1.
Nutrition in chronic critical illness.
Pingleton, SK
Clinics in chest medicine. 2001;(1):149-63
Abstract
Nutritional management of patients with respiratory failure can be a model of nutritional management in chronically critically ill patients. This model requires recognition of the differing metabolic states of starvation and hypermetabolism. Starvation can result in malnutrition, with adverse effect on respiratory muscle strength, ventilatory drive, and immune defense mechanisms. General nutritional goals include preservation of lean body mass by providing adequate energy and positive nitrogen balance. General nutritional prescriptions for both states include a substrate mix of 20% protein, 60% to 70% carbohydrates, and 20% to 30% fat. Positive nitrogen balance is difficult to attain in hypermetabolic patients and energy requirements are increased compared with starved patients. Enteral nutrition should be the mode of initial nutrient delivery unless the gastrointestinal tract is nonfunctional. Monitoring of nutritional support is essential. Complications of nutritional support are multiple. Nutritional hypercapnia is an important complication in a chronically critically ill patient. Outcomes of selected long-term acute patients are poor, with only 8% of patients fully functional 1 year after discharge. Appropriate nutritional therapy is one aspect of management of these patients that has the possibility of optimizing function and survival.
2.
Defective natural killer and phagocytic activities in chronic obstructive pulmonary disease are restored by glycophosphopeptical (inmunoferón).
Prieto, A, Reyes, E, Bernstein, ED, Martinez, B, Monserrat, J, Izquierdo, JL, Callol, L, de LUCAS, P, Alvarez-Sala, R, Alvarez-Sala, JL, et al
American journal of respiratory and critical care medicine. 2001;(7):1578-83
Abstract
We have investigated both modifications in natural (innate) immunity caused by chronic obstructive pulmonary disease (COPD) and the effects of a glycophosphopeptical immunomodulator (Inmunoferón) treatment on COPD-associated immunoalterations. In a double-blinded clinical trial, 60 patients with COPD received glycophosphopeptical or placebo during 90 consecutive days at oral doses of 3 g/d. Fifty-six sex- and age-matched healthy control subjects were included as a reference group for immunologic parameters. Peripheral blood natural killer (PBNK) cell cytotoxic activity and phagocytic activity of peripheral monocytes/macrophages (Mo/Ma) and polymorphonuclear (PMN) cells were assessed at baseline and then again at the end of treatments. We found both PBNK activity and phagocytic activity to be significantly decreased in patients with COPD compared with levels in healthy volunteers. The treatment with glycophosphopeptical provoked significant stimulatory effects on PBNK cytotoxic activity. This stimulation was not mediated by an increase in CD3(-)CD56(+) NK cells. Further, glycophosphopeptical significantly increased the percentage of monocytes and PMNs that phagocytize Escherichia coli in vitro, as well as increased phagocytic indices. We conclude that peripheral blood cells of patients with COPD show clear defects in natural immunity that are partially rescued by glycophosphopeptical.