A resposta metabólica ao trauma cranioencefálico é autolimitada? Análise das proteínas de fase aguda e glicemia

Nos últimos anos tem havido referências à limitação da resposta metabólica nas duas primeiras semanas após trauma cranioencefálico (TCE). Foi feita proposta de estudo a partir de experimento clínico em pacientes com trauma encefálico grave, que foram avaliados por volta de 7 dias após a lesão (M1). A segunda avaliação ocorreu 4 dias após (M2), e a terceira 3 a 4 dias após (M3). em um período de 2 anos, foram selecionados 28 pacientes do sexo masculino, com trauma encefálico grave, escala de gravidade de Glasgow entre 4 e 6. Dentre os 28 pacientes, 6 completaram o estudo proposto. Os pacientes foram acompanhados clinicamente durante toda a fase do experimento. em cada um dos momentos de análise, foram feitas análises da excreção nitrogenada e proteínas de fase aguda. da mesma forma foram feitas determinações da glicemia plasmática, N-amínico e triglicerídeos. Os resultados do estudo demonstraram não haver modificações no balanço nitrogenado, normalização da proteína-C-reativa e redução relativa da glicemia ao final do experimento. Os autores tecem considerações sobre os possíveis mecanismos envolvidos na modulação da resposta metabólica e concluem que o hipermetabolismo, a basear-se na análise da glicemia e das proteínas de fase aguda, não persiste além do 13° dia do período de recuperação pós-trauma. São feitas sugestões de estudos futuros que possam elucidar os mecanismos envolvidos na normalização do hipercatabolismo e hipermetabolismo observados nas duas primeiras semanas após TCE.There are many reports supporting a self-limitation mechanism involved with hypermetabolic response after severe cranial injury. It was proposed a study with severe head injury patients, in three stages of the evolution. The first 7 days after admission (moment 1- M1), the second three days latter (M2) and the last 7 days after the first (M3). Among male patients with severe head injury, attended between January 1992 and December 1993 in University Hospital of Botucatu, UNESP, were selected 28 male patients, with Glasgow severity scale between 4 and 6, with pO2< 70 mm Hg, weighting 60 kg or more. Among these patients, 6 finished the study, including analysis of the excretion of N, acute phase proteins, glycemia, triglycerides and amine nitrogen. During the study there were no changes in nitrogen balance and there was a decrease in protein C-reative. Glycemia tends to fall within two weeks after injury. The authors make some considerations about possible mechanisms involved in brain modulation associated with the period of dependence of hypermetabolism and hypercatabolism after closed brain injury. There are some evidences that the brain responds to head trauma with a gobal non specific way, which tends to be reorganized beyond the first two weeks after lesion. The study does not show any influence of the type and severity of head trauma

Effects of active smoking on airway and systemic inflammation profiles in patients with chronic obstructive pulmonary disease

Background: The markers that characterize local and systemic inflammation in chronic obstructive pulmonary disease (COPD) remain unclear, as do their correlations with smoking status and presence of disease. The aim of this study was to assess markers of inflammation in the peripheral blood and airways of current smokers without COPD, of current smokers with COPD and of ex-smokers with COPD. METHODS: In this study, 17 current smokers with COPD (mean age: 58.2 ± 9.6 years; mean forced expiratory volume in 1 second [FEV1]: 56.1 ± 15.9%), 35 ex-smokers with COPD (mean age: 66.3 ± 7.3 years; mean FEV1: 47.9 ± 17.2%) and 20 current smokers without COPD (mean age: 49.1 ± 6.2 years; mean FEV1: 106.5 ± 15.8%) were evaluated. Spirometry findings, body composition and serum/induced sputum concentrations of tumor necrosis factor α (TNF-α), interleukin (IL)-6, IL-8 and IL-10, together with serum C-reactive protein (CRP) levels, were assessed. RESULTS: Serum TNF-α concentration was higher in all current smokers than in ex-smokers with COPD. In current smokers without COPD, serum CRP level was lower than in ex-smokers with COPD and significantly lower than in current smokers with COPD. Sputum TNF-α concentration was higher in current and ex-smokers with COPD than in current smokers without COPD. Multiple regression analyses showed that serum TNF-α was associated with active smoking, and serum CRP and sputum TNF-α were associated with COPD diagnosis. CONCLUSIONS: Smoking is associated with higher systemic inflammation in patients with COPD. Current findings also support the hypothesis that smoking and COPD have different effects on the regulation of airway and systemic inflammatory processes. © 2013 Lippincott Williams and Wilkins

Plasma levels of transthyretin and retinol-binding protein in child-a cirrhotic patients in relation to protein-calorie status and plasma amino acids, zinc, vitamin a and plasma thyroid hormones

Transthyretin and retinal-binding protein are sensitive markers of acute protein-calorie malnutrition both for early diagnosis and dietary evaluation. A preliminary study showed that retinal-binding protein is the most sensitive marker of protein-calorie malnutrition in cirrhotic patients, even those with the mild form of the disease (Child A). However, in addition to being affected by protein-calorie malnutrition, the levels of these short half-life-liver-produced proteins are also influenced by other factors of a nutritional (zinc, tryptophan, vitamin A, etc) and non-nutritional (sex, aging, hormones, renal and liver functions and inflammatory activity) nature. These interactions were investigated in 11 adult male patients (49.9 ± 9.2 years of age) with alcoholic cirrhosis (Child-Pugh grade A) and with normal renal function. Both transthyretin and retinol binding protein were reduced below normal levels in 55% of the patients, in close agreement with their plasma levels of retinal. In 67% of the patients (4/6), the reduced levels of transthyretin and retinal-binding protein were caused by altered liver function and in 50% (3/6) they were caused by protein-calorie malnutrition. Thus, the present data, taken as a whole, indicate that reduced transthyretin and retinal-binding protein levels in mild cirrhosis of the liver are mainly due to liver failure and/or vitamin A status rather than representing an isolated protein-calorie malnutrition indicator

Utilização do metabolismo protéico ( 15N-glicina) na detecção precoce de agravamento da atividade da doença em pacientes portadores de retocolite ulcerativa inespecífica

Disease activity was assessed in 10 (five males and five females) ulcerative colitis patients through the following parameters: clinical, laboratory, sigmoidoscopic and histological. Protein metabolism was also assessed with 15N-glycine and urinary ammonia as end product. Only one patient had exacerbation of the disease two months after the study started. This patient presented in the beginning of the study protein synthesis and breakdown of 4.51 and 3.47 g protein/kg/day, respectively, values higher than all other patients, showing an hypermetabolic state, suggesting an increase of the disease activity. However, this increase was not detected by others indicators and indexes utilised. These data allow to suggest the hypothesis that protein metabolism predicts precociously the exacerbation of disease activity in ulcerative colitis patients