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In the past few years, copeptin, which is a stable surrogate marker for arginine vasopressin (AVP) activity, has emerged as a marker for disease severity and as a predictor for outcome in the setting of acute illness.1 2 Increased levels of copeptin have been shown in septic shock,1 acute stroke,3 in myocardial infarction,4 and in community-acquired pneumonia.5 However, little is known about the dynamics of copeptin levels in acute illness and about its response to anti-inflammatory treatment. Earliest evidence for corticosteroid-dependent regulation of AVP comes from studies dating back to 1967 showing that administration of corticosteroids reduced AVP levels in patients with adrenal cortisol deficiency. Furthermore, corticosteroid treatment was shown to reduce AVP expression in the posterior pituitary.6 7 In 2008, a first study addressed the question of corticosteroid-dependent AVP regulation in a human model of endotoxinemia.8 Thereby, pretreatment with corticosteroids dose dependently inhibited the increase in copeptin levels. However, no study so far has investigated the dynamics of copeptin in acute disease treated with and …
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