Loss of TCR-beta F1 and/or EZRIN expression is associated with unfavorable prognosis in nodal peripheral T-cell lymphomas.

Nodal peripheral T-cell lymphoma (nodal PTCL) has an unfavorable prognosis, and specific pathogenic alterations have not been fully identified. The biological and clinical relevance of the expression of CD30/T-cell receptor (TCR) genes is a topic under active investigation. One-hundred and ninety-three consecutive nodal PTCLs (89 angioimmunoblastic T-cell lymphomas (AITL) and 104 PTCL-unspecified (PTCL-not otherwise specified (NOS)) cases) were analyzed for the immunohistochemical expression of 19 molecules, involving TCR/CD30 pathways and the associations with standard prognostic indices. Mutually exclusive expression was found between CD3 and TCR-beta F1 with CD30 expression. Taking all PTCL cases together, logistic regression identified a biological score (BS) including TCR molecules (TCR-beta F1 and EZRIN) that separates two subgroups of patients with a median survival of 34.57 and 5.20 months (P<0.001). Multivariate analysis identified BS and the prognostic index for PTCL (PIT) score as independent prognostic factors. This BS maintained its significance in multivariate analysis only for the PTCL-NOS subgroup of tumors. In AITL cases, only a high level of ki67 expression was related to prognosis. A BS including molecules involved in the TCR signaling pathway proved to be an independent prognostic factor of poor outcome in a multivariate analysis, specifically in PTCL-NOS patients. Nevertheless, validation in an independent series of homogeneously treated PTCL patients is required to confirm these data.

A fatal case of community acquired methicillin resistant Staphylococcus aureus brain abscess in a previously healthy adolescent.

A 16-year-old adolescent presented with fever, lethargy and vomiting associated with mild dehydration. This was followed less than 24-hours later by loss of consciousness, seizures and clinical brain death. She had no prior medical illness, no hospital or frequent antibiotic exposure. There was no evidence of soft tissue or skin infection. Management included intravenous fluids, ampicillin and cefotaxime parenterally, dexamethasone, endotracheal intubation and mechanical ventilation. Her neurologic examination remained unchanged with areflexia, flaccid paralysis and fixed pupils. Post-mortem examination revealed an eight-centimetre right fronto-parietal lobe brain abscess. Cultures were positive for methicillin resistant Staphylococcus aureus. Although formerly a nosocomial pathogen affecting debilitated patients in the hospital setting, S aureus that is methicillin resistant is emerging as a community acquired pathogen affecting previously well patients.

A fatal case of community acquired methicillin resistant Staphylococcus aureus brain abscess in a previously healthy adolescent / Un Caso Fatal de Estafilococo Dorado Resistente a la Meticilina, Adquirido en la Comunidad, por una Adolescente Previamente Sana

A 16-year-old adolescent presented with fever, lethargy and vomiting associated with mild dehydration. This was followed less than 24-hours later by loss of consciousness, seizures and clinical brain death. She had no prior medical illness, no hospital or frequent antibiotic exposure. There was no evidence of soft tissue or skin infection. Management included intravenous fluids, ampicillin and cefotaxime parenterally, dexamethasone, endotracheal intubation and mechanical ventilation. Her neurologic examination remained unchanged with areflexia, flaccid paralysis and fixed pupils. Post-mortem examination revealed an eight-centimetre right fronto-parietal lobe brain abscess. Cultures were positive for methicillin resistant Staphylococcus aureus. Although formerly a nosocomial pathogen affecting debilitated patients in the hospital setting, S aureus that is methicillin resistant is emerging as a community acquired pathogen affecting previously well patients.

