Copeptin is associated with mortality and outcome in patients with acute intracerebral hemorrhage

Zweifel, Christian; Katan, Mira; Schuetz, Philipp; Siegemund, Martin; Morgenthaler, Nils G.; Merlo, Adrian; Müeller, Beat; Christ‐Crain, Mirjam

doi:10.1186/1471-2377-10-34

Cited by 74 publications

(51 citation statements)

References 33 publications

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“…Although copeptin is not a specific marker, unlike other neuromarkers it directly bypasses the blood-brain barrier and is excreted into systemic circulation and thus it reflects the intracerebral condition better (14). A significant correlation has been shown between copeptin levels and prognosis and the GCS at presentation, not only in patients presenting with ischemic stroke but also for acute intracerebral hemorrhages (15).…”

Section: Discussionmentioning

confidence: 99%

Copeptin levels in carbon monoxide poisoning

Güler¹,

Çevik²,

Keskin³

et al. 2017

Turk J Med Sci

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IntroductionCarbon monoxide (CO) poisoning is a health problem that frequently occurs in Turkey and worldwide. In Turkey, it accounts for 30% of the poisoning cases that end with death (1).This colorless, odorless, tasteless, and nonirritating gas is produced as a result of the incomplete burning of organic matter that can easily be absorbed by the lungs. CO poisoning can cause cerebral, cardiac, and general ischemia. The poisoning can be diagnosed according to the blood carboxyhemoglobin (COHb) levels. There is a weak correlation between blood COHb levels and organ damage. Poisonings higher than 60% end with death and at lower levels clinical findings range from mild to severe. It is not always possible to identify this using the COHb level (2). Biochemical markers other than COHb are being studied to identify the clinical outcomes of this poisoning with neurotoxic and cardiotoxic effects in particular (3).Copeptin is excreted from the posterior hypophysis simultaneously with vasopressin and reflects the amount of vasopressin in circulation. Copeptin is more stable than vasopressin in plasma and serum. Studies conducted have reported that copeptin and vasopressin levels float parallel to each other both in healthy individuals and in the critically ill patient population. Recently copeptin has been investigated as a diagnostic and prognostic factor in many diseases like pneumonia, heart failure, and hemorrhagic and septic shock and it has been identified that its levels rise in correlation with the severity of the disease (4-7).The aim of this study is to identify the copeptin levels in patients presenting to the emergency department with CO poisoning and to investigate its correlation with neurological damage.Background/aim: The aim of this study is to identify the copeptin levels in patients presenting with carbon monoxide (CO) poisoning to the emergency department and to investigate its correlation with the neurological effects. Materials and methods:The study group consisted of patients presenting with CO poisoning and carboxyhemoglobin levels >10%. Blood samples for copeptin levels were obtained twice, first at presentation then at the fourth hour of observation. The data were analyzed using SPSS 16 for Windows. Results:The median copeptin levels of the patient group were identified as 0.63 (0.39-1.06) ng/mL at hour 0 and 0.41 (0.31-0.49) at hour 4. The copeptin levels of the control group were 0.34 (0.25-0.42) ng/mL and were significantly lower than those of the patient group (P < 0.000). According to our results, 0.345 ng/mL for plasma copeptin level as the best cut-off level may be used with sensitivity of 94.0% and specificity of 60%. The copeptin levels at hour 0 were statistically significantly higher in the neurologically affected patients than those not affected (P < 0.001). Conclusion:In this study it was shown that blood copeptin levels increase in patients presenting to the emergency department with CO poisoning.

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Section: Discussionmentioning

confidence: 99%

Copeptin levels in carbon monoxide poisoning

Güler¹,

Çevik²,

Keskin³

et al. 2017

Turk J Med Sci

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“…Moreover, high levels of copeptin allowed prediction of 30-day mortality (AUC of 0.88) and poor functional outcome at 90 days (AUC of 0.68) [80]. In a larger study, it was shown that copeptin independently predicted 1-year mortality and poor outcome as well as early neurologic deterioration [81].…”

Section: Selection Of Blood Biomarkers In Ichmentioning

confidence: 99%

Potential Role of Blood Biomarkers in the Management of Nontraumatic Intracerebral Hemorrhage

Senn

Elkind

Montaner³

et al. 2014

Cerebrovasc Dis

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Background: Intracerebral hemorrhage (ICH), a subtype of stroke associated with high mortality and disability, accounts for 13% of all strokes. Basic and clinical research has contributed to our understanding of the complex pathophysiology of neuronal injury in ICH. Outcome rates, however, remain stable, and questions regarding acute management of ICH remain unanswered. Newer research is aiming at matching measured levels of serum proteins, enzymes, or cells to different stages of brain damage, suggesting that blood biomarkers may assist in acute diagnosis, therapeutic decisions, and prognostication. This paper provides an overview on the most promising blood biomarkers and their potential role in the diagnosis and management of spontaneous ICH. Summary: Information was collected from studies, reviews, and guidelines listed in PubMed up to November 2013 on blood biomarkers of nontraumatic ICH in humans.We describe the potential role and limitations of GFAP, S100B/RAGE, and ApoC-III as diagnostic biomarkers, F-Amyloid as a biomarker for etiological classification, and 27 biomarkers for prognosis of mortality and functional outcome. Within the group of prognostic markers we discuss markers involved in coagulation processes (e.g., D-Dimers), neuroendocrine markers (e.g., copeptin), systemic metabolic markers (e.g., blood glucose levels), markers of inflammation (e.g., IL-6), as well as growth factors (e.g., VEGF), and others (e.g., glutamate). Some of those blood biomarkers are agents of pathologic processes associated with hemorrhagic stroke but also other diseases, whereas others play more distinct pathophysiological roles and help in understanding the basic mechanisms of brain damage and/or recovery in ICH. Key Messages: Numerous blood biomarkers are associated with different pathophysiological pathways in ICH, and some of them promise to be useful in the management of ICH, eventually contributing additional information to current tools for diagnosis, therapy monitoring, risk stratification, or intervention. Up to date, however, no blood biomarker of ICH has been studied sufficiently to find its way into clinical routine yet; well-designed, large-scale, clinical studies addressing relevant clinical questions are needed. We suggest that the effectiveness of biomarker research in ICH might be improved by international cooperation and shared resources for large validation studies, such as provided by the consortium on stroke biomarker research (http://stroke-biomarkers.com/page.php?title=Resources). i 2014 S. Karger AG, Basel

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“…Serum copeptin levels may correlate with the volume of brain edema, but this has not been confirmed [113]. Levels are positively correlated with hematoma volume, death at 30 days following ICH, and poor functional outcome at 3 months as measured by the mRS and the Barthel Index [113]. Vasopressin inhibitors have been investigated as a potential therapeutic intervention [114].…”

Section: Othersmentioning

confidence: 97%