ABSTRACT
El osteocondroma representa la lesión tumoral más frecuente del hueso. La característica radiológica patognomónica de este tumor es la continuidad cortical y medular de las lesiones con el hueso del que surgen. Las lesiones pueden ser solitarias o múltiples, formando esta última parte del síndrome de exostosis hereditaria múltiple. Estas lesiones también se pueden presentar con complicaciones como deformidades óseas, fracturas, compromiso neurológico o vascular, formación de bursa y más raramente transformación maligna. El diagnóstico requiere de un trípode clave: clínica, estudio histopatológico/biopsia y estudios de imagen que son necesarios para el tratamiento y planificación de exéresis quirúrgica y anestésica como es el caso que se relata a continuación.
Osteochondroma represents the most frequent tumoral lesion of the bone. The pathognomonic radiological characteristic of this tumor is the cortical and medullary continuity of the lesions with the bone from which they arise. The lesions can be solitary or multiple, forming this last part of the syndrome of multiple hereditary exostosis. These lesions can also present with complications such as bone deformities, fractures, neurological or vascular compromise, bursa formation and, more rarely, malignant transformation. The diagnosis requires a key tripod: clinical, histopathological study / biopsy and imaging studies that are necessary for the treatment and planning of surgical and anesthetic excesses, as is the case reported below.
Subject(s)
Humans , Male , Adolescent , Orthopedics , Osteochondroma , NeoplasmsABSTRACT
Las fracturas de la cabeza radial son infrecuentes y hay que hacer el diagnóstico diferencial con triada terrible de codo. El resultado de estas fracturas depende en gran medida de la gravedad de la lesión. Por lo general, resultan de una caída en el brazo extendido con el codo en pronación y flexión parcial. Por lo tanto, el diagnóstico en este tipo de lesiones óseas se basa en el mecanismo del trauma, la clínica y el estudio radiográfico y tomográfico en 3D. El tratamiento adecuado es esencial para recuperar la estabilidad y las actividades funcionales del codo y minimizar las secuelas. Debido a la importancia de este tema presentamos un caso quirúrgico de una fractura de cabeza radial Mason IV, manejada con artroplastia de cúpula radial que destaca el abordaje y procedimiento quirúrgico.
Fractures of the radial head are infrequent and the differential diagnosis must be made with a terrible elbow triad. The outcome of these fractures depends to a large extent on the severity of the injury. They usually result from a fall in the arm extended with the elbow in pronation and partial flexion. Therefore, the diagnosis in this type of bone lesions is based on the mechanism of the trauma, the clinic and the radiographic and tomographic study in 3D. Adequate treatment is essential to recover the stability and functional activities of the elbow and minimize the sequelae. Due to the importance of this topic we present a surgical case of a radial head fracture Mason IV, managed with radial dome arthroplasty that highlights the surgical approach and procedure.
Subject(s)
Humans , Female , Adolescent , Arthroplasty , Tomography , ElbowABSTRACT
In response to microenvironmental cues, macrophages undergo a profound phenotypic transformation acquiring distinct activation phenotypes ranging from pro-inflammatory (M1) to anti-inflammatory (M2). To study how activation phenotype influences phagocytosis and production of reactive oxygen species (ROS) mediated by receptors for IgG antibodies (Fcγ receptors) and by CD13, human monocyte-derived macrophages were polarized to distinct phenotypes using IFN-γ (MÏ-IFN-γ), IL-4 (MÏ-IL-4), or IL-10 (MÏ-IL-10). Phenotypically, MÏ-IFN-γ were characterized as CD14+CD80+CD86+ cells, MÏ-IL-4 as CD209highCD206+CD11b+CD14low, and MÏ-IL-10 as CD16+CD163+ cells. Compared to non-polarized macrophages, FcγRI expression increased in MÏ-IFN-γ and MÏ-IL-10 and FcγRIII expression increased in MÏ-IL-10. None of the polarizing cytokines modified FcγRII or CD13 expression. Functionally, we found that cytokine-mediated activation significantly and distinctively affected FcγR- and CD13-mediated phagocytosis and ROS generation. Compared to non-polarized macrophages, FcγRI-, FcγRII-, and CD13-mediated phagocytosis was significantly increased in MÏ-IL-10 and decreased in MÏ-IFN-γ, although both cytokines significantly upregulated FcγRI expression. IL-10 also increased phagocytosis of Escherichia coli, showing that the effect of IL-10 on macrophage phagocytosis is not specific for a particular receptor. Interestingly, MÏ-IL-4, which showed poor FcγR- and CD13-mediated phagocytosis, showed very high phagocytosis of E. coli and zymosan. Coupled with phagocytosis, macrophages produce ROS that contribute to microbial killing. As expected, MÏ-IFN-γ showed significant production of ROS after FcγRI-, FcγRII-, or CD13-mediated phagocytosis. Unexpectedly, we found that MÏ-IL-10 can also produce ROS after simultaneous stimulation through several phagocytic receptors, as coaggregation of FcγRI/FcγRII/CD13 induced a belated but significant ROS production. Together, these results demonstrate that activation of macrophages by each cytokine distinctly modulates expression of phagocytic receptors, FcγR- and CD13-mediated phagocytosis, and ROS production.
