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1.
Rev. esp. patol ; 52(2): 87-91, abr.-jun. 2019. ilus, graf
Artigo em Inglês | IBECS | ID: ibc-182694

RESUMO

We present a case of a nasal rhabdomyosarcoma (RMS) in a 27-year-old male with epistaxis and nasal obstruction due to a mass, which was subjected to prophylactic tumor embolization. However, histopathological study on the nasal biopsy was impossible due to necrotic changes. As blast cells were present in peripheral blood samples, a bone marrow biopsy was recommended in order to reach a definitive diagnosis. The possibility of an RMS in cases of bone marrow infiltration by a diffuse tumor constituted by small, round, blast-like cells mimicking acute leukemia should be assessed. Immunohistochemical staining in bone marrow biopsy and flow cytometry in aspirate samples may help to establish the diagnosis (CD45 negativity and CD56 positivity) and cytogenetic studies can be useful in identifying a RMS subtype. When clinically possible, it is desirable to await the results of the tumor immunophenotype and those of the primary mass or bone marrow biopsy to avoid possible errors of diagnosis and treatment


Se presenta el caso de un rabdomiosarcoma (RMS) en un varón de 27 años de edad con cuadro de epistaxis y obstrucción por masa nasal, que fue sometido a embolización tumoral profiláctica. El estudio en sangre periférica, fundamentalmente por la detección de células de apariencia blástica, recomendó biopsia de médula ósea que fue determinante para el diagnóstico, debido a que la embolización tumoral en la biopsia nasal, invalidó por cambios necróticos su estudio histopatológico. Se debe evaluar la posibilidad diagnóstica de un RMS, en casos de infiltración de médula ósea por un tumor difuso constituido por células pequeñas, redondas y similares a blastos que imitan una leucemia aguda. La tinción inmunohistoquímica en la biopsia de médula ósea y la citometría de flujo en muestras de aspirado, pueden ayudar a establecer el diagnóstico (negatividad CD45 y positividad CD56) y los estudios citogenéticos pueden ayudar a diferenciar el subtipo de RMS. Cuando sea clínicamente posible, se debe esperar a los resultados del inmunofenotipo celular del tumor y los de la masa primaria o la biopsia de la médula ósea, para así evitar posibles errores de diagnóstico y tratamiento


Assuntos
Humanos , Masculino , Adulto , Rabdomiossarcoma Embrionário/patologia , Neoplasias da Medula Óssea/patologia , Neoplasias da Medula Óssea/secundário , Metástase Neoplásica/patologia , Leucemia Mieloide Aguda/patologia , Diagnóstico Diferencial
2.
Rev Esp Patol ; 52(2): 87-91, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-30902383

RESUMO

We present a case of a nasal rhabdomyosarcoma (RMS) in a 27-year-old male with epistaxis and nasal obstruction due to a mass, which was subjected to prophylactic tumor embolization. However, histopathological study on the nasal biopsy was impossible due to necrotic changes. As blast cells were present in peripheral blood samples, a bone marrow biopsy was recommended in order to reach a definitive diagnosis. The possibility of an RMS in cases of bone marrow infiltration by a diffuse tumor constituted by small, round, blast-like cells mimicking acute leukemia should be assessed. Immunohistochemical staining in bone marrow biopsy and flow cytometry in aspirate samples may help to establish the diagnosis (CD45 negativity and CD56 positivity) and cytogenetic studies can be useful in identifying a RMS subtype. When clinically possible, it is desirable to await the results of the tumor immunophenotype and those of the primary mass or bone marrow biopsy to avoid possible errors of diagnosis and treatment.

