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Aplasia medular: Actualización
Machín García,Sergio; Svarch,Eva; Dorticós Balea,Elvira;
Revista Cubana de Hematolog?-a, Inmunolog?-a y Hemoterapia , 1999,
Abstract: bone marrow aplasia according to its etiology may be congenital or acquired. the latter is the most frequent. haemopoietic failure seems to be caused by several factors. the causes of acquired medullary aplasia and its physiopathological mechanisms are reviewed. emphasis is made on th immune mechanisms, which play an important role in its physiopathology. the diagnostic criteria as well as the elements of an unfavorable diagnosis and the disease that must be taken into consideration to make the differential diagnosis are analyzed in this paper. the most effective treatments at present are the immunosuppressors and bone marrow transplantation. each has advantages and disadvantages and requires specific indications
Aplasia medular: Actualización Bone marrow aplasia: Update
Sergio Machín García,Eva Svarch,Elvira Dorticós Balea
Revista Cubana de Hematolog?-a, Inmunolog?-a y Hemoterapia , 1999,
Abstract: La aplasia medular, según su etiología puede ser congénita y adquirida; esta última es la más frecuente. La causa del fallo de la hematopoyesis parece ser multifactorial. Se revisan las causas de aplasia medular adquirida, sus mecanismos fisiopatológicos y se hace énfasis en los mecanismos inmunes, que desempe an un papel central en su fisiopatología. Se actualizan los criterios diagnósticos, los elementos de pronóstico desfavorable, así como las enfermedades con las que debe hacerse el diagnóstico diferencial. Las terapéuticas actuales más efectivas son los inmunosupresores y el trasplante de médula ósea, cada uno de ellos ofrece ventajas y desventajas y requiere de indicaciones precisas Bone marrow aplasia according to its etiology may be congenital or acquired. The latter is the most frequent. Haemopoietic failure seems to be caused by several factors. The causes of acquired medullary aplasia and its physiopathological mechanisms are reviewed. Emphasis is made on th immune mechanisms, which play an important role in its physiopathology. The diagnostic criteria as well as the elements of an unfavorable diagnosis and the disease that must be taken into consideration to make the differential diagnosis are analyzed in this paper. The most effective treatments at present are the immunosuppressors and bone marrow transplantation. Each has advantages and disadvantages and requires specific indications
Aplasia medular tratada exitosamente con ciclosporina en un paciente en hemodiálisis crónica
Vega S,Jorge; Rodríguez S,María de los Angeles; Vásquez G,Alejandro; Torres F,Carlos;
Revista médica de Chile , 2004, DOI: 10.4067/S0034-98872004000800012
Abstract: a 28 years old male on chronic hemodialysis for 40 months due to a iga crescentic glomerulonephritis developed pancytopenia (hematocrit 16%, white blood cell count 3.800 mm3 and platelets 11.000 mm3. the bone marrow aspirate showed erythropoietic hyperplasia. hemolytic anemia, folate or vitamin b12 deficiency and paroxysmal nocturnal hemoglobinuria were ruled out. steroids were given with a transient elevation of red cells and platelets, which lasted only for some weeks. afterwards, intravenous immunoglobulin was given without benefit. two months after, a bone marrow biopsy and a bone marrow magnetic resonance imaging showed severe aplasia. cyclosporine was started with a rapid increase in blood cells count. eight months later, he received a renal transplant from a cadaveric donor. immunosupression was achieved with cyclosporine, prednisone and mycofenolate mofetil. the patient required hemodialysis for the first three weeks and a mild acute cellular rejection was treated with methylprednisolone. at discharge, 6 weeks later, serum creatinine was 2.4 mg/dl and creatinine clearance 37.6 ml/min. during the first months after transplant, platelet count and hemoglobin decreased and a bone marrow biopsy showed only mild hypoplasia. four months after renal transplant the hematocrit was 43%, white blood cell count 6.600 mm3 and platelets, 150.000 mm3 and did not change during the first year of follow up (rev méd chile 2004; 132: 989-94
Aplasia medular tratada exitosamente con ciclosporina en un paciente en hemodiálisis crónica Bone marrow aplasia during hemodialysis successfully treated with cyclosporine. Report of one case  [cached]
Jorge Vega S,María de los Angeles Rodríguez S,Alejandro Vásquez G,Carlos Torres F
Revista médica de Chile , 2004,
