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| 1 | 2012
Klinisk Biokemi i Norden
failure may be in connection with therapeutic vaso-
pressin inhibition in selected heart failure patients.
Selective vasopressin receptor (V
2
)
blockers, the so-
called Vaptans, have been tested in heart failure treat-
ment with only limited effects (23). However, copeptin
measurement prior to Vaptan therapy may help iden-
tify patients where vasopressin receptor blockade will
be beneficial and also patients where the therapeutic
effects are contraindicated. For instance, high copep-
tin concentrations combined with low plasma sodium
concentrations seem to be a reasonable patient group
eligible for vasopressin receptor blockade, whereas
patients suffering from hypovolemia and hypona-
triemia should not receive such treatment. Clinical
trials are currently being conducted in this important
field, and copeptin measurement may turn out to be
a biochemical “gate keeper” for this potent treatment
regimen.
Copeptin pitfalls
A few potential pitfalls in clinical measurement seem
reasonable to briefly address here. First of all, water
intake acutely affects the copeptin concentration in
plasma (3). In fact, this feature is used in testing for
diabetes insipidus. But for standard plasma measu-
rement in for instance cardiac patients, there is no
standardisation concerning this frequent and phy-
siological event. While water intake may not grossly
affect the results in larger clinical studies, it may still
have a crucial impact on singular patients that are mis-
takenly identified as being at high-risk for morbidity
and death, while the increased copeptin concentration
only reflected water intake prior to blood sampling.
In AMI, the potential impact of water intake is less
severe, as it will not lead to missed diagnoses. It may
though blur the clinical interpretation, and some
discussion of water intake prior to blood sampling
should at least be considered. Second, patients with
severe bleedings may also display increased copeptin
concentrations, for which the underlying mechanism
has been elegantly demonstrated in monkeys (24).
This association to (presumably rapid) changes in
blood volume needs to be explored further in order
to identify possible thresholds for copeptin secretion.
Third, glucocorticoid treatment is known to attenuate
the copeptin response, a fact that could be important
if copeptin is implemented as a rapid rule-out test in
AMI. Finally, the mechanism behind increased copep-
Condition
Copeptin levels
in patients with
favorable out-
come (pmol/L)
Copeptin levels
in patients that
died or with
adverse outcome
(
pmol/L)
AUC for
predicting
death or adverse
outcome
Reference
Acute Heart failure - (14 days)
24 (11–49)
135 (56–272)
0.80 (0.76–0.84) 25
Chronic heart failure - (3.6 years) 16.1 (1.7–143)
28.8 (1.1–111.9) 0.72 (0.64–0.80) 26
Myocardial infarction
7.2(0.3–523)
32(2.4–330)
0.79(0.73–0.86)
27
Ischemic stroke
8.2(4.5-14-5)
19.4(9.7-36-6)
0.73(0.67-0.78)
28
Intracerebral hemorrhage
11.9(3.2-19.8)
32.4(9.5-97.8)
0.88(0.75-1.0)
29
Traumatic brain injury
N.A.
1
N.A.
1
0.87(0.79-0.93)
30
Chronic obstructive pulmonary
disease
9.6(5-21)
23.5(10.7-44)
N.R.
2
31
Sepsis
59.1(8.45–386)
144(46.5–504)
0.75(0.61–0.86)
24
Pneumonia
12.4(4.9–22.6)
44.2(32.0–83.4)
0.86(0.83–0.89)
32
1
Not applicable. Copeptin measu-
red with method not comparable
with standard method.
2
Not reported.
Median value.
Inter quartile
range in paren-
thesis
Median value.
Inter quartile
range in paren-
thesis
95%
confidence interval in
parenthesis
Table 1.
Copeptin concentrations in critical diseases.
(
Fortsat fra side 25)
