RESUMO
When the supply of energetic substrates is insufficient to slow the development of the catabolism, the next step is to focus on the neuro-endocrine mechanism which regulates the anabolism-catabolism balance. In this work, we review the endocrine response to stress and its implications in protein metabolism, in order to evaluate the different therapeutic possibilities available. Pharmacological blocking of the secretion of catabolic hormones (glucagon and catecholamines) has been unsuccessful up to now. Insulin is the only hormone which produces anabolism in all energetic substrates, but the results published about its administration with glucose and amino acids and its effects upon the nitrogen balance are controversial. The administration of anabolic steroids such as nandrolone, stanolone, and methenolone are usually associated with protein anabolism with minimum androgenizing action. The most recent works lead to the study of the effects of the use of GH and IGF-1 with clearly hopeful results. We have not yet acquired enough experience to use these methods in the habitual clinical practice. At the moment, the clinical studies are in the experimental stage and their application in nutrition is not accepted by the official authorities.
Assuntos
Hormônios/uso terapêutico , Fenômenos Fisiológicos da Nutrição/fisiologia , Metabolismo Energético/efeitos dos fármacos , Hormônios/fisiologia , Humanos , Apoio Nutricional , Cuidados Pós-Operatórios , Proteínas/efeitos dos fármacos , Proteínas/metabolismo , Estresse Fisiológico/metabolismo , Estresse Fisiológico/terapiaRESUMO
Two cases of bisalbuminaemia are hereby studied: a congenital case and an acquired or transitory case. In the first one, this hereditary disturbance is studied on four affected members of one Spanish family, being associated in two of them with multiple lipomatosis. This kind of association is considered as casual. As in most of the informed cases, ours belongs to the slow kind. The second case deals with a bisalbuminaemia of transitory character or pseudobisalbuminaemia which, appeared in a woman in the course of an acute pancreatitis of biliolithiasic origin, with a pancreatic pseudocyst and pleural effusion, the evolution in the inflamatory pancreatic process being advantageous in spite of the prsence of bisalbuminaemia. Briefly revised, are exposed the causes of this interesting and rare alteration in the electrophoretic fractioning of plasmatic proteins: congenital, and adquired causes due to administration of betalactamines and during the course of acute pancreatitis.