Abstract: A 28 years old male on chronic hemodialysis for 40 months due to a IgA crescentic glomerulonephritis developed pancytopenia (hematocrit 16%, white blood cell count 3.800 mm3 and platelets 11.000 mm3. The bone marrow aspirate showed erythropoietic hyperplasia. Hemolytic anemia, folate or vitamin B12 deficiency and paroxysmal nocturnal hemoglobinuria were ruled out. Steroids were given with a transient elevation of red cells and platelets, which lasted only for some weeks. Afterwards, intravenous immunoglobulin was given without benefit. Two months after, a bone marrow biopsy and a bone marrow magnetic resonance imaging showed severe aplasia. Cyclosporine was started with a rapid increase in blood cells count. Eight months later, he received a renal transplant from a cadaveric donor. Immunosupression was achieved with cyclosporine, prednisone and mycofenolate mofetil. The patient required hemodialysis for the first three weeks and a mild acute cellular rejection was treated with methylprednisolone. At discharge, 6 weeks later, serum creatinine was 2.4 mg/dl and creatinine clearance 37.6 ml/min. During the first months after transplant, platelet count and hemoglobin decreased and a bone marrow biopsy showed only mild hypoplasia. Four months after renal transplant the hematocrit was 43%, white blood cell count 6.600 mm3 and platelets, 150.000 mm3 and did not change during the first year of follow up (Rev Méd Chile 2004; 132: 989-94
Megakaryocytic Aplasia
Dheeraj Gandotra, Charu Jandial*, Sudesh Kumar, Shazia Hamid, Kuldeep Koul**
JK Science : Journal of Medical Education & Research , 2007,
Abstract: Acquired Megakaryocytic aplasia is a rare disorder defined by severe thrambocytopenia with no otherhaematological and absent or severely marow megakaryocytes.
Efecto de la ticlopidina en los cambios morfológicos de cultivos endoteliales inducidos por la interacción endotoxina plaqueta
Martínez de Lima,Nina;
Revista de la Facultad de Medicina , 2007,
Abstract: induced by lipopolysaccharide is inhibited by ticlopidina. we investigated if ticlopidina could modify the effect of the lipopolysaccharide -platelets interaction, on endothelial cell morphology. the endothelial cells were isolated from rat embryos dermal microvasculature. the cultures were incubated with: lipopolysaccharide; lipopolysaccharide + platelet rich plasma; lipopolysaccharide + platelet rich plasma from rats treated with ticlopidina; lipopolysaccharide + ticlopidina solution; lipopolysaccharide + control platelet rich plasma + ticlopidina; ticlopidina solution. the results evidenced citoplasmatic alterations with lipopolysaccharide. this cellular damage was strengthen by platelet rich plasma; however, in the presence of platelet rich plasma from rats pretreated with ticlopidina, these changes did not become present. we concluded that ticlopidina suppresses some derived adverse effects of the lipopolysaccharide -platelet interaction on the endothelium, thus ticlopidina could have a therapeutic potential on septic shock
Bilateral maxillary sinus aplasia  [cached]
Seied Mehdi Sonbolestan,Seied Mohammad Javad Marashi,Hamed Abasi
Journal of Research in Medical Sciences , 2007,
Abstract: Bilateral maxillary sinus aplasia is an extremely rare congenital anomaly. Only a few cases have been reported in the literature. We present a 24- year-old woman with bilateral maxillary sinus aplasia associated with the bilateral absence of the uncinate process and infundibular passage on CT images. KEY WORDS: Maxillary sinus, aplasia, computed tomography.
Colitis pseudomembranosa asociada al uso de antibióticos
Alejandra Orellana,Salazar Esmeralda
Acta Odontológica Venezolana , 2009,
Abstract: La colitis asociada a antibióticos es una inflamación aguda de la mucosa intestinal que algunas veces ocurre a continuación del tratamiento con antibióticos y es causada por toxinas producidas por la bacteria Clostridium difficile. El diagnóstico está basado en el cuadro clínico y en cultivos y pruebas inmunológicas para detectar las toxinas. Cuando no hay respuesta al tratamiento conservador (retiro del antibiótico y terapia de apoyo), el Metronidazol o la Vancomicina deberían ser suministrados. Recurrencias hasta de un 20% son frecuentes. Medidas preventivas contra su extensión son esenciales, debido a la elevada transmisión a través del cuidado personal y de los instrumentos. Antibiotic-associated colitis is an acute inflammation of the intestinal mucosa that sometimes occurs following antibiotic treatment and is caused by toxins produced by the bacterium Clostridium difficile. Diagnosis is based on culture and immunological tests to detect its toxins. When there is no response to conservative treatment (withdrawal of the antibiotic and support therapy), metronidazole or vancomycin should be given. Recurrences, up to 20%, are frequent. Preventive measures of its spreading are essential due to the elevated transmission through health care personnel and instruments.
