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ORIGINAL ARTICLE
Year : 2020  |  Volume : 33  |  Issue : 1  |  Page : 152-156

Study of serum leptin level in children with cyanotic and acyanotic congenital heart disease


Department of Pediatrics, Faculty of Medicine, Menoufia University Hospitals, Menoufia University, Shebin Elkom, Egypt

Date of Submission03-Jan-2017
Date of Decision01-Mar-2017
Date of Acceptance03-Mar-2017
Date of Web Publication25-Mar-2020

Correspondence Address:
Rania S.H. Ali
Tala City, Menoufia Governorate
Egypt
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/mmj.mmj_21_17

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  Abstract 


Objective
The aim of this study was to measure serum leptin levels in children with cyanotic and acyanotic congenital heart disease and to examine its possible role in growth in these children.
Background
Leptin has been shown to be an integral component of energy homeostasis and regulation of body weight. Leptin regulates adipose tissue mass and correlates with the fat mass. Research on the physiological function of leptin has primarily focused on its role in the pathogenesis of obesity. Children with congenital heart disease are at increased risk for poor growth. Several factors may play a role in poor growth, including feeding difficulties, increased caloric requirements, and the effects of cardiac lesions on growth regulation.
Patients and methods
This study was carried out over 1 year on 35 patients with congenital heart disease [20 patients were acyanotic (12 boys, 8 girls) and 15 patients were cyanotic (9 boys, 6 girls)] in the Pediatric Cardiology Department in Menoufia University Hospital and 35 apparently healthy children of the same age (range: 3 months–12 years), sex, and socioeconomic status. All patients and controls were subjected to a complete assessment of history, a thorough clinical examination, chest radiograph, ECG, echocardiography, and measurement of serum leptin level.
Results
Children with cyanotic congenital heart disease had statistically significant lower weight, length, mid-arm circumference, and BMI. There was no statistically significant difference in serum leptin levels in the cyanotic, acyanotic, and control groups. Serum leptin level was correlated positively with BMI and mid-arm circumference in all groups.
Conclusion
Serum leptin level did not change in children with acyanotic and cyanotic congenital heart disease, suggesting that other factors may regulate nutrient intake, growth, weight, and energy input and output in these children.

Keywords: congenital heart disease, growth, leptin


How to cite this article:
Hassan FM, Khatab AA, El-Zayat RS, Habib MS, Ali RS. Study of serum leptin level in children with cyanotic and acyanotic congenital heart disease. Menoufia Med J 2020;33:152-6

How to cite this URL:
Hassan FM, Khatab AA, El-Zayat RS, Habib MS, Ali RS. Study of serum leptin level in children with cyanotic and acyanotic congenital heart disease. Menoufia Med J [serial online] 2020 [cited 2020 Mar 30];33:152-6. Available from: http://www.mmj.eg.net/text.asp?2020/33/1/152/281272




  Introduction Top


Congenital heart disease (CHD) is the most common cause of major congenital anomalies, representing a major global health problem. Twenty-eight percent of all major congenital anomalies consist of heart defect. The prevalence of CHD varies widely among studies worldwide. The estimate of eight per 1000 live births is generally accepted as the best approximation[1].

CHD is a type of defect or malformation in one or more structures of the heart or blood vessels that occurs before birth in the early weeks of pregnancy when the heart is in the process of being formed. Such an abnormality is often present in any part of the heart at birth, and may produce symptoms at birth, during childhood, and sometimes not until adulthood. This defect is among the most common birth defects and is a leading cause of death. This abnormality may be so slight that the baby appears healthy at birth, even for many years, or might be so severe that infants develop a life-threatening condition. Almost 40–50% of infants with CHD are diagnosed within the first week, whereas 50–60% will be detected during the first month[2].

Ventricular septal defect is the most common CHD[3]. Atrial septal defects are the second most common congenital lesion in adults after bicuspid aortic valves[4].

Leptin has been shown to be an integral component of energy homeostasis and regulation of body weight. Leptin regulates adipose tissue mass and correlates with the fat mass; however, the circulating levels are altered by energy intake[5].

