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      Respuesta adrenal en pacientes críticos del Hospital de Clínicas de Asunción, Paraguay Translated title: Adrenal response in critically ill patients of the Hospital de Clínicas of Asuncion, Paraguay

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          Abstract

          RESUMEN El pronóstico de los pacientes críticos depende en gran medida de una interacción entre el sistema endocrino, nervioso e inmune. El eje hipotálamo - hipofiso - adrenal constituye el paradigma de estas interacciones, con respuestas secretorias variables. Por ello, este estudio de cohorte fue realizado con el objetivo de determinar el nivel medio de cortisol sérico en pacientes críticos al momento de su ingreso, a fin de analizar la relación entre dichos niveles y el pronóstico que tuvieron los mismos. Se incluyeron 122 sujetos ingresados a UCIA de junio de 2005 a enero de 2006 que fueron distribuidos en tres grupos (G1,G2,G3) de acuerdo al nivel de cortisol sérico que presentaban. El nivel medio de cortisol fue de 55.46ug-dL. Fallecieron 42.3% (12/29) de los pacientes con niveles de cortisol más bajos (G1) y el 33.3% (17/51) de los que presentaban niveles de cortisol intermedio (G2) RR:1.91,(p=0.5 ),así como el 61.90% (26/42) de los que tenían los niveles más elevados(G3)RR:1.78, (p=0.01).Si bien, el nivel medio de cortisol fué elevado, como era de esperar, los peores pronósticos estuvieron asociados a niveles bajos de cortisol (inferiores a 20ug-dL)como así también a aquellos que presentaron niveles superiores a 40 ug-dL, donde observamos una mortalidad significativamente mayor.

          Translated abstract

          ABSTRACT The prognosis of critically ill patients mainly depends on an interaction between the endocrinous, nervous and immune systems. The hypothalamic-pituitary-adrenal axis constitutes the paradigm of these interactions with variable secretory responses. Due to this, this cohort study was carried out in order to determine the mean serum cortisol level in critically ill patients at their hospital admission and to analyze the relation between those levels and the patient prognosis. One hundred and twenty two patients that entered the AICU from June 2005 to January 2006 were included and distributed in three groups (G1,G2,G3) according to their serum cortisol level. The mean cortisol level was 55.46 µg/dL.In the group with the lowest cortisol levels (G1), 42.3% of the patients (12/29) died, as well as 33.3% (17/51) of the patients with medium cortisol levels (G2) (RR:1.91, (p=0.5) and 61.90% (26/42) of the patients with the highest levels (G3) (RR:1.78, (p=0.01).Although the mean cortisol level was high, as expected the worse prognoses were associated to low cortisol levels (lower than 20 µg/dL) as well as to those that presented levels higher than 40 µg/dL in whom a significantly higher mortality was observed.

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          Aggressive nutritional support does not prevent protein loss despite fat gain in septic intensive care patients.

          It is current clinical practice to give intravenous nutrition (IVN) to critically ill postoperative septic intensive care patients to prevent loss of body protein, although it has not hitherto been possible to confirm this by direct measurement of body composition. Using a neutron activation analysis facility adapted to provide an intensive care environment and tritiated water dilution we directly measured total body water, protein and fat before and after 10 days of IVN (mean daily non-protein energy and amino acid intakes 2,750 kcal and 127 gm) in eight adult intensive care patients. All patients had recovered from the septic shock syndrome but were still ventilator dependent at the start of IVN. Six patients survived to leave hospital. As a group, the patients lost 12.5% of body protein (mean loss 1.5 +/- SE 0.3 kg; p = 0.001) despite a gain in fat (mean 2.2 +/- 0.8 kg; p = 0.026). There were, in addition, large losses of body water in most patients (mean, 6.8 +/- 2.6 kg; p = 0.036). We conclude that substantial losses of body protein occur in critically ill septic patients despite aggressive nutritional support and that further research is urgently required on the fate of infused substrates and the efficacy of alternative nutritional therapies.
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            Perioperative glucocorticoid coverage. A reassessment 42 years after emergence of a problem.

