24
| 1 | 2012
Klinisk Biokemi i Norden
(
Fortsat fra side 23)
nostic performance. However, a ratio where the relative
copeptin increase during the test was divided with the
plasma sodium concentration at the end of the test was
able to separate central DI from primary polydipsia
with a sensitivity of 86% and specificity of 100%. Thus,
these findings suggest that copeptin measurement may
soon be included in the complex diagnostic algorithm
for diagnosing polydipsia.
Copeptin and early rule out of myocardial infarc-
tion
According to current guidelines, diagnosis of the
60-70%
of patients with acute myocardial infarction
(
AMI) without obvious electrocardiographic findings
relies on baseline plasma concentrations and the
dynamic response of the myocardial necrosis markers
troponin T or troponin I. These markers have low
diagnostic performance early after the onset of chest
pain due to a delayed cellular release after myocardial
damage. Patients presenting with chest pain must
therefore be observed for 6-9 hours before a potential
AMI diagnosis can be excluded (6). Introduction of
high-sensitive troponin assays and lowering of the
troponin cut-off limit to the 99
th
percentile has further
complicated the diagnostic performance of troponin
measurement (7). This is partly due to a high preva-
lence of stable troponin elevations in older patients and
in patients with chronic conditions such as heart fai-
lure or kidney failure. Consequently, there is a need for
early markers that will perform independently of myo-
cardial necrosis to increase the spatial performance of
biochemical markers in patients with suspected AMI.
Vasopressin is released after AMI in both humans
(8)
and in animal models. Vasopressin secretion in
AMI is not fully understood but may be triggered by
altered cardiac dynamics and a decrease in systemic
blood pressure. Also, vasopressin secretion may be
stimulated as a generalized response to life-threatening
disease along with ACTH and cortisone as part of the
rapid stress response. Experimental induction of AMI
in sheep has shown that vasopressin is released as early
as 40 minutes after occlusion of coronary arteries and
remains elevated for 12 hours (9).
Foto: Henrik Alfthan
