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RESUMENLos queratinocitos multinucleados son un hallazgo histopatológico específico en el diagnóstico de algunas enfermedades infecciosas virales de la piel. Desde hace más de 30 años otro tipo de queratinocitos multinucleados se han identificado en afecciones diversas no relacionadas a procesos infecciosos cutáneos tales como el eczema, la atipia multinuclear vulvar, la dermatitis facticia, la psoriasis y enfermedades del tejido conectivo; sin embargo, muy pocos casos clínicos han sido publicados hasta el momento y su fisiopatología no es del todo conocida. Se presenta un caso clínico con hallazgo de queratinocitos multinucleados en un paciente masculino de mediana edad, con diagnóstico final de eczema crónico. ABSTRACTMultinucleated keratinocytes are a specific histopathological finding in the diagnosis of some viral infectious skin diseases. For more than 30 years, other types of multinucleated keratinocytes have been identified in various conditions unrelated to cutaneous infectious processes such as eczema, multinuclear vulvar atypia, factitious dermatitis, psoriasis, connective tissue diseases and even alterations in the mucous membranes of the digestive tract (esophagus and intestine); however, very few clinical cases have been published so far and their pathophysiology is not entirely known. We present a clinical case Revista Médica Sanitas 183 QUERATINOCITOS MULTINUCLEADOS EN ECZEMA CRÓNICO: REPORTE DE CASO

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This technique may be useful in the prenatal diagnosis of conotruncal anomalies and in the assessment of the spatial relationships of abnormal vascular connections in the upper mediastinum. P01.34Maternal lipopolysaccharide depresses fetal cardiovascular function in mouse S. Rounioja, J. Räsänen, H. Autio-Harmainen, M. Ojaniemi, V. Glumoff, K. Mäkikallio, M. Hallman University of Oulu, FinlandBackground: Intra-amniotic lipopolysaccharide (LPS) causes a fetal inflammatory response and cardiac dysfunction in mice. We hypothesized that the placenta serves as a barrier against bacterial toxins delaying the onset of a fetal inflammatory response and cardiac failure. Methods: At 14-15 days of gestation DBA strain mice were randomized to receive LPS (∼ 70 µg) or vehicle intraperitoneally. Doppler ultrasonography of fetal cardiovascular hemodynamics was performed before and six hours after LPS. The expression and production of cytokines and other inflammatory mediators were determined using ribonuclease protection assay and cytometric bead array. Histopathology and immunostaining of toll-like receptor (TLR) in placenta were carried out. Results: Six hours after LPS injection, there was no evidence of stasis in maternal lung or liver, although tumor necrosis factoralpha (TNF-á) and interleukin (IL)-6 were increased in serum (p < 0.05). In contrast, placenta showed severe dilatation and stasis most distinctly in maternal vessels. The expression of TNF-á, IL-1á and IL-6 (p < 0.05) increased in placenta, whereas no inflammatory activation was evident in fetal tissues, and amniotic fluid revealed no increase in cytokines. The expression of TLR2 (p < 0.05) was increased in labyrinthine macrophages, which could serve as target for LPS. The fetal cardiac outflow mean velocity, was lowered (p < 0.005) in the LPS group. The pulsatility indices (PI) of the umbilical artery and the descending aorta and the PI for veins from the ductus venosus were higher after LPS. In the LPS group 65% of the fetuses had atrioventricular valve regurgitation, compared to only 4% in the vehicle group. Conclusions: Maternally administered LPS acutely induced cytokine expressions in placental tissue with histologic lesions. Inflammatory response was not evident in the fetal compartment. However, placental congestion increased the cardiac afterload, leading to fetal cardiovascular dysfunction.