Leptin is a hormone that decreases food intake and increases energy expenditure[6]. It has been suggested that leptin may act as a starvation signal, such that low levels trigger the hypothalamic–pituitary–adrenal axis and high levels may play a role in the negative-feedback function of this axis[7].

Research on the physiological function of leptin has primarily focused on its role in the pathogenesis of obesity. However, its role in the negative energy imbalance is unclear. Increased energy expenditure is a primary factor in the reduced growth in infants with cyanotic CHD[5].

Children with CHD are at increased risk for poor growth. Several factors may play a role in poor growth, including feeding difficulties, increased caloric requirements, and the effects of cardiac lesions on growth regulation[8].

In patients with CHD, leptin, ghrelin, and tumor necrosis factor-α, serum levels appear to regulate nutrient intake, growth, weight, and energy intake and output. It is also claimed that there is a relationship between CHD, malnutrition, and growth retardation among children[2].

The aim of this study was to measure serum leptin levels in children with cyanotic and acyanotic CHD and to examine its possible role in growth in these children.


  Patients and Methods Top


The study was carried out on 35 patients with CHD (20 patients were acyanotic, with a mean age of 20.8 ± 35.52 months, and 15 patients were cyanotic, with a mean age of 19.4 ± 36.59 months) in the Pediatric Cardiology Department of Menoufia University Hospital and 35 apparently healthy children with a mean age of 22.2 ± 39.13 months between July 2014 and July 2015. The study was approved by the Ethical Committee of Menoufia Faculty of Medicine and informed consent was obtained from the guardian of each patient.

Inclusion criteria

Children with acyanotic CHD and cyanotic CHD were included in the study.

Exclusion criteria

Patients with congenital anomalies, chromosomal abnormalities, other chronic disease, and acquired heart disease were excluded from the study.

All patients and controls were subjected to the following:

  1. Complete assessment of history including age, sex, nutritional history, family history, admission to hospital, and the reason for admission to the hospital


  2. Thorough clinical examination with a special focus on the following:


    1. Vital signs
    2. Anthropometric measurements including height (cm), weight (kg), mid-arm circumference (MAC) (cm), and BMI (kg/m2) using the Z-score


  3. Cardiac examination: inspection, palpation, percussion, and auscultation
  4. Investigations: oxygen saturation by arterial blood gases and pulse oximetry, chest radiograph, ECG, echocardiography using a Philips HD 11 (Philips Health Care Company, Amsterdam, Holland) machine, serum leptin level (ng/ml) using the DRG Leptin EL1SA Kit (DRG International, Inc., Springfield Township, New Jersey, United States).


Statistical analysis

The data collected were tabulated and analyzed using the statistical package for the social science software 20 (SPSS Inc., Chicago, Illinois, USA) on an IBM compatible computer.

The results were described as ranges, means ± SD. The χ2-test, the Mann–Whitney U-test, the t-test, and the Kruskal–Wallis test were used. A P value less than 0.05 was considered to be significant.

The Pearson correlation was used for normally distributed quantitative variables, whereas Spearman's correlation was used for quantitative variables that were not normally distributed or when one of the variables was qualitative.


  Results Top


Cyanotic patients had significantly insufficient feeding compared with acyanotic patients (P < 0.05) [Table 1].
Table 1: Comparison of feeding data between the groups studied

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Children with cyanotic CHD had statistically significantly lower weight and length (P < 0.001) [Table 2].
Table 2: Comparison of anthropometric measures between the groups studied

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Children with cyanotic CHD had statistically significantly lower MAC and BMI (P < 0.05) [Table 2].

There was no statistically significant difference in serum leptin levels between the acyanotic, cyanotic, and control groups (serum leptin levels were 2.71 ± 1.79, 2.31 ± 1.51, and 2.49 ± 1.91 ng/ml, respectively; P > 0.05) [Table 3] and [Figure 1].
Table 3: Comparison of serum leptin between the groups studied

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Figure 1: Serum leptin level among groups.