3.
Rev. esp. patol ; 50(4): 268-272, oct.-dic. 2017. ilus
Artigo em Espanhol | IBECS | ID: ibc-166046

RESUMO

Se describe el caso de un varón de 38 años que consultó por distensión abdominal, saciedad precoz y pérdida de 7kg de peso de 2 meses de evolución. Presentaba una masa pétrea abdominal y una tumoración umbilical de 3cm que había aumentado de tamaño en las semanas previas. En la analítica destacaba elevación de lactato deshidrogenasa y beta-2 microglobulina, así como hipogammaglobulinemia. Se realizó una tomografía computarizada abdominal, en la cual se observó un gran tumor retroperitoneal que englobaba el riñón izquierdo y desplazaba la aorta, esplenomegalia, afectación peritoneal, adenopatías mesentéricas y un nódulo umbilical. El diagnóstico anatomopatológico fue de linfoma no Hodgkin de células grandes B inmunofenotipo centro germinal (según algoritmo de Hans). Las metástasis umbilicales, también denominadas «nódulo de la hermana María José», son infrecuentes, generalmente asociadas a neoplasias gastrointestinales y ginecológicas diseminadas. Solo se han descrito unos pocos casos en linfomas, asociados en general a mejor pronóstico (AU)


A 38-year-old patient presented with abdominal distention, anorexia and a weight loss of 7kg over the previous two months. Physical examination revealed a solid abdominal mass and a 3cm umbilical nodule. He had raised lactate dehydrogenase and beta-2 microglobulin levels, as well as hypogammaglobulinemia. An abdominal CT showed a solid retroperitoneal mass invading the left kidney and displacing the aorta, splenomegaly and an umbilical nodule. Histopathology revealed a diffuse large b cell lymphoma germinal center type. Umbilical metastases, also known as Sister Mary Joseph's nodule, are uncommon and usually associated with disseminated gastrointestinal and gynecological malignancies; indeed only a few cases of lymphomas with this presentation have been reported, most of which have a much better prognosis (AU)


Assuntos
Humanos , Masculino , Adulto , Linfoma Difuso de Grandes Células B/complicações , Linfoma Difuso de Grandes Células B/diagnóstico , Linfoma Difuso de Grandes Células B/patologia , Linfoma não Hodgkin/patologia , Linfoma não Hodgkin , Nódulo da Irmã Maria José/patologia , Neoplasias Abdominais/patologia , Patologia/métodos , Umbigo/patologia , Neoplasias Retroperitoneais/patologia , Metástase Neoplásica/patologia , Metástase Neoplásica , Tomografia por Emissão de Pósitrons/métodos , Diagnóstico Diferencial
4.
Rev. esp. enferm. dig ; 108(9): 588-591, sept. 2016.
Artigo em Espanhol | IBECS | ID: ibc-156136

RESUMO

En la cirrosis hepática es frecuente que se produzca activación de la trombina y microtrombosis en las raicillas de la vena porta intrahepática, en parte debido al déficit de proteína C, y en parte a alteración del equilibrio coagulación-anticoagulación-fibrinólisis. Por eso hay una incidencia aumentada de trombosis portal. La trombina no solo puede generar la formación de un trombo, sino que puede activar a las células estrelladas y estimular la fibrogénesis. Además, la isquemia asociada a la trombosis puede promover la síntesis de factores de crecimiento involucrados en la fibrogénesis. La coincidencia en un mismo paciente de mutaciones protrombóticas, como factor V Leiden o polimorfismos del PAI- 1, puede acelerar todo este proceso. Presentamos dos casos de cirrosis criptogenética en los que los únicos factores identificables capaces de causar fibrogénesis acelerada fueron mutaciones del factor V y del PAI-1. Estas observaciones, además de apoyar la hipótesis de que las citadas mutaciones puedan por sí mismas llegar a provocar cirrosis, sugieren que es recomendable determinar si existen polimorfismos del factor V, PAI-1 y protrombina en el estudio de la cirrosis criptogenética (AU)


