ABSTRACT
The rationale for betablocker use in heart failure, based on neurohormonal physiology, has been established over the past 20 years. Recent trials have shown the unequivocal benefits of betablockers in patients with chronic systolic heart failure. The benefits include improve survival (35%) reduced need for hospitalization and improve of left ventricular function. However, betablockers may also make a patient with heart failure worse, especially when treatment begins and there is reluctance to use betablockade therapy. Complications can generally be avoided by starting with extremely low doses and increasing the dose very slowly. Despite this, further questions remain regarding the use of these agents in cardiac failure, including the role in the progression of the disease, the selection of individual betablocker, and the use in very severe disease or very old patients.
Subject(s)
Adrenergic beta-Antagonists/therapeutic use , Heart Failure/drug therapy , Adrenergic beta-Antagonists/administration & dosage , Adrenergic beta-Antagonists/adverse effects , Clinical Trials as Topic , HumansABSTRACT
El conocimiento de la implicación del sistema adrenérgico en la fisiopatología de la insuficiencia cardiaca (ICC) ha justificado una intensa investigación sobre el papel de los betabloqueadores en el tratamiento de esta enfermedad. Recientemente se han publicado varios ensayos clínicos de gran calidad que demuestran claramente que el tratamiento de la ICC sistólica con betabloqueadores disminuye la mortalidad en un 35 por ciento, la frecuencia de hospitalización y mejora la función ventricular. Sin embargo, existen muchas reticencias para su uso debido a que pueden empeorar el cuadro en algunos pacientes, sobre todo al principio del tratamiento. Esto puede evitarse con un cuidadoso comienzo y un progresivo ajuste de dosis. Todavía quedan cuestiones por responder como la elección del betabloqueador, el efecto del tratamiento en la progresión de la enfermedad y su utilidad en pacientes muy graves o muy ancianos (AU)
Subject(s)
Humans , Adrenergic beta-Antagonists/therapeutic use , Heart Failure/drug therapy , Adrenergic beta-Antagonists/administration & dosage , Adrenergic beta-Antagonists/adverse effects , Clinical Trials as TopicABSTRACT
La gastropatía inducida por antiinflamatorios no esteroideos es muy frecuente. Las lesiones gástricas ocasionadas por el uso de estos fármacos son subclínicas e intrascendentes en la mayoría de ocasiones, pero algunas veces los antiinflamatorios determinan la aparición de úlceras gástricas o duodenales que pueden complicarse con la aparición de hemorragia digestiva o de perforación. La prevención de estas alteraciones pasa, en primer lugar, por el uso más juicioso de los antiinflamatorios y, en segundo lugar, por la administración de algunos fármacos con finalidad protectora. Sin embargo, está plenamente demostrado que el uso de estos fármacos con fines profilácticos es necesario en pocos casos. En este artículo se revisan las recomendaciones actuales de la profilaxis farmacológica de la gastropatía inducida por antiinflamatorios no esteroideos (AU)
Subject(s)
Humans , Anti-Inflammatory Agents, Non-Steroidal/adverse effects , Stomach Diseases/chemically induced , Stomach Diseases/prevention & control , Anti-Ulcer Agents/therapeutic use , Risk FactorsABSTRACT
Low expression of the mitochondrial 3-hydroxy-3-methylglutaryl-CoA (HMG-CoA) synthase gene during development correlates with an unusually low hepatic ketogenic capacity and lack of hyperketonaemia in piglets. Here we report the isolation and characterization of the 5' end of the pig mitochondrial HMG-CoA synthase gene. The 581 bp region proximal to the transcription start site permits transcription of a reporter gene, confirming the function of the promoter. The pig mitochondrial HMG-CoA synthase promoter is trans-activated by the peroxisomal proliferator-activated receptor (PPAR), and a functional response element for PPAR (PPRE) has been localized in the promoter region. Pig PPRE is constituted by an imperfect direct repeat (DR-1) and a downstream sequence, both of which are needed to confer PPAR-sensitivity to a thymidine kinase promoter and to form complexes with PPAR.retinoid X receptor heterodimers. A role of PPAR trans-activation in starvation-associated induction of gene expression is suggested.
Subject(s)
Hydroxymethylglutaryl-CoA Synthase/genetics , Peroxisome Proliferators/metabolism , Promoter Regions, Genetic , Response Elements , Swine/genetics , Amino Acid Sequence , Animals , Base Sequence , Cloning, Molecular , Lipid Metabolism , Mitochondria/enzymology , Models, Genetic , Molecular Sequence Data , Protein Binding , Receptors, Retinoic Acid/metabolism , Retinoid X Receptors , Species Specificity , Transcription Factors/metabolism , Transcriptional ActivationABSTRACT
We report on a patient whose clinical, radiologic, and histopathologic findings are compatible with the Piepkorn type of lethal short-limb osteochondrodysplasia, but who also showed multinucleated giant chondrocytes in cartilage. Multinucleated giant cells are an unusual finding in osteochondrodysplasias, having been reported in atelosteogenesis type I and boomerang dysplasia. This uncommon histopathologic finding and the clinical and radiographic findings strongly support the diagnosis of boomerang dysplasia in the present patient. Our patient supports the previously suggested existence of an entity including atelosteogenesis and boomerang dysplasia. If this is so, the current patient and that described by Piepkorn et al. [1977: Teratology 16:345-350] could represent the most severe clinical expression of that condition.
Subject(s)
Cartilage/pathology , Giant Cells/pathology , Osteochondrodysplasias/pathology , Fatal Outcome , Humans , Male , Osteochondrodysplasias/diagnostic imaging , Phenotype , RadiographyABSTRACT
A de novo interstitial deletion of 6q16.2q21 was observed in a 23-month-old boy with mental and psychomotor delay, obese appearance, minor craniofacial anomalies, and brain anomalies. We compare clinical manifestations of this patient with those observed in previously reported cases with similar 6q interstitial deletions. It is interesting to note the clinical similarities between some patients with interstitial deletions of 6q16 or q21 bands and patients with Prader-Willi syndrome (PWS) and it may help to keep in mind cytogenetic studies of patients with some PWS findings.
