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Cardiac troponin-I in the serum of infants of diabetic mothers

Published online by Cambridge University Press:  24 May 2005

Bülent Oran
Affiliation:
Department of Paediatrics, Meram Medicine Faculty, Selçuk University, Turkey
Lokman Çam
Affiliation:
Department of Paediatrics, Meram Medicine Faculty, Selçuk University, Turkey
Osman Başpınar
Affiliation:
Department of Paediatrics, Meram Medicine Faculty, Selçuk University, Turkey
Tamer Baysal
Affiliation:
Department of Paediatrics, Meram Medicine Faculty, Selçuk University, Turkey
İsmail Reisli
Affiliation:
Department of Paediatrics, Meram Medicine Faculty, Selçuk University, Turkey
Harun Peru
Affiliation:
Department of Paediatrics, Meram Medicine Faculty, Selçuk University, Turkey
Sevim Karaaslan
Affiliation:
Department of Biochemistry, Meram Medicine Faculty, Selçuk University, Turkey
Hasan Koç
Affiliation:
Department of Paediatrics, Meram Medicine Faculty, Selçuk University, Turkey
Mehmet Gürbilek
Affiliation:
Department of Biochemistry, Meram Medicine Faculty, Selçuk University, Turkey

Abstract

A transient form of hypertrophic cardiomyopathy has been previously described in infants of diabetic mothers. When it occurs, it is generally benign. The purpose of our study was to establish the extent of injury to the cardiomyocytes in symptomatic and asymptomatic patients with and without hypertrophic cardiomyopathy.

Thus, we compared 35 consecutive patients to 20 healthy controls, establishing the significance, if any, of differences in cardiac troponin-I and creatine kinase, including its MB-fraction, and seeking to establish the value of these parameters in the diagnosis of cardiac injury. We also determined to levels of glucose and insulin in the serum, and took note of electrocardiographic and echocardiographic investigations. Values were determined at the 1st and 7th days after admission in the patients, while parameters were measured in the control group only on the first day.

We found that the levels of cardiac troponin-I in the serum, known to be a marker for cardiac injury, were significantly elevated in symptomatic patients with life-threatening respiratory or haemodynamic distress. We speculate that transient ventricular hypertrophy is neither the cause nor the consequence of damage to the cardiomyocytes. It would be interesting, nonetheless, to determine the relationship, if any, between cardiomyocytic damage and clinical outcome.

Type
Original Article
Copyright
© 2003 Cambridge University Press

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