Presepsin is a soluble fragment of the cluster-of-differentiation marker protein 14 (CD14) involved in pathogen recognition by innate immunity. We evaluated the relation between its circulating concentration, host response, appropriateness of antibiotic therapy, and mortality in patients with severe sepsis.

Cette mise au point a pour objet de montrer le rôle positif de l'insuline sur l'anabolisme protéique chez le sujet dénutri ou catabolique. De nombreux travaux chez l'homme sont disponibles :-études, avec témoins contrôles, chez des sujets pouvant supporter une charge de glucose avec et sans administration d'insuline,-études, avec témoins contrôles, faisant varier à la fois la charge d'insuline et de glucose tout en maintenant un apport énergétique constant,-études avec différents niveaux d'apport en insuline et en glucose,-études sur la réponse à l'insuline et son rôle dans l'anabolisme induit par la nutrition. La seconde partie de cet article passe en revue les différentes études cliniques concernant les effets métaboliques de la nutrition chez le patient agressé. Celles-ci permettent, selon le concept de l'entraînement anabolique lié aux nutriments ou anabolic drive, d'essayer de définir une composition optimale de l'apport calorique non protéique. Les études retenues portaient à la fois sur des sujets modérément agressés et avec des degrés de malnutrition variables et sur des sujets en état de stress sévère. Par ailleurs, si l'on considère les 42 groupes retenus de patients cataboliques, des résultats cliniquement satisfaisants (c'est-à-dire avec un bilan d'azote au pire faiblement négatif) ont été obtenus pour 13 groupes sur 22 recevant un système mixte glucose/lipide et pour 18 groupes sur 20 recevant uniquement du glucose. Ainsi, l'effet anabolique de l'insuline est également démontré chez le sujet catabolique.

PURPOSE:To evaluate the effect induced on gas exchange and on urea excretion by glucose and insulin infusion in injured patients. The magnitude and time necessary for the full development of the metabolic effect were investigated. METHODS:Six injured patients were investigated. During the first 24 hours, the fasting period, patients received 1 mg/kg*min of glucose; during the second 24 hours, the treatment period, infusion was increased to about the 95% of the energy production rate; during the last 8 hours, (stop period) the infusion rate was again set to 1 mg/kg*min. Gas exchange was determined in two consecutive 12-hour series, for 30 minutes every hour, either during a stabilized treatment or after its variation. Urea excretion was determinated on 4-hour samples. RESULTS:With respect to the fasting period, during the last 4 hours of the treatment period, the energy production rate did not vary; urea excretion (-25%) and oxygen consumption (-9%) decreased significantly. Carbon dioxide production (+16%), total respiratory quotient, and minute ventilation (+5%) increased significantly. Carbon dioxide production varied linearly with time (glucose infusion +1.74 mL/min*m2*h, P < .05; glucose withdrawal -1.89 mL/min*m2*h, P < .01). Minute ventilation decreased only during the withdrawal period by 65 mL/min*m2*h (P < .05). CONCLUSIONS:The infusion of glucose and insulin, in an amount slightly lower than the metabolic expenditure, leads to a consistently reduced amino acid catabolism and to a decreased oxygen consumption, without affecting energy requirements. Although it leads to an increase of carbon dioxide production, the measured change is so small and slow that it is not harmful unless there is severe respiratory insufficiency.

To investigate the kinetics of body nitrogen (N) excretion during 24 h glucose infusion (relating glycemia with insulin supply) and during subsequent 24 h saline infusion in injured patients during a full blown stress reaction. To define the lag time between the start or the withdrawal of glucose and insulin infusion, and the modification in the N loss from the body, and the time span to reach the maximum effect and its size. The knowledge of these variables is mandatory to plan short term studies in critically ill patients, while assuring the stability of the metabolic condition during the study period, and also to assess the possible weaning of the effect on protein breakdown during prolonged glucose and insulin infusion.