Thrombin activation and microthrombosis of intrahepatic portal venules is a common feature in liver cirrhosis, due in part to relative protein C deficiency and altered coagulation-anticoagulation-fibrinolysis balance. Extension of this microthrombotic process to larger portal vessels explains the increased incidence of portal vein thrombosis in liver cirrhosis. Thrombin not only leads to thrombosis, but also activates liver stellate cells and promotes fibrogenesis. Also, ischemia associated with thrombosis up-regulates the expression and secretion of growth factors involved in fibrogenesis. The coincidence in a given patient of prothrombotic mutations, such as factor V Leiden or PAI-1 polymorphisms, can accelerate the fibrogenetic process. We hereby present two cases of liver cirrhosis in which etiologic evaluation was negative except for the finding of a factor V Leiden mutation in one case and the 4G/5G PAI polymorphism in the second case. These observations support the hypothesis that these mutations may be involved in the etiology of some cases of cirrhosis, or, at least, accelerate the evolution of the disease. It is therefore convenient to search for the presence of prothrombotic mutations in patients with cryptogenetic cirrhosis(AU)


Assuntos
Humanos , Feminino , Pessoa de Meia-Idade , Idoso , Cirrose Hepática/complicações , Fator V/genética , Veia Porta , Trombose Venosa/genética , Fatores de Risco , Predisposição Genética para Doença , Proteína C-Reativa/análise
5.
Rev Esp Enferm Dig ; 108(9): 588-91, 2016 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-26785615

RESUMO

Thrombin activation and microthrombosis of intrahepatic portal venules is a common feature in liver cirrhosis, due in part to relative protein C deficiency and altered coagulation-anticoagulation-fibrinolysis balance. Extension of this microthrombotic process to larger portal vessels explains the increased incidence of portal vein thrombosis in liver cirrhosis. Thrombin not only leads to thrombosis, but also activates liver stellate cells and promotes fibrogenesis. Also, ischemia associated with thrombosis up-regulates the expression and secretion of growth factors involved in fibrogenesis. The coincidence in a given patient of prothrombotic mutations, such as factor V Leiden or PAI-1 polymorphisms, can accelerate the fibrogenetic process. We hereby present two cases of liver cirrhosis in which etiologic evaluation was negative except for the finding of a factor V Leiden mutation in one case and the 4G/5G PAI polymorphism in the second case. These observations support the hypothesis that these mutations may be involved in the etiology of some cases of cirrhosis, or, at least, accelerate the evolution of the disease. It is therefore convenient to search for the presence of prothrombotic mutations in patients with cryptogenetic cirrhosis.


Assuntos
Cirrose Hepática/genética , Mutação/genética , Protrombina/genética , Idoso , Fator V/genética , Evolução Fatal , Feminino , Humanos , Cirrose Hepática/complicações , Pessoa de Meia-Idade
6.
Crit Care Med ; 43(12): e551-9, 2015 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-26308427

RESUMO

OBJECTIVES: Pulmonary endothelial cell injury is central to the pathophysiology of acute lung injury. Mechanical ventilation can cause endothelial disruption and injury, even in the absence of preexisting inflammation. Platelet-endothelial cell adhesion molecule-1 is a transmembrane protein connecting adjacent endothelial cells. We hypothesized that injurious mechanical ventilation will increase circulating lung endothelial-derived microparticles, defined as microparticles positive for platelet-endothelial cell adhesion molecule-1, which could serve as potential biomarkers and mediators of ventilator-induced lung injury. DESIGN: Prospective randomized, controlled, animal investigation. SETTING: A hospital preclinical animal laboratory. SUBJECTS: Forty-eight Sprague-Dawley rats. INTERVENTIONS: Animals were randomly allocated to one of the three following ventilatory protocols for 4 hours: spontaneous breathing (control group), mechanical ventilation with low tidal volume (6 mL/kg), and mechanical ventilation with high tidal volume (20 mL/kg). In both mechanical ventilation groups, positive end-expiratory pressure of 2 cm H2O was applied. MEASUREMENTS AND MAIN RESULTS: We analyzed histologic lung damage, gas exchange, wet-to-dry lung weight ratio, serum cytokines levels, circulating endothelial-derived microparticles, platelet-endothelial cell adhesion molecule-1 lung protein content, and immunohistochemistry. When compared with low-tidal volume mechanical ventilation, high-tidal volume ventilation increased lung edema score and caused gas-exchange deterioration. These changes were associated with a marked increased of circulating endothelial-derived microparticles and a reduction of platelet-endothelial cell adhesion molecule-1 protein levels in the high-tidal volume lungs (p < 0.0001). CONCLUSIONS: There is an endothelial-derived microparticle profile associated with disease-specific features of ventilator-induced lung injury. This profile could serve both as a biomarker of acute lung injury and, potentially, as a mediator of systemic propagation of pulmonary inflammatory response.