Efecto de la ticlopidina en los cambios morfológicos de cultivos endoteliales inducidos por la interacción endotoxina plaqueta
Nina Martínez de Lima
Revista de la Facultad de Medicina , 2007,
Abstract: La endotoxina (lipopolisacárido) induce estados trombogénicos en el shock séptico. La agregación plaquetaria inducida por lipopolisacárido es inhibida por ticlopidina. Investigamos si ticlopidina podía modificar el efecto de la interacción lipopolisacárido - plaqueta sobre la morfología de cultivos endoteliales. Las células fueron aisladas de la microvasculatura dérmica de embriones de rata. Los cultivos fueron incubados con: lipopolisacárido; lipopolisacárido + plasma rico en plaquetas; lipopolisacárido + plasma rico en plaquetas de ratas pretratadas con ticlopidina; lipopolisacárido + solución de ticlopidina; lipopolisacárido + plasma rico en plaquetas + solución de ticlopidina; solución de ticlopidina. Se evidenció da o celular con lipopolisacárido, que se acentuó en presencia de plasma rico en plaquetas, pero con plasma rico en plaquetas procedente de ratas pretratadas con ticlopidina, estas alteraciones no estuvieron presentes. En conclusión ticlopidina suprimió las alteraciones derivadas de la interacción lipopolisacárido - plaqueta sobre el endotelio por lo que podría tener un potencial terapéutico en el shock séptico induced by lipopolysaccharide is inhibited by ticlopidina. We investigated if ticlopidina could modify the effect of the lipopolysaccharide -platelets interaction, on endothelial cell morphology. The endothelial cells were isolated from rat embryos dermal microvasculature. The cultures were incubated with: lipopolysaccharide; lipopolysaccharide + platelet rich plasma; lipopolysaccharide + platelet rich plasma from rats treated with ticlopidina; lipopolysaccharide + ticlopidina solution; lipopolysaccharide + control platelet rich plasma + ticlopidina; ticlopidina solution. The results evidenced citoplasmatic alterations with lipopolysaccharide. This cellular damage was strengthen by platelet rich plasma; however, in the presence of platelet rich plasma from rats pretreated with ticlopidina, these changes did not become present. We concluded that ticlopidina suppresses some derived adverse effects of the lipopolysaccharide -platelet interaction on the endothelium, thus ticlopidina could have a therapeutic potential on septic shock
Aplasia irreversible por el tratamiento con mesilato de Imatinib en una leucemia mieloide crónica: Presentación de un caso
Agramonte Llanes,Olga; Pavón Morán,Valia; Hernández Padrón,Carlos; Losada Buchillón,Rafael; Mesa Cuervo,José; Ramón Rodríguez,Luis Gabriel; ávila Cabrera,Onel; Silva Aguiar,Roberto;
Revista Cubana de Hematolog?-a, Inmunolog?-a y Hemoterapia , 2007,
Abstract: a 45-year-old female patient who was diagnosed chronic myeloid leukemia ph+ in march 1984, and had treatment with busulfan, hydroxyurea, interferon and cytosine arabinoside during 15 years is presented. in march 2003, the transformation stage was diagnosed and, in april, she began to receive imatinib at daily doses of 600 mg. evolutively, she had mild bone pain, palpebral edema and, on the 35th day, severe pancytopenia that caused the suspension of the treatment. bone marrow samples were taken by aspiration and biopsy, and a severe medular aplasia was diagnosed. treatment with wide-spectrum antibiotic therapy, hemoderivates, and granulocyte colony-stimulating factor was applied. in spite of these therapeutic measures, the patient died 46 days after interrupting the treatment with imatinib, with a clinical picture of irreversible medular aplasia and respiratory distress, complications attributable to imatinib
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