Queratoquistes odontogénicos en el síndrome de carcinoma basocelular de tipo nevoide (SCBCN o S. de Gorlin) evaluación TC y RM

Introducción: El síndrome de carcinoma basocelular de tipo nevoide (SCBCN o S. de Gorlin) es un desorden autosómico dominante, caracterizado por múltiples carcinomas basocelulares, queratoquistes odontogénicos, calcificaciones durales, deformidades óseas y faciales, tumores que incluyen meduloblastoma y fibromas ováricos y grados variables de retardo mental. Los hallazgos imagenológicos característicos del SCBCN son queratoquistes odontogénicos de la mandíbula y del maxilar, prognatismo, labio-paladar hendido, macrocefalia, cavidades paranasales prominentes, calcificaciones de la hoz interhemisférica, anomalías vertebrales (cifoescoliosis y segmentación anormal), fusión de cuerpos costales, cuarto metacarpiano corto y lesiones óseas escleróticas. Material y métodos: Presentamos un caso de un paciente masculino de 13 años de edad, con antecedentes familiares de SCBCN, quien presentó drenaje serosanguinolento fétido bucal, prognatismo e hipertelorismo. Los estudios imagenológicos mostraron lesiones quísticas bilaterales en el ángulo de la mandíbula y antros maxilares. La RM con imágenes potenciadas en T2 y T1 con Gadolinium demostró múltiples lesiones quísticas de contornos lobulados, con realce periférico luego de la administración del Gadolinium, algunas con nivel líquido secundario a un componente hemorrágico. La RM cerebral demostró mínimo adelgazamiento del cuerpo calloso y discreta prominencia del sistema ventricular para la edad. La serie ósea no mostró alteraciones diferentes a las ya descritas. Discusión: A pesar de que la TC es útil en el diagnóstico de las anomalías faciales asociadas al SCBCN; la RM es superior por su capacidad de demostrar la composición interna y estructuras de la queratosis odontogénica.(AU)

CT-angiography for the detection of a lower gastrointestinal bleeding source.

The evaluation of lower gastrointestinal bleeding (LGIB) often involves the collaborative efforts of the gastroenterologist, radiologist, and surgeon. Efforts to localize the acute LGIB have traditionally involved colonoscopy, technetium-labeled red blood cell (RBC) scintigraphy, angiography, or a combination of these modalities. The sensitivity of each method of diagnosis is limited, with the most common cause of a negative study the spontaneous cessation of hemorrhage. Other technical factors include vasospasm, lack of adequate contrast volume or exposure time, a venous bleeding source, and a large surface bleeding area. We report the use of multidetector computed tomography (MDCT), or CT-angiography (CT-A), in the initial evaluation of LGIB, and speculate on the incorporation of this technique into a diagnostic algorithm to treat LGIB. MDCT may offer a very sensitive means to evaluate the source of acute LGIB, while avoiding some of the morbidity and intense resource use of contrast angiography, and may provide unique morphologic information regarding the type of pathology. Screening with the more rapid and available MDCT, followed by either directed therapeutic angiography or surgical management, may represent a reasonable algorithm for the early evaluation and management of acute LGIB in which an active bleeding source is strongly suspected.

Interleukin-1 beta activates expression of cyclooxygenase-2 and inducible nitric oxide synthase in primary hippocampal neuronal culture: platelet-activating factor as a preferential mediator of cyclooxygenase-2 expression.

Interleukin-1 beta (IL-1beta) is an inflammatory cytokine whose expression is elevated in brain during seizures, ischemia, and injury. Expression of IL-1beta and its receptor can also be observed in normal brain. Platelet-activating factor (PAF) is also a dual mediator that promotes neuronal plasticity responses as well as inflammation. We have determined the role of PAF in the regulation of cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS) genes by IL-1beta in rat primary hippocampal cultures. As assessed by reverse transcriptase/polymerase chain reaction (RT/PCR), recombinant mouse IL-1beta (1 nM) led to an induction of COX-2 mRNA which peaked at 2 hours, declined to baseline levels by 4 hours, began to rise again by 6 hours, and remained elevated at 24 hours post-treatment. iNOS mRNA was also induced, but unlike COX-2, its abundance peaked at 4 hours and decreased by 6 hours to a plateau lasting through 24 hours. Pretreatment with PAF antagonist BN50730 blocked induction of COX-2 mRNA by 2-hour IL-1beta treatment, and 2-hour treatment with the PAF analog mcPAF mimicked the effects of IL-1beta on COX-2 mRNA levels. Following injury, synaptic plasticity changes may be affected by IL-1beta-PAF-COX-2 neuronal signaling.

Exogenous and endogenous opioids as biological response modifiers.

Narcotic opioid compounds are among the most widely prescribed drug interventions for individuals suffering pain. Among the unwarranted side effects of respiratory depression, constipation, and physical dependence are the immunosuppressive qualities, particularly those which affect cell-mediated immunity. The immunosuppressive characteristics of opioid narcotics (e.g., morphine) have recently come into focus with the advent of acquired immune deficiency syndrome (AIDS) and the putative causative agent, human immunodeficiency virus type 1 (HIV-1). Specifically, a vast reservoir of HIV-1-infected individuals exists among drug abusers. Moreover, experimental evidence would suggest narcotic opioids may increase viral load in infected individuals by modifying the cellular machinery of activated leukocytes. Likewise, investigators have shown that opioids modify tumor growth and development. In this review, a comparison between endogenous opioid peptides and exogenous opiates on cell-mediated immunity and its relationship to viral infection and tumors is described.