Assuntos
Moléculas de Adesão Celular/metabolismo , Micropartículas Derivadas de Células/metabolismo , Células Endoteliais/metabolismo , Lesão Pulmonar Induzida por Ventilação Mecânica/fisiopatologia , Animais , Citocinas/metabolismo , Imuno-Histoquímica , Pulmão/patologia , Masculino , Estudos Prospectivos , Troca Gasosa Pulmonar , Distribuição Aleatória , Ratos , Ratos Sprague-Dawley , Volume de Ventilação Pulmonar
7.
Crit Care ; 19: 138, 2015 Apr 03.
Artigo em Inglês | MEDLINE | ID: mdl-25871971

RESUMO

INTRODUCTION: Most patients with sepsis and acute lung injury require mechanical ventilation to improve oxygenation and facilitate organ repair. Mast cells are important in response to infection and resolution of tissue injury. Since tryptase secreted from mast cells has been associated with tissue fibrosis, we hypothesized that tryptase would be involved in the early development of ventilator-induced pulmonary fibrosis in a clinically relevant model of sepsis-induced lung injury. METHODS: Prospective, randomized, controlled animal study using Sprague-Dawley rats. Sepsis was induced by cecal ligation and perforation. Animals were randomized to spontaneous breathing or two ventilatory strategies for 4 h: protective ventilation with tidal volume (VT) = 6 ml/kg plus 10 cmH2O positive end-expiratory pressure (PEEP) or injurious ventilation with VT = 20 ml/kg plus 2 cmH2O PEEP. Healthy, non-ventilated animals served as non-septic controls. We studied the following end points: histology, serum cytokine levels, hydroxyproline content, tryptase and proteinase-activated receptor-2 (PAR-2) protein level in lung homogenates, and tryptase and PAR-2 immunohistochemical localization in the lungs. RESULTS: All septic animals developed acute lung injury. Animals ventilated with high VT had a significant increase of pulmonary fibrosis, hydroxyproline content, tryptase and PAR-2 protein levels compared to septic controls (P <0.0001). However, protective ventilation attenuated sepsis-induced lung injury and decreased lung tryptase and PAR-2 protein levels. Immunohistochemical staining confirmed the presence of tryptase and PAR-2 in the lungs. CONCLUSIONS: Mechanical ventilation modified tryptase and PAR-2 in injured lungs. Increased levels of these proteins were associated with development of sepsis and ventilator-induced pulmonary fibrosis early in the course of sepsis-induced lung injury.


Assuntos
Pulmão/metabolismo , Respiração com Pressão Positiva/efeitos adversos , Receptor PAR-2/metabolismo , Sepse/complicações , Triptases/metabolismo , Lesão Pulmonar Induzida por Ventilação Mecânica/metabolismo , Animais , Ceco/cirurgia , Citocinas/sangue , Modelos Animais de Doenças , Masculino , Estudos Prospectivos , Fibrose Pulmonar/etiologia , Distribuição Aleatória , Ratos , Ratos Sprague-Dawley , Sepse/metabolismo , Volume de Ventilação Pulmonar/fisiologia , Lesão Pulmonar Induzida por Ventilação Mecânica/patologia
8.
Crit Care ; 18(5): 568, 2014 Oct 21.
Artigo em Inglês | MEDLINE | ID: mdl-25331176