Una adolescente de 16 años de edad se presentó con fiebre, letargia y vómitos, asociados con deshi-dratación ligera. Estos síntomas fueron seguidos en menos de 24 horas por pérdida de conciencia, ataques y muerte clínica del cerebro. Con anterioridad, la paciente no había tenido enfermedad médica, ni hospitalización, ni tratamiento frecuente con antibióticos. No había evidencia de tejidos blandos o infección de la piel. El tratamiento incluyó líquidos intravenosos, ampicilina y cefotaxima de forma parenteral, dexametasona, entubación endotraqueal, y ventilación mecánica. El examen neurológico permaneció invariable con areflexia, parálisis flácida, y pupilas fijas. El examen post-mortem reveló un absceso cerebral de ocho centímetros en el lóbulo fronto-parietal derecho. Los cultivos resultaron positivos al Staphylococcus aureus resistente a la meticilina. Aunque visto an-teriormente como un patógeno nosocomial que afecta a los pacientes debilitados en el entorno hos-pitalario, el S aureus resistente a la meticilina está surgiendo como un patógeno extrahospitalario (ie adquirido en la comunidad) y afecta a pacientes previamente sanos. 1Equivalente acuñado aquí para el término inglés caseness, a saber, criterios que definen el estatus de caso sobre la base de la presencia de sintomatologia clinicamente significativa.

Hemorragia digestiva como forma de presentación de hipernefroma diseminado con metástasis gástricas / Digestive bleeding as the clinical presentation of disseminated renal-cell cancer with gastric metastases

Una mujer de 70 años ingresó en nuestro hospital para evaluación de melenas y anemización. Tres meses antes, en relación con la detección de síndrome anémico, se le realizó una endoscopia digestiva alta, y se practicó exéresis de un pólipo gástrico pequeño. Durante su estancia hospitalaria se le realizaron diversos estudios, y la ecografía y la tomografía computarizada abdominal revelaron una gran masa sobre el polo superior de riñón derecho, con una biopsia compatible con carcinoma de células renales. Una nueva endoscopia digestiva alta reveló la presencia de pequeños pólipos gástricos y mucosa duodenal anacarada. En la colonoscopia se apreció una sigmoiditis inespecífica. La biopsia de la mucosa gástrica y de la masa abdominal mostró la presencia de células claras como expresión de carcinoma renal. Se comenta la rareza de las metástasis gástricas de carcinoma renal, así como su inicio como hemorragia digestiva (AU)

[Adrenocortical macronodular hyperplasia with massive enlargement of the gland. A rare variant of autonomous hypercortisolism]. / Hiperplasia macronodular corticosuprarrenal con agrandamiento masivo de la glándula. Una rara variante de hipercortisolismo autónomo.

OBJECTIVE: To present a case of Cushing's syndrome due to massive adrenocortical macronodular hyperplasia that gave the gland the appearance of a pseudotumor. METHODS: In a review of the surgical pathology of the adrenal gland recently performed in our hospital, 82 adrenalectomy specimens obtained from 1978-1998 were found. Of these 82 surgical specimens, 44 (53.6%) were cortical pathologies and 10 of these (12.1%) were hyperplasia. There was only one with massive adrenocortical macronodular hyperplasia. A 53-year-old male, chronic alcoholic with cushingoid obesity and hypercortisolism is described. RESULTS: Ultrasound and CT assessment showed enlarged, asymmetrical adrenal glands and macronodules. The analytical and MRI study of the sella turcica showed primary adrenal hypercortisolism. Adrenalectomy of the dominant gland (the left adrenal whose activity was demonstrated on the 131Iodine scintiscan) was performed. The postoperative cortisol levels returned to normal and remain normal up to the present time, 18 months after surgery. The surgical specimen weighed 104 gms and was completely macronodular. CONCLUSIONS: Massive adrenocortical macronodular hyperplasia is a rare cause of pituitary-independent autonomous primary adrenal hypercortisolism. It is always bilateral. Adrenal weight is significantly increased (total weight of both adrenals 60-180 gms) and present yellow or golden, non-encapsulated nodules of a few millimeters to up to 4 cms, comprised of cells with scanty activity, therefore massive enlargement of the glands is necessary to produce Cushing's syndrome. The clinical, biochemical and surgical aspects can cause confusion and can be suggestive of an adrenocortical neoplasm. Treatment is by adrenalectomy.