ABSTRACT
The exposure to certain species of Nontuberculous Mycobacteria (NTM) can modulate the immune response induced by Mycobacterium bovis BCG. Mycobacterium avium has been postulated as a weak inducer of dendritic cell (DC) maturation. However, how the DC exposure to M. avium could contribute to the modulation of a BCG-specific CD4+ T cell response and the molecules involved remain unknown. Here, we exposed bone marrow-derived DCs (BMDCs) to M. avium either prior to exposure to BCG or as a unique stimulus. We found that M. avium induces high expression of PD-L2 (B7-DC) in BMDCs. This was dependent on IL-10 production through the TLR2-p38 MAPK signaling pathway. Exposure to M. avium prior to BCG results in BMDCs that do not express co-stimulatory molecules and pro-inflammatory cytokines, while the expression of PD-L2 and IL-10 was maintained. BMDCs exposed to M. avium impaired the activation of BCG-specific T cells through the PD-1: PD-L interaction. This suggests that a M. avium-induced phenotype in DCs might be implicated in the induction of mechanisms of tolerance that could impact the T cell response induced by BCG vaccination.
Subject(s)
BCG Vaccine/immunology , CD4-Positive T-Lymphocytes/immunology , Dendritic Cells/immunology , Lymph Nodes/immunology , Mycobacterium avium/immunology , Programmed Cell Death 1 Ligand 2 Protein/immunology , Tuberculosis, Pulmonary/prevention & control , Animals , Down-Regulation , Interleukin-10/immunology , Lymphocyte Activation , Male , Mice , Mice, Inbred BALB C , Programmed Cell Death 1 Ligand 2 Protein/genetics , Tuberculosis, Pulmonary/genetics , Tuberculosis, Pulmonary/immunologyABSTRACT
Lymphocytic infiltrates and lymphoid follicles with germinal centers are often detected in autoimmune thyroid disease (AITD), but the mechanisms underlying lymphocyte entry and organization in the thyroid remain unknown. We tested the hypothesis that CCL21, a chemokine that regulates homeostatic lymphocyte trafficking, and whose expression has been detected in AITD, is involved in the migration of lymphocytes to the thyroid. We show that transgenic mice expressing CCL21 from the thyroglobulin promoter (TGCCL21 mice) have significant lymphocytic infiltrates, which are topologically segregated into B and T cell areas. Although high endothelial venules expressing peripheral lymph node addressin were frequently observed in the thyroid tissue, lymphocyte recruitment was independent of L-selectin or lymphotoxin-alpha but required CCR7 expression. Taken together, these results indicate that CCL21 is sufficient to drive lymphocyte recruitment to the thyroid, suggest that CCL21 is involved in AITD pathogenesis, and establish TGCCL21 transgenic mice as a novel model to study the formation and function of lymphoid follicles in the thyroid.
Subject(s)
Chemokines, CC/physiology , Lymphocytes/pathology , Thyroid Gland/pathology , Adoptive Transfer , Animals , Cell Movement , Chemokine CCL21 , Female , L-Selectin/analysis , Lymphotoxin-alpha/physiology , Mice , Mice, Inbred C57BL , Mice, Inbred DBA , Mice, Transgenic , Rats , Receptors, CCR7 , Receptors, Chemokine/physiology , Thyroid Diseases/etiologyABSTRACT
Invasive aspergillosis is a common and devastating pneumonia in immunocompromised hosts. Neutrophils are critical for defense against this infection, and ELR+ CXC chemokines are potent neutrophil chemoattractants. We hypothesized that transient lung-specific overexpression of one such ligand, KC, in mice with invasive aspergillosis improves the outcome of disease. We generated mice in which transgenic expression of KC was limited to the lungs and occurred only upon exposure to tetracycline analogues, and we exposed them to doxycycline after the onset of invasive aspergillosis. Transgenic mice had a threefold greater survival, a 74% lower lung fungal burden, a greater magnitude of lung KC induction, and an earlier and higher peak of lung neutrophil influx compared with wild-type mice. In addition to a higher number of neutrophils, we found a 1.8-fold higher number of monocytes-macrophages in the lungs of transgenic mice as compared with wild-type mice. Furthermore, transgenic mice had greater lung expression of interferon-gamma and interleukin-12 in response to infection, suggesting that transgenic expression of KC indirectly regulated the expression of other cytokines associated with improved host defense against this pathogen. Taken together, these data suggest that overexpression of KC in the lung in the setting of established invasive aspergillosis results in improved host defense and outcome of disease.