RESUMO

INTRODUCTION: The mechanisms of lung repair and fibrosis in the acute respiratory distress syndrome (ARDS) are poorly known. Since the role of WNT/ß-catenin signaling appears to be central to lung healing and fibrosis, we hypothesized that this pathway is activated very early in the lungs after sepsis. METHODS: We tested our hypothesis using a three-step experimental design: (1) in vitro lung cell injury model with human bronchial epithelial BEAS-2B and lung fibroblasts (MRC-5) cells exposed to endotoxin for 18 hours; (2) an animal model of sepsis-induced ARDS induced by cecal ligation and perforation, and (3) lung biopsies from patients who died within the first 24 hours of septic ARDS. We examined changes in protein levels of target genes involved in the Wnt pathway, including WNT5A, non-phospho (Ser33/37/Thr41) ß-catenin, matrix metalloproteinase-7 (MMP7), cyclin D1, and vascular endothelial growth factor (VEGF) by Western blotting and immunohistochemistry. Finally, we validated the main gene targets of this pathway in experimental animals and human lungs. RESULTS: Protein levels of WNT5A, non-phospho (Ser33/37/Thr41) ß-catenin, total ß-catenin, MMP7, cyclin D1, and VEGF increased after endotoxin stimulation in BEAS-2B and MRC-5 cells. Lungs from septic animals and from septic humans demonstrated acute lung inflammation, collagen deposition, and marked increase of WNT5A and MMP7 protein levels. CONCLUSIONS: Our findings suggest that the WNT/ß-catenin signaling pathway is activated very early in sepsis-induced ARDS and could play an important role in lung repair and fibrosis. Modulation of this pathway might represent a potential target for treatment for septic and ARDS patients.


Assuntos
Lesão Pulmonar Aguda/metabolismo , Mucosa Respiratória/metabolismo , Sepse/metabolismo , Proteínas Wnt/metabolismo , Lesão Pulmonar Aguda/etiologia , Lesão Pulmonar Aguda/patologia , Animais , Células Cultivadas , Fibrose/metabolismo , Fibrose/patologia , Humanos , Masculino , Ratos , Ratos Sprague-Dawley , Mucosa Respiratória/patologia , Sepse/complicações , Sepse/patologia , Proteína Wnt-5a
9.
Front Neuroanat ; 8: 84, 2014.
Artigo em Inglês | MEDLINE | ID: mdl-25206324

RESUMO

Nowadays it is assumed that besides its roles in neuronal processing, dopamine (DA) is also involved in the regulation of cerebral blood flow. However, studies on the hemodynamic actions of DA have been mainly focused on the cerebral cortex, but the possibility that vessels in deeper brain structures receive dopaminergic axons and the origin of these axons have not been investigated. Bearing in mind the evidence of changes in the blood flow of basal ganglia in Parkinson's disease (PD), and the pivotal role of the dopaminergic mesostriatal pathway in the pathophysiology of this disease, here we studied whether striatal vessels receive inputs from midbrain dopaminergic neurons. The injection of an anterograde neuronal tracer in combination with immunohistochemistry for dopaminergic, vascular and astroglial markers, and dopaminergic lesions, revealed that midbrain dopaminergic axons are in close apposition to striatal vessels and perivascular astrocytes. These axons form dense perivascular plexuses restricted to striatal regions in rats and monkeys. Interestingly, they are intensely immunoreactive for tyrosine hydroxylase (TH) phosphorylated at Ser19 and Ser40 residues. The presence of phosphorylated TH in vessel terminals indicates they are probably the main source of basal TH activity in the striatum, and that after activation of midbrain dopaminergic neurons, DA release onto vessels precedes that onto neurons. Furthermore, the relative weight of this "vascular component" within the mesostriatal pathway suggests that it plays a relevant role in the pathophysiology of PD.

10.
Rev. esp. patol ; 45(4): 218-223, oct.-dic. 2012. tab, ilus
Artigo em Espanhol | IBECS | ID: ibc-107860

RESUMO

Hemos realizado una evaluación semicuantitativa de la cantidad de pigmento hemosiderínico, en biopsias de médula ósea mediante tinción de Perls, en un total de 75 pacientes a los que se realizó esta prueba por diferentes motivos. Coincidentes en el tiempo, se han determinado a estos mismos pacientes los valores séricos de ferritina e índice de saturación de la transferrina. En el análisis de los resultados hemos observado que existe correlación estadísticamente significativa entre la intensidad de los depósitos medulares de pigmento hemosiderínico y los niveles de ferritina e índice de saturación de la transferrina. Esta observación es sugestiva de que, a pesar de las limitaciones de la tinción de Perls como técnica de rutina en biopsias de médula ósea, cuando los depósitos de pigmento hemosiderínico son detectables e intensos, el procedimiento, al menos en ciertos casos, nos da una idea de la sobrecarga férrica de los pacientes. De este modo, en algunas situaciones la detección de dicho pigmento en las biopsias de médula ósea podría complementar otros exámenes hematológicos(AU)