In sixteen severely catabolic patients, two different nutritional treatments with the same nitrogen input (0.30 gN.kg-1.die-1) but with a different caloric support: 30 kcal.kg-1.die-1 foe group A and 15 kcal.kg-1.die-1 for group B were infused. Body nitrogen balance (BN), muscle nitrogen balance (BNm) and, calculated as a difference of the two, visceral nitrogen balance were measured in every patient on basal day and on the second day of total parenteral nutrition. Both nutritional treatment reduced the catabolic state in the same amount: this was confirmed by a less negative body BN and by the reduced excretion of 3-MEH and amino acidic catabolic markers. Otherwise in the other compartments the treatments showed different effects: the metabolic support was more reduced by treatment A than it was by B, supplying to visceral compartment a lower nitrogen amount: the nitrogen dismission from muscle compartment, available for visceral tissues, is greater with treatment B than with treatment A. In conclusion, even if both treatments show the same effect on body nitrogen balance, they penalize either one of the examined compartment or the other. To avoid this problem, the study and the use of tissue-specific nutrients are desiderable. Tissue-specific solutions may warrant the balance among body compartment without any further increase of the nitrogen rate.

Ten-three patients were investigated during the early postoperative phase after orthotopic liver transplantation to assess the adequacy of the amino acid (AA) supply during both parenteral (days 1-5) and enteral (days 6-9) nutrition. Plasma AA profile was determined preoperatively, on day 4 and 5 during TPN and on day 8 and 9 during EN, urea production rate was measured every day. Calories input was 28 kcal.kg-.day as glucose, nitrogen intake was 0.25 g.kg- day, supplying individual AA on the basis of previous studies. Urea nitrogen production during TPN (9-11 gN/m2.day) outlines the ability of the transplanted liver to manage the overall nitrogen load. Individual AA plasma profile was considered the expression of an adequate input when comprised between 1 and 1.5 times the normal value, in this respect we obtained adequate levels of all essential AAs. Particularly phenylalanine, methionine and branched chain AA, critical during liver failure, were kept in this range by supplying 68, 48 and 500 mg.kg-1.day. According to AA profile the supply of cystine and tyrosine (conditionally essential AAs), and of histidine, taurine, proline and serine could be safely increased. Not given dispensable AAs (glutamine, asparagine, citrulline and alfa amino butyric) showed a plasma level below the norm and should be added to the diet.

In 16 critically ill patients with full-blown stress reaction and without severe organ failure, we studied the kinetics of the arterial plasma amino acid (aa) profile during the first 48 h of total parenteral nutrition (TPN) in order to assess the time necessary to reach the steady-state condition during infusion. Each patient was treated with one of three different amino acid solutions giving, with the same nitrogen load, different intakes of individual amino acids. We found four different responses to the administered amino acids. Some amino acids showed a different trend depending on the dose given. At lower doses a steady state was achieved sooner. Plasma levels of amino acids not supplied in the TPN were unaffected or decreased, achieving a steady state at various times during the study period. We conclude that, in critically ill patients, stable arterial plasma amino acid concentrations are obtained within 24 h of starting TPN. In such patients, valid studies of the effect of amino acid solutions may therefore be carried out over short periods of time, thereby minimizing errors due to a fluctuating and unstable clinical state.

A plasmatic concentration for each aminoacid, between 1 and 1.5 times the normal value in fasting healthy subjects, is considered as an optimal target during total parenteral nutrition (TPN) in malnourished patients. We have analyzed the correlation between the aminoacid input and the aminoacid plasmatic concentration during TPN at different aminoacid composition. By exponential regression curves we then calculated the input required to keep each aminoacid plasma concentration in the optimal range.

The aim of this study was to evaluate the kinetics of arterial plasma amino acid profile during the first 48 h of clinical TPN in order to assess the time necessary to reach the steady-state condition during infusion. Each patient was treated with one of three different amino acid solutions yielding, in the same nitrogen intake, different intakes of individual amino acids. We found four different kinetics for the administered amino acids: an increase of plasma levels immediately after the start of the TPN with no variations during the steady period; the same trend with the steady-state obtained after 6-24 h of TPN infusion; no influence at all; a decrease of fasting plasma levels with the steady-state attained variably during the study period. Each given amino acid showed a different trend partly depending on the supply, suggesting that the steady-state was reached sooner for most amino acids, when the supply was larger. With lower intakes, plasma levels were unaffected or decreased. We conclude that in critically ill patients at least 24 h are needed to obtain stable arterial plasma amino acid concentration during TPN with adequate intakes of amino acid. Knowledge offers the possibility for a quick and accurate assessment of the adequacy of a given preparation (tailored for critically ill patients), it reduces the time span of the study and, as a consequence, the influence of varied metabolic conditions.