Carditrophin-1 (CT-1) level and Echocardiographic changes in macrosomic neonate infants

Document Type : Original Article

Authors

1 Department of Pediatrics, Faculty of Medicine, Minia University, El-Minya, Egypt.

2 Department of Pediatrics, Faculty of Medicine, Minia University, El-Minya, Egypt

3 2 Departments of Clinical Pathology, Faculty of Medicine, Minya University, El-Minya, Egypt

Abstract

Background: Fetal macrosomia, or otherwise large-for-gestational - age (LGA) fetus/infant, 
applies to birth weight (BW) between 4000 and 4500g, and BW > 90th percentile for 
gestational age. Cardiotrophin-1(CT-1), cardiomyocytes-produce chemokine, member of the 
interleukin- 6 cytokine family, which acts upon the glycoprotein (GP) 130 trans- membrane 
receptor, plays fundamental role in fetal heart development this is up-regulated by hypoxia 
and inflammation and exerts potent hypertrophic action on cardiac cells. It mediates the 
hyperglycemia/hyperinsulinemia-induced myocardial hypertrophy and systemic atherosclerosis, and are actively involved in cardiovascular pathology. Aim of the study: To evaluate the 
Cardiotrophin-1level and echocardiographic findings in the macrosomic neonate's in maternity 
and children hospital. Methods: It is a case control study. A total 80 neonates enrolled. They 
were divided into 2 groups; 40 neonates' were macrosomic, 40 neonates control were healthy. Cord 
blood was collected and analyzed for plasma level of cardiotrophin-1 and echo study for cases 
and control. The two groups were subjected to careful detailed history perinatal history, 
complete clinical examination, echo study, and laboratory investigations including plasma 
level of cardiotrophin-1, random blood sugar. Results: There was a significant difference in 
weight, length, body area surface of macrosomic neonates at p <0.001. CT-1 is significantly 
high in Macrosomic neonates p<0.001. ASD was comment defect in our study present in 
eighteen (56.3%) Macrosomic neonates, while the increase in IVSD was highly significant in 
macrosomic neonates compared to control. A subgroup analysis (in the Macrosomic group) 
showed increased cord blood CT-1 concentrations in Macrosomic neonates with CHD, as 
compared to Macrosomic neonates without CHD (p1 =0.029). Subgroup analysis (in the 
Macrosomic group) showed increased cord blood CT-1 concentrations in IDM median 
280(pg. /mL) as compared to controls median 59(pg. /mL) p2 <0.001, CT-1 concentrations 
was significantly elevated in Macrosomic of IDM Median 280(pg. /mL) as compared to 
Macrosomic of Non-diabetic mothers p1<0.001, but still significantly high in Macrosomic 
neonates of Non-diabetic mothers Median was 280 (pg. /mL) versus (59) in control p3<0.001.
CT-1 concentrations were similar in Macrosomic with CHD and Macrosomic without CHD 
neonates, and positively correlated with Infant RBS (r =0.949, r = 0.948 respectively 
p<0.001). CT-1 concentrations were positively correlated with body surface area and birth 
weight in Macrosomic with CHD (r =0.888, r =0.800 respectively) and Macrosomic without 
CHD neonates (r =0.917, r =0.920 respectively). Conclusion: plasma cardiotrophin-1 level is 
significant high in macrosomic neonates, cardiac hypertrophy and anomalies are common on 
macrosomic neonates.

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