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Serum leptin level was correlated positively with BMI in cyanotic and acyanotic groups and MAC in all groups (r = 0.38, P < 0.05; r = 0.75, P < 0.001; r = 0.84, P < 0.001; r = 0.40, P < 0.05; respectively) [Table 4] and Figs. 2–4).
Table 4: Correlation between serum leptin level and some variables

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  Discussion Top


The cause of growth retardation in CHD is multifactorial[9]. In cyanotic CHD, many patients clearly show loss of fat. Increased energy expenditure is a primary factor in the reduced growth in infants with cyanotic CHD[10]. Leptin is an adipocyte-derived hormone that is essential for normal regulation of body weight. Leptin regulates adipose tissue mass and correlates with fat mass[11].

In our study, nutritional history obtained from the mother in terms of the quality and quantity of feeding and time of weaning showed that cyanotic patients had significantly insufficient feeding than acyanotic patients.

Varan et al.[9] found that cyanotic patients with pulmonary hypertension had significantly less nutrient intake than acyanotic patients.

In contrast to our results, Hallioglu et al.[5] found that calorie and protein intake was increased in the cyanotic group on the basis of the mothers' records of intake of nutrients of patients; 3-day dietary data were obtained. These records were analyzed and quantified for the daily average calorie and protein intake.

In our study, patients with cyanotic CHD showed greater growth retardation as they had statistically significantly lower weight, length, MAC, and BMI than acyanotic patients and healthy controls.

Hallioglu et al.[5] found that patients with congenital cyanotic heart diseases had statistically significantly lower height, MAC, and BMI than acyanotic patients, which support our results.

Our results are also supported by the results of Aydin et al.[12], who found that BMI levels were significantly lower in the cyanotic group compared with the acyanotic group. Zhang et al.[13] found that patients with CHD had lower BMI.

In contrast to our results, Shahramian et al.[2] found that there was no significant difference in weight, height, and BMI between cyanotic, acyanotic patients, and healthy controls.

Leptin is a hormone that decreases food intake and increases energy expenditure[5].

In our study, there was no statistically significant difference between acyanotic patients, cyanotic patients, and healthy controls in serum leptin levels, suggesting that other factors affect growth retardation in children with CHD. Shahramian et al.[2] also found the same result.

Hallioglu et al.[5] and Aydin et al.[12] found that there was no significant difference in plasma leptin levels between cyanotic and acyanotic patients despite lower BMI in cyanotic patients and this is in agreement with our study and indicates that there are factors other than BMI affecting serum leptin level in children with CHD.

In contrast to our results, Rao et al.[14] found that children with CHD had significantly lower serum leptin levels than healthy controls.

El-Melegy et al.[15] and Zhang et al.[13] found that serum leptin level in all children with CHD was significantly higher than that of the healthy controls and this is not in agreement with our results.

This difference in serum leptin levels in children with CHDs among different studies may be because of multiple factors affecting serum leptin levels in those children. It is well known that leptin is correlated positively with BMI in humans[12], but other factors such as hypoxia, severe pulmonary stenosis, cardiomegaly, and/or heart failure lead to an increase in serum leptin levels in children with CHD[16].

Previous studies have shown that in humans, circulating leptin level is positively correlated with BMI. Our findings of a positive correlation between serum leptin level with BMI and MAC in cyanotic patients, acyanotic patients, and healthy controls support this view. Shahramian et al.[2] and Hallioglu et al.[5] found that there is a positive correlation between serum leptin level and BMI in cyanotic and acyanotic patients.

Hallioglu et al.[5] found that there is a positive correlation between plasma leptin level and MAC in cyanotic and acyanotic patients, which supports our results.

Rao et al.[14] found that there is a positive correlation between serum leptin level and BMI in obese, overweight, and normal controls and children with CHD.

In the study carried out by Aydin et al.[12], plasma leptin levels were correlated positively with BMI only in the acyanotic group, but not in the cyanotic group.

In our study, there was a negative correlation between serum leptin level and arterial oxygen saturation, but this was not statistically significant. This is supported by the study carried out by Aydin et al.[12].


  Conclusion Top


Children with cyanotic CHD are at an increased risk for poor growth. Chronic hypoxia and decreased nutrient intake are important factors in growth retardation in children with CHDs.

