Copeptin for All

Calprotectin: a biomarker for both infant/childhood and adult disease

“…There is accumulating evidence suggesting that the origin of some forms of adult disease may occur during fetal life. The reported changes in copeptin 5,6 and calprotectin 1,4 levels support the "fetal programming" (or "fetal origins of adult disease") hypothesis which implies that alterations in fetal nutrition may result in developmental adaptations that permanently change the physiology and metabolism of the offspring, thereby predisposing individuals to metabolic, endocrine and cardiovascular disorders later in life 7,8 .…”

“…Another biomarker which may predict cardiovascular disease both in adults and in infants is copeptin 5,6 . Copeptin levels increase in cardiovascular diseases (such as ischemic stroke, acute myocardial infarction, heart failure and intracerebral hemorrhage) and traumatic brain injury 5,6 . Copeptin levels also increase in conditions associated with perinatal stress, such as birth acidosis, asphyxia, chorioamnionitis and sepsis 6 .…”

Inflammatory Mediators Across the Spectrum of Ankle-Brachial Index

“…These findings suggest that PTX3 is a better indicator for obstructive PAD than hsCRP. Copeptin, the C terminal fragment of proarginine vasopressin, is a stress hormone released in response to various stimuli 16) . The stimulation of hypothalamo-pituitary axis by several inflammatory mediators such as TNF- α , IL-1, and IL-6 is known to increase the copeptin levels 16) .…”

“…Copeptin, the C terminal fragment of proarginine vasopressin, is a stress hormone released in response to various stimuli 16) . The stimulation of hypothalamo-pituitary axis by several inflammatory mediators such as TNF- α , IL-1, and IL-6 is known to increase the copeptin levels 16) . Herein, we demonstrated that copeptin was negatively correlated with ABI and was a strong determinant of obstructive PAD.…”

“…Experimental studies have provided evidence on the relation of a wide range of cytokines revealing mortality with the cardiovascular diseases. These include the proatherogenic cytokines such as pentraxin-3 (PTX3), high sensitivity C- reactive protein (hsCRP), and soluble triggering receptor expressed on myeloid cells-1 (sTREM-1); pleiotropic cytokines like neopterin; and biomarkers of hemodynamic stress such as copeptin and N terminal probrain natriuretic peptide (NT-proBNP) 11–16) . PTX3 and hsCRP are the two most characteristic acute phase proteins from the pentraxin family; sTREM-1 is a recently identified cell surface receptor that propagates the proinflammatory cytokines, all of which are mediated through the nuclear factor kappa beta (NF- κ B)signaling, the key inflammatory pathway in the pathogenesis of atherosclerosis ( Fig.…”