6.7 years) were compared with 21 healthy volunteers (10 men and 11 women, 24.2 5.6 years). The markers of thrombotic activation used were fragment 1 + 2, ATM complex, PDF/pdf, D-dimer, and beta-thromboglobulin. Fibrinolysis was evaluated before and after venous occlusion, together with euglobulin lysis time, t-PA, and PAI-1 titers. RESULTS: The markers of thrombotic state were significantly higher in patients with chronic Chagas' disease than in controls: F1 + 2 (p < 0.0001), ATM (p < 0.0001), PDF/pdf (p < 0.05), and D dimer (p < 0.05). There was no significant difference in beta-thromboglobulin (p = 0.06). Euglobulin lysis time, a global fibrinolytic marker, differed significantly (p < 0.0001) between patients with Chagas' disease and healthy volunteers. However, the more specific fibrinolytic markers t-PA and PAI-1 did not differ significantly between the two study groups. CONCLUSIONS: Although there were no significant differences in fibrinolytic markers between patients with chronic Chagas' disease and healthy volunteers, the significant increase in thrombosis markers (F1 + 2, ATM complex, PDF/pdf, and D dimer) suggests the presence of a prothrombotic state in the early stages of chronic Chagas' disease.