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Bei kritisch kranken PatientInnen kommt es häufig zum Auftreten einer Hyperglykämie welche eindeutig mit einer gesteigerten Mortalitätsrate assoziiert ist. Der aktuell verfügbaren Datenlage entsprechend sollte eine intravenöse Insulintherapie bei Blutzuckerwerten > 180 mg/dl begonnen werden und ein Zielbereich zwischen meist 140–180 mg/dl angestrebt werden. In critical illness hyperglycemia is associated with increased mortality. Based on the currently available evidence, an intravenous insulin therapy should be initiated when blood glucose is above 180 mg/dl. After initiation of insulin therapy blood glucose should be maintained between 140 and 180 mg/dl. Version of record

Laboruntersuchungen helfen Ursachen von Osteopathien aufzudecken und Geschwindigkeit und Bilanz des Knochenumbaus zu beurteilen. Diese Faktoren können durch Resorptions- und Anbaumarker erfaßt werden. Für einige Marker haben wir geschlechtsspezifische Referenzbereiche evaluiert. Die Konzentrationsveränderungen zirkulierender Biomarker zeigen Erfolg oder Mißerfolg von osteoprotektiven Therapien erheblich rascher an als densitometrische Messungen. Die zur Interpretation von Verlaufsbeobachtungen wichtigen kleinsten signifikanten Änderungen der Markerspiegel liegen zwischen 15 % und 60%.

Adequate adrenocortical function is essential to survive critical illness. Most critically ill patients display an elevated plasma Cortisol level, reflecting activation of the pituitary-adrenal axis, which is considered to be a homeostatic adaptation. In the setting of critical illness, the failure of an appropriate neuroendocrine response can lead to the picture of vasopressor-dependent refractory hypotension. In randomised trials with patients in septic shock, a more rapid haemodynamic recovery was obtained with physiological doses of hydrocortisone than with placebo. The observed haemodynamic response following hydrocortisone administration supports the concept of relative adrenal insufficiency. Causes of this relative adrenal insufficiency are a dysfunction of the hypothalamic-pituitary-adrenal axis and/or Cortisol resistance. There is increasing evidence that Cortisol physiology and regulation are substantially altered in the course of septic shock. Several controlled studies have shown that stress doses of hydrocortisone given in patients with septic shock reduce the time to shock reversal and decrease mortality. A multicenter large-scale trial (CORTICUS) is on the way investigating the benefit of stress doses of hydrocortisone on the mortality of septic shock. In this review glucocorticoid physiology and regulation during septic shock and the effects of hydrocortison administration in the course of septic shock are being discussed.

BACKGROUND AND AIM: Several basic science studies support the existence of non-genomic glucocorticoid signaling in pancreas, liver, and adipocytes, but its clinical relevance has not yet been elucidated. This study aimed at investigating the rapid effects of hydrocortisone on the human metabolic response to glucose. SUBJECTS AND METHODS: In a randomized placebo-controlled crossover study, ten healthy men received an i.v. bolus of 0.6 mg/kg hydrocortisone once and placebo once 4 min before the administration of 330 mg/kg glucose. Cortisol, glucose, insulin, C-peptide, ghrelin, and peptide YY (PYY) levels were measured during the following 3 h. Minimal model analysis was performed for evaluating the metabolic response. RESULTS: Hydrocortisone attenuated the rise in plasma glucose during the initial 15 min following glucose administration (P=0.039), and it led to lower glucose levels during the first 2 h (P=0.017). This was accompanied by enhanced circulating insulin (P=0.02) and C-peptide (P=0.03) levels during the initial 15 min, and a 35% increase in the first-phase beta-cell function (P=0.003). Hydrocortisone decreased PYY concentrations during the initial 30 min (P=0.014), but it did not affect the ghrelin response to glucose. CONCLUSION: One i.v. bolus of hydrocortisone induces rapid effects on carbohydrate metabolism increasing the first-phase beta-cell function. The modulation of PYY plasma levels suggests the possible non-genomic effects of glucocorticoids on appetite-regulatory hormones.

Plasma concentrations of Epidermal Growth Factor (EGF) in healthy control persons do not change significantly during adult lifetime and no diurnal changes could be detected. In addition, no alterations of plasma EGF concentrations occur during acute and chronic stress and in all three trimesters of pregnancy. Thus, the previously suggested theories that EGF might play a causative role in the activation of the hypothalamic-pituitary adrenal axis during the stress reaction and in the prevention of peptic ulcers in pregnancy could not be confirmed by the present data.