Research Article

Correlations among copeptin, ischemia-modified albumin, and the extent of myocardial injury in patients with acute carbon monoxide poisoning

Published: September 01, 2015
Genet. Mol. Res. 14 (3) : 10384-10389 DOI: https://doi.org/10.4238/2015.September.1.5
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Abstract

This study evaluated the relationships among copeptin, ischemia-modified albumin (IMA), and extent of myocardial injury in patients with acute carbon monoxide poisoning (ACOP). A total of 110 patients with different degrees of ACOP were selected as the poisoning group, and 30 healthy individuals as the control group. The levels of troponin I (cTnI), IMA, and copeptin were detected. Based on the presence of complications, the patients were assigned to the complication (26 patients) or non-complication (84 patients) group. Levels of cTnI, IMA, and copeptin were compared among the control, complication, and non-complication groups. Compared with the control group, in the 2 h after admission, the IMA levels decreased and copeptin levels increased in the poisoning group; these changes were more significant in patients with severe ACOP than in those with mild ACOP, and the difference was statistically significant (P < 0.05). There were no differences in the IMA and copeptin levels between the groups 7 days after admission; the cTnI levels increased more significantly in patients with severe ACOP than in patients with mild and moderate ACOP, and the differences were statistically significant (P < 0.05). In the complication group, at 7 days after admission, the IMA levels decreased whereas the copeptin and cTnI levels were significantly higher than in the non-complication group, with a statistically significant difference (P < 0.05). IMA was negatively correlated with copeptin. IMA and copeptin detection is clinically useful in the early diagnosis and prognosis of ACOP-related myocardial injury and in guiding early clinical drug application.

This study evaluated the relationships among copeptin, ischemia-modified albumin (IMA), and extent of myocardial injury in patients with acute carbon monoxide poisoning (ACOP). A total of 110 patients with different degrees of ACOP were selected as the poisoning group, and 30 healthy individuals as the control group. The levels of troponin I (cTnI), IMA, and copeptin were detected. Based on the presence of complications, the patients were assigned to the complication (26 patients) or non-complication (84 patients) group. Levels of cTnI, IMA, and copeptin were compared among the control, complication, and non-complication groups. Compared with the control group, in the 2 h after admission, the IMA levels decreased and copeptin levels increased in the poisoning group; these changes were more significant in patients with severe ACOP than in those with mild ACOP, and the difference was statistically significant (P < 0.05). There were no differences in the IMA and copeptin levels between the groups 7 days after admission; the cTnI levels increased more significantly in patients with severe ACOP than in patients with mild and moderate ACOP, and the differences were statistically significant (P < 0.05). In the complication group, at 7 days after admission, the IMA levels decreased whereas the copeptin and cTnI levels were significantly higher than in the non-complication group, with a statistically significant difference (P < 0.05). IMA was negatively correlated with copeptin. IMA and copeptin detection is clinically useful in the early diagnosis and prognosis of ACOP-related myocardial injury and in guiding early clinical drug application.