La autopsia blanca

En Patología Forense, frecuentemente nos encontramos con autopsias de muertes súbitas en las que se observan lesiones inespecíficas (edema pulmonar y/o cerebral) como únicos hallazgos macroscópicos y en ocasiones también microscópicos. La información clínica suele ser escasa, la muerte normalmente ocurre sin testigos y el lugar del levantamiento aporta pocos datos orientativos. Nos encontramos, en principio, ante la llamada incorrectamente «autopsia blanca». En estos casos, es imprescindible descartar la participación de tóxicos o trastornos electrolíticos, así como estar familiarizados con todas aquellas patologías que puedan cursar con una muerte súbita. La casuística en este tipo de muertes es reducida debido a su escasa frecuencia y a la dificultad de inscribir correctamente la causa de muerte en los registros de mortalidad. Este artículo trata de revisar aquellas patologías extracardíacas que, con mayor frecuencia, nos podemos encontrar en este tipo de autopsias: muerte súbita e inesperada del epiléptico, trauma cerebral mínimo, asma bronquial, hipertensión pulmonar, microembolismo, diabetes mellitus tipo I y cetoacidosis alcohólica. En muchos de estos casos, los estudios químico-toxicológicos e histológicos postmortem pueden establecer la causa de muerte, si los datos clínicos y los obtenidos en el momento del levantamiento son compatibles con la misma.Sudden death autopsy is a frequent event in forensic pathology. In a percentage of these cases, unspecific pathology (pulmonary and/or cerebral edema) is the only feature observed in postmortem examination. Deaths are usually witnessed. Clinical data, scene information and circumstances of death are insufficient. The aim of this paper is to review the most frequent extracardiac diseases that could result in a negative autopsy: SUDEP (sudden unexplained death in epilepsy), bronchial asthma, minimal traumatic brain injury, pulmonary hypertension, microembolism (fat, amniotic fluid and air embolism), type I diabetes mellitus (dead in bed syndrome) and alcoholic ketoacidosis. Laboratory tests and careful histological examination may establish the cause of death in cases where clinical and scene data are compatible.Molina Aguilar, Pilar, [email protected] ; Dasi Martinez, Concha, [email protected] ; Gisbert Grifo, Marina, [email protected]

Oxidative Stress and DNA Damage in Human Gastric Carcinoma: 8-Oxo-7\u278-dihydro-2\u27-deoxyguanosine (8-oxo-dG) as a Possible Tumor Marker

We characterized the oxidative stress (OS) status by the levels of reduced/oxidized glutathione (GSH/GSSG), malondialdehyde (MDA) and the mutagenic base 8-oxo-7\u278-dihydro-2\u27-deoxyguanosine (8-oxo-dG) in human gastric carcinoma (HGC) samples and compared the results with normal tissue from the same patients. We also analyzed 8-oxo-dG in peripheral mononuclear cells (PMNC) and urine from healthy control subjects and in affected patients in the basal state and one, three, six, nine and twelve months after tumor resection. The levels of DNA repair enzyme mRNA expression (hOGG1, RAD51, MUYTH and MTH1) were determined in tumor specimens and compared with normal mucosa. Tumor specimens exhibited increased levels of MDA and 8-oxo-dG compared with normal gastric tissue. GSH levels were also increased, while GSSG levels remained stable. DNA repair enzyme mRNA expression was induced in the tumor tissues. Levels of 8-oxo-dG were significantly elevated in both urine and PMNC of gastric cancer patients compared with healthy controls. After gastrectomy, the levels of the damaged base in urine and PMNC decreased progressively to values close to those found in the healthy population. The high levels of 8-oxo-dG in urine may be related to the increased induction of DNA repair activity in tumor tissue, and the changes observed after tumor resection support its potential use as a tumor marker