            The authors review the historical basis for the provision of perioperative glucocorticoid coverage, and detail the evolution in the understanding of the role of the hypothalamic-pituitary-adrenal cortical (HPA) axis in response to physical stressors. New recommendations are proposed for glucocorticoid-dependent patients who require anesthesia and surgery. In 1952, a patient developed surgery-associated adrenal insufficiency as a result of preoperative withdrawal from glucocorticoid therapy. That case report, and one other in the ensuing 12 months, prompted the publication of recommendations for perioperative glucocorticoid coverage, which became the standard of care. The understanding of the role of the HPA axis in the stress response has been subsequently refined; however, recommendations for perioperative glucocorticoid coverage have not been altered in parallel. Studies were identified beginning with the first reports of the physiologic actions of the adrenal glands (1855) and the description and clinical use of cortisone (1930-1993). Studies were selected for review if they were related to or evaluated the provision of stress-related glucocorticoid administration. All clinical studies were evaluated to determine the basis for the provision of perioperative glucocorticoid coverage and the validity of the data used to justify these conclusions. Clinical and experimental evidence support the concept that the current amount of perioperative glucocorticoid coverage is excessive and has been based on anecdotal information. New recommendations are proposed which suggest that the amount and duration of glucocorticoid coverage should be determined by: a) the preoperative dose of glucocorticoid taken by the patient, b) the preoperative duration of glucocorticoid administration, and c) the nature and anticipated duration of surgery.
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              Novel insights into the neuroendocrinology of critical illness.

              An unexplained hallmark of prolonged critical illness is the fact that food does not prevent or reverse protein wasting, while fat is paradoxically accrued. This 'wasting syndrome' often persists after the underlying disease has been resolved and thus perpetuates intensive care dependency. Although the crucial role of an intact hypothalamus-pituitary axis for homeostasis during stress is well recognized, the differences between the neuroendocrine changes observed in acute and prolonged critical illness were only recently described. Novel insights in this area are reviewed here. The initial endocrine stress response consists primarily of a peripheral inactivation of anabolic pathways while pituitary activity is essentially amplified or maintained. These responses presumably provide the metabolic substrates and host defense required for survival and to delay anabolism, and thus should be considered as adaptive and beneficial. Persistence of this acute stress response throughout the course of critical illness was hitherto assumed. This assumption has now been invalidated, since a uniformly reduced pulsatile secretion of ACTH, TSH, LH, prolactin (PRL) and GH has been observed in protracted critical illness, causing diminished stimulation of several target organs. Impaired pulsatile secretion of anterior pituitary hormones in the chronic phase of critical illness seems to have a hypothalamic rather than a pituitary origin, as administration of relevant releasing factors evoked immediate and pronounced pituitary hormone release. A reduced availability of TRH, one of the endogenous ligands of the GH-releasing peptide (GHRP) receptor (such as the recently discovered ghrelin) and, in very long-stay critically ill men, also of GHRH, appear to be involved. This hypothesis was further explored by investigating the effects of continuous i.v. infusion of GHRH, GHRP, TRH and their combinations for several days. Pulsatile secretion of GH, TSH and PRL was re-amplified by relevant combinations of releasing factors which also substantially increased circulating levels of IGF-I, GH-dependent binding proteins, thyroxine and tri-iodothyronine (T3) while avoiding a rise in reverse T3. Active feedback-inhibition loops prevented overstimulation of target organs and metabolic improvement was noted with the combined infusion of GHRP and TRH. Whether this novel endocrine strategy will also enhance clinical recovery from critical illness remains to be explored.
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                Journal
                anales
                Anales de la Facultad de Ciencias Médicas (Asunción)
                An. Fac. Cienc. Méd. (Asunción)
                EFACIM. Editorial de la Facultad de Ciencias Médicas - Universidad Nacional de Asunción (Asunción, Central, Paraguay )
                1816-8949
                June 2009
                : 42
                : 1
                : 27-36
                Article
                S1816-89492009000100004
                d80da136-1218-45b6-ad46-e15cf7d68613

                This work is licensed under a Creative Commons Attribution 4.0 International License.

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                Figures: 0, Tables: 0, Equations: 0, References: 23, Pages: 10
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                SciELO Paraguay

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                Cortisol levels,Niveles de cortisol,pacientes críticos,critical ill patient

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