Actualización en diagnóstico de divertículo de Meckel como causa de hemorragia gastrointestinal / Update in diagnosis of Meckel's diverticulum as a cause of gastrointestinal hemorrhage

El Divertículo de Meckel es la malformación congénita más común del sistema gastrointestinal1 , se produce al obliterarse el conducto onfalomesentérico a nivel proximal formando un divertículo verdadero en el borde anti mesentérico a nivel del íleon, el cual debería cerrarse entre la 5ta y 6ta semana de gestación normalmente. Sus alteraciones pueden dar lugar a pólipos ductales, bandas fibrosas, quistes ductales, fístulas íleoumbilicales o más frecuentemente al Divertículo de Meckel; estas variaciones pueden asociarse a otras malformaciones en el sistema nervioso o cardiovascular2 . Los remanentes onfalomesentéricos son más frecuentes en hombres que en mujeres, con una relación 2:1, siendo la incidencia general de un 2%3 . La mayoría de los casos se mantienen asintomáticos, pero algunos pacientes, sobre todo en edades pediátricas, pueden presentar síntomas como hemorragia gastrointestinal, torsión intestinal, obstrucción o infección4 . Dada su escasa e inespecífica sintomatología, es que podría llevar al clínico a confundirlo con otros diagnósticos diferenciales tales como la Enfermedad Inflamatoria Intestinal, Úlceras u otras patologías. Esta una de las razones por las que nos parece relevante realizar una revisión de las técnicas diagnósticas disponibles en la actualidad con el fin de determinar las mejores opciones diagnosticas dependiendo del medio en que se desenvuelva el clínico.

Meckel Diverticulum is the most common congenital malformation of the gastrointestinal system1 , it occurs when the omphalomesenteric duct is obliterated proximally, forming a true diverticulum in the anti-mesenteric border at the level of the ileum, which should be closed usually between the 5th and 6th week of gestation. Its alterations can give rise to ductal polyps, fibrous bands, ductal cysts, ileo-umbilical fistulas or more frequently to Meckel's diverticulum; These variations can be associated with other malformations in the nervous or cardiovascular system2 . Omphalomesenteric remnants are more frequent in men than in women, with a 2: 1 ratio, with a general incidence of 2% 3 . Most cases remain asymptomatic, but some patients, especially at pediatric ages, may present symptoms such as gastrointestinal bleeding, intestinal torsion, obstruction or infection4 . Given its scarce and unspecific symptomatology, it could lead the clinician to confuse it with other differential diagnoses such as Inflammatory Bowel Disease, Ulcers or other pathologies. This is one of the reasons why it seems relevant to review the diagnostic techniques currently available to determine the best diagnostic options depending on the environment in which the clinician operates

Increased expression of the transient receptor potential melastatin 7 channel is critically involved in lipopolysaccharide-induced reactive oxygen species-mediated neuronal death.

AIMS: To assess the mechanisms involved in lipopolysaccharide (LPS)-induced neuronal cell death, we examined the cellular consequences of LPS exposure in differentiated PC12 neurons and primary hippocampal neurons. RESULTS: Our data show that LPS is able to induce PC12 neuronal cell death without the participation of glial cells. Neuronal cell death was mediated by an increase in cellular reactive oxygen species (ROS) levels. Considering the prevalent role of specific ion channels in mediating the deleterious effect of ROS, we assessed their contribution to this process. Neurons exposed to LPS showed a significant intracellular Ca(2+) overload, and nonselective cationic channel blockers inhibited LPS-induced neuronal death. In particular, we observed that both LPS and hydrogen peroxide exposure strongly increased the expression of the transient receptor protein melastatin 7 (TRPM7), which is an ion channel directly implicated in neuronal cell death. Further, both LPS-induced TRPM7 overexpression and LPS-induced neuronal cell death were decreased with dithiothreitol, dipheniliodonium, and apocynin. Finally, knockdown of TRPM7 expression using small interference RNA technology protected primary hippocampal neurons and differentiated PC12 neurons from the LPS challenge. INNOVATION: This is the first report showing that TRPM7 is a key protein involved in neuronal death after LPS challenge. CONCLUSION: We conclude that LPS promotes an abnormal ROS-dependent TRPM7 overexpression, which plays a crucial role in pathologic events, thus leading to neuronal dysfunction and death.