Subject(s)
Aspergillosis/genetics , Chemokines, CXC , Chemokines/analysis , Chemokines/genetics , Chemotactic Factors/analysis , Chemotactic Factors/genetics , Gene Expression/genetics , Growth Inhibitors/analysis , Growth Inhibitors/genetics , Intercellular Signaling Peptides and Proteins/analysis , Intercellular Signaling Peptides and Proteins/genetics , Outcome Assessment, Health Care , Animals , Aspergillosis/immunology , Aspergillosis/mortality , Aspergillus fumigatus/genetics , Aspergillus fumigatus/immunology , Aspergillus fumigatus/pathogenicity , Chemokine CXCL1 , Chemokines/immunology , Chemotactic Factors/immunology , Disease Models, Animal , Gene Expression/immunology , Growth Inhibitors/immunology , Intercellular Signaling Peptides and Proteins/immunology , Mice , Mice, Transgenic , Severity of Illness IndexABSTRACT
Con el objeto de establecer la historia natural de la Cirrosis Hepática, se determinó las características de las variables relacionadas a la edad, sexo, etiología, morfología, cuadro clínico, complicaciones y enfermedades concomitantes. Este es un estudio de tipo retrospectivo, descriptivo y analítico para lo cual se seleccionaron 134 historias clínicas desde enero 1990 hasta diciembre de 1998, con el morfológico; y en la presentación de sus complicaciones que se constituyeron en la manifestación más importante para llegar al diagnóstico. En el análisis de información se utilizó cuadros de distribución de frecuencia de una y doble entrada con valores absolutos y relativos. Predominó el sexo masculino en un 53.7 por ciento; siendo el promedio de edad de 61.5 años. El alcoholismo en un 65 por ciento fue la causa más frecuente. El síntoma y signo predominante fue el edema de miembros inferiores y ascitis. La ascitis y las infecciones fueron las complicaciones mas frecuentes en nuestro estudio constituyendo un 69 por ciento y 64 por ciento respectivamente;. Las enfermedades con mayor frecuencia encontradas fueron colicistitis litiásica con 16 por ciento e infección de vías urinarias con un 15 por ciento. Se concluye que la cirrosis hepática en nuestro hospital constituye una enfermedad en su forma avanzada, con etiología principalmente alcohólica, predominantemente en pacientes de sexo masculino con un promedio de edad de 61.5 años para ambos sexos y cuyas complicaciones más frecuentes fueron: ascitis, infecciones, hipertensión portal, encefalopatía hepática, hemorragia digestiva.
Subject(s)
Male , Female , Adult , Liver Cirrhosis , Epidemiology, Descriptive , Retrospective StudiesABSTRACT
Se estudiaron retrospectivamente 2268 pacientes con diagnóstico clínico de Cólera admitidos al Departamento de Medicina del Hospital Eleazar Guzmán Barrón de Chimbote, entre los meses de enero a mayo de 1991. El objetivo principal fue determinar los factores predisponentes, causas de Insuficiencia Renal Aguda (IRA) secundario al Cólera y a la letalidad. Se revisaron las historias clínicas, el libro de registro de Emergencia, los informes estadísticos de ingresos y egresos y se hizo una ficha de evaluación para cada paciente portador del Cólera. Se hospitalizaron 713 (31 por ciento) pacientes, de procedencia urbano marginal 53 por ciento (378) y de zonas rurales el 33 por ciento; 182 (26 por ciento) pacientes ingresaron en estado de choque, 102 (43.4 por ciento) procedían de zonas rurales. Hicieron IRA 206 (28.9 por ciento) pacientes, teniendo como factor predisponente la edad avanzada en el 78.5 por ciento (84) de los pacientes; menor porcentaje representaron lo diabéticos, hipertensos, gestantes y los tuberculosos. Los mayores de 60 años fueron los de mayor riesgo con 71 por ciento (84) de letalidad; la hipovolemia con choque fue causa de IRA en 91.2 por ciento (188) de los pacientes. En 97 por ciento (200) de pacientes con IRA el tratamiento fue conservador y solo 3 por ciento (6) recibió apoyo dialítico en el IPSS. De los casos de IRA fallecieron 24 (11.6 por ciento) y 1 por ciento de la muestra total. Los incrementos de úrea y creatinina en sangre se asociaron a la mortalidad, siendo uremia la principal causa de muerte en el 50 por ciento de los pacientes con compromiso renal.