Serum leptin level did not change in children with acyanotic and cyanotic CHD, suggesting that other factors may regulate nutrient intake, growth, weight, and energy input and output in these children. Further investigations are needed to assess the role of different factors in growth failure among children with CHD.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Van der Linde D, Konings EE, Slager MA, Witsenburg M, Helbing WA, Takkenberg JJ et al. Birth prevalence of congenital heart disease. J Am Coll Cardiol 2011; 58:2241–2247.  Back to cited text no. 1
    
2.
Shahramian I, Noori MN, Hashemi M, Sharafi E, Baghbanian A. Study of serum levels of leptin, ghrelin and tumour necrosis factor-alpha in child patients with cyanotic and acyanotic congenital heart disease. J Pak Med Assoc 2013; 63:1332–2013.  Back to cited text no. 2
    
3.
Rubio AE, Lewin MB. Ventricular septal defects. In: Allen HD, Driscoll DJ, Feltes TF, Shaddy RE, editors. Moss and Adams heart disease in infants, children and adolescents. 8th ed. Philadelphia: PA 19103 USA: Williams & Wilkins; 2013. pp. 713–715.  Back to cited text no. 3
    
4.
Badran HM, Sultan GD, Atwa AM. Atrial septal defects: clinical presentation and recent approach in its diagnosis and treatment. Menouf Med J 2014; 27145–151.  Back to cited text no. 4
    
5.
Hallioglu O, Alehan D, Kandemir N. Plasma leptin levels in children with cyanotic and acyanotic congenital heart disease and correlations with growth parameters: Int J Cardiol 2003; 92:93–97.  Back to cited text no. 5
    
6.
Murdoch DR, Rooney E, Dargie HJ, Morton JJ, McMurray JJ. Inappropriately low plasma leptin concentration in the cachexia associated with chronic heart failure. Heart 1999; 82:352–356  Back to cited text no. 6
    
7.
Soliman AT, Elzalabany MM, Salama BM, Ansari BM. Serum leptin concentration leptin during severe protein energy malnutrition: correlation with growth parameters and endocrine function. Metabolism 2000; 49:819–825.  Back to cited text no. 7
    
8.
Daymont C, Neal A, Prosnitz A, Cohen MS. Growth in children with congenital heart disease: Pediatrics 2013; 131:236–242.  Back to cited text no. 8
    
9.
Varan B, Takel K, Yilma ZG. Malnutrition and growth failure in cyanotic and acyanotic congenital heart disease with and without pulmonary hypertension. Arch Dis Child 1999; 81:49–52.  Back to cited text no. 9
    
10.
Leitch CA, Karn CA, Peppard RJ. Increased energy expenditure in infants with cyanotic congenital heart disease. J Pediatr 1998; 133:755–760.  Back to cited text no. 10
    
11.
Kavazarakis E, Moustaki M, Gourgiotis D. Relation of serum leptin levels to lipid profile in healthy children. Metabolism 2001; 50:1091–1094.  Back to cited text no. 11
    
12.
Aydin HI, Yozgat Y, Demirkaya E, Olgun A, Okutan V, Lenke MK, et al. Correlation between vascular endothelial growth factor and leptin in children with cyanotic congenital heart disease. Turk J Pediatr 2007; 49:360–364.  Back to cited text no. 12
    
13.
Zhang YH, Xiang RL, Hu XT. Changes of serum leptin and vascular endothelial growth factor in children with congenital heart disease. Chin J Contemp Pediatr 2009; 10:802–805.  Back to cited text no. 13
    
14.
Rao GSN, Gurumurthy P, Gururajor P, Arumugano SB, Cherian KM. Clinical and biochemical parameters in relation to serum leptin levels in south Indian children and adolescents. Indian J Pediatr 2010; 77:555–559.  Back to cited text no. 14
    
15.
EL-Melegy NT, Mohamed NA. Angiogenic biomarkers in children with congenital heart disease: possible implications. Ital J Pediatr 2010; 36:32–45.  Back to cited text no. 15
    
16.
Soliman AT, Yasin M, Kassem A. Leptin in pediatrics, a hormone from adipocytes that wheels several functions in children. Indian J Endocrinol Metab 2012; 16:577–587.  Back to cited text no. 16
    


    Figures

  [Figure 