A semiquantitative assessment of the amount of haemosiderin pigment in bone marrow biopsies was made using Perls’ staining in a total of 75 patients with different diagnoses. Simultaneously, the serum ferritin and transferrin saturation index were measured. It was found that there is a statistically significant correlation between the intensity of the deposits of haemosiderin pigment and the serum parameters analyzed. Thus, despite the limitations of Perls’ staining as a technique for routine bone marrow biopsies, it can provide an indication of iron overload when the deposits are detectable and intense. Therefore, the detection of pigment in bone marrow biopsies could complement other haematological tests in some cases(AU)


Assuntos
Humanos , Masculino , Feminino , Hemossiderina , Medula Óssea/patologia , Medula Óssea/cirurgia , Biópsia/instrumentação , Biópsia/métodos , Biópsia , Ferritinas , Biomarcadores/sangue
11.
Dermatol Reports ; 3(3): e51, 2011 Oct 05.
Artigo em Inglês | MEDLINE | ID: mdl-25386303

RESUMO

Mantle cell lymphoma is a type of non-Hodgkin lymphoma that affects extranodal areas, especially, bone narrow, digestive tract and Waldeyer ring. Here we report a case of mantle cell lymphoma IV Ann Arbor stage with cutaneous lesions on nasal dorsum and glans penis as the first manifestations. Skin involvement is a very rare manifestation and less than 20 cases have been reported in the literature. The importance of establishing multidisciplinary relationships for a global approach has been shown by this clinical case.

12.
Prog. obstet. ginecol. (Ed. impr.) ; 53(6): 240-243, jun. 2010. tab, ilus
Artigo em Espanhol | IBECS | ID: ibc-79622

RESUMO

La enfermedad de Bowen vulvar o neoplasia vulvar intraepitelial (VIN) es una lesión preinvasora en los genitales externos. La VIN de etiología viral está relacionada con la infección por virus del papiloma humano (VPH) (principalmente los serotipos 16 y 18), sobre todo a edades tempranas y en relación con cambios en la conducta sexual. Presentamos el caso clínico que corresponde a una paciente joven, portadora del VPH 16 y en control por neoplasia intraepitelial de cuello uterino tipo III (CIN III) tras una conización, que desarrolló una VIN extensa. Se realizó tratamiento quirúrgico (ninfectomía) sin recidiva a los 3 años y con buen resultado estético (AU)


Bowen’s disease of the vulva, also called vulvar intraepithelial neoplasia (VIN), is considered a premalignant lesion of the external genitalia. VIN of viral etiology is most often associated with human papillomavirus (HPV) subtypes 16 and 18 and typically occurs in younger premenopausal women. The main risk factor for HPV acquisition is sexual activity. We report the case of a young patient, a carrier of HPV subtype 16, with cervical intraepithelial neoplasia grade 3, who developed severe VIN. Wide local excision of the labia minora was performed. The cosmetic results were satisfactory and the patient has had no relapses after 3 years of follow-up (AU)


Assuntos
Humanos , Feminino , Adulto , Doença de Bowen/complicações , Doença de Bowen/diagnóstico , Doença de Bowen/terapia , Neoplasias Vulvares/complicações , Neoplasias Vulvares/diagnóstico , Imuno-Histoquímica , Doença de Bowen/etiologia , Doença de Bowen/fisiopatologia , Infecções por Papillomavirus/complicações , Infecções por Papillomavirus/patologia , Neoplasia Intraepitelial Cervical/complicações , Neoplasia Intraepitelial Cervical/patologia , Diagnóstico Diferencial
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