[Clinical characteristics of spinal cord injury caused by infection]. / Características clínicas de la lesión medular de causa infecciosa.

INTRODUCTION: Infections account for 3% of all non-traumatic spinal cord injuries. The demographic distribution and clinical course are still not fully understood in these patients. AIMS: The aim of this study was to determine the clinical-epidemiological characteristics and clinical course in patients with infectious spinal cord injury referred to our centre. PATIENTS AND METHODS: A retrospective study (over the period 1997-2003) was carried out. Variables examined included age, sex, type of injury, aetiology, causing agent, ASIA classification on admission and discharge. RESULTS: N = 27 (8% of the total number of non-traumatic spinal cord injuries). Mean age: 37.3 years (range: 14-75). Higher prevalence was found between the ages of 20 and 39 years (48.1%) and in males (70.4%). A prevalence of dorsal injuries (59.3%) was also observed. On hospital admission most of the injuries were incomplete (70.4%) and this figure increased to 77.8% on discharge. Spondylodiscitis was the most frequent cause (51.9%) and Staphylococcus aureus was found to be the most common microbiological causing agent. The greatest prevalence of complete injuries was observed in cases of dorsal injuries (43.75%). All cases of tuberculosis were situated in the dorsal region (p < 0.05). CONCLUSIONS: In our care centre, non-traumatic spinal cord injuries of an infectious origin seem to be most often caused by spondylodiscitis due to S. aureus, with a higher incidence in the dorsal region. They predominantly affect males in their thirties and forties, and usually give rise to incomplete injuries.

Características clínicas de la lesión medular de causa infecciosa / Clinical characteristics of spinal cord injury caused by infection

Introducción. La etiología infecciosa representa el 3% de la lesión medular no traumática. La distribución demográfica y evolución clínica no son completamente conocidas en estos pacientes. Objetivos. Conocer las características clinicoepidemiológicas y la evolución en pacientes con lesión medular infecciosa remitidos a nuestro centro. Pacientes y métodos. Estudio retrospectivo (período 1997-2003). Variables: edad, sexo, tipo de lesión, etiología, agente causal, clasificación ASIA al ingreso y al alta. Resultados. N = 27 (8% del total de lesiones medulares no traumáticas). Edad media: 37,3 años (rango: 14-75). Mayor prevalencia en edades comprendidas entre 20 y 39 años (48,1%) y en varones (70,4%). Se observa una mayor prevalencia de lesiones dorsales (59,3%). Al ingreso la mayoría de lesiones fueron incompletas (70,4%), y aumentaron hasta un 77,8% al alta. La espondilodiscitis fue la causa más frecuente (51,9%), y el Staphylococcus aureus, el agente microbiológico etiológico más frecuente. La mayor prevalencia de lesiones completas se observa en lesiones dorsales (43,75%). El 100% de los casos de tuberculosis asentaron en la región dorsal (p < 0,05). Conclusiones. En nuestro centro, la lesión medular de causa no traumática de etiología infecciosa parece estar producida en mayor frecuencia por espondilodiscitis por S. aureus, con una mayor incidencia en la región dorsal. Afecta predominantemente a varones en la tercera y cuarta décadas de la vida y suele producir lesiones incompletas (AU)

Introduction. Infections account for 3% of all non-traumatic spinal cord injuries. The demographic distribution and clinical course are still not fully understood in these patients. Aims. The aim of this study was to determine the clinicalepidemiological characteristics and clinical course in patients with infectious spinal cord injury referred to our centre. Patients and methods. A retrospective study (over the period 1997-2003) was carried out. Variables examined included age, sex, type of injury, aetiology, causing agent, ASIA classification on admission and discharge. Results. N = 27 (8% of the total number of nontraumatic spinal cord injuries). Mean age: 37.3 years (range: 14-75). Higher prevalence was found between the ages of 20 and 39 years (48.1%) and in males (70.4%). A prevalence of dorsal injuries (59.3%) was also observed. On hospital admission most of the injuries were incomplete (70.4%) and this figure increased to 77.8% on discharge. Spondylodiscitis was the most frequent cause (51.9%) and Staphylococcus aureus was found to be the most common microbiological causing agent. The greatest prevalence of complete injuries was observed in cases of dorsal injuries (43.75%). All cases of tuberculosis were situated in the dorsal region (p < 0.05). Conclusions. In our care centre, non-traumatic spinal cord injuries of an infectious origin seem to be most often caused by spondylodiscitis due to S. aureus, with a higher incidence in the dorsal region. They predominantly affect males in their thirties and forties, and usually give rise to incomplete injuries (AU)

Regulation of glutamate transport and transport proteins in a placental cell line.

We utilized HRP.1 cells derived from midgestation rat placental labyrinth to determine that the primary pathway for glutamate uptake is via system X, a Na(+)-dependent transport system. Kinetic parameters of system X activity were similar to those previously determined in rat and human placental membrane vesicle preparations. Amino acid depletion caused a significant upregulation of system X activity at 6, 24, and 48 h. This increase was reversed by the addition of glutamate and aspartate but not by the addition of alpha-(methylamino)isobutyric acid. Immunoblot analysis of the three transport proteins previously associated with system X activity indicated a trend toward an increase in GLT1, EAAC1, and GLAST1 immunoreactive protein contents by 48 h; cell surface expression of the same was enhanced by 24 h. Inhibition analysis suggested key roles for EAAC1 and GLAST1 in basal anionic amino acid transfer, with an enhanced role for GLT1 under conditions of amino acid depletion. In summary, amino acid availability as well as intracellular metabolism regulate anionic amino acid uptake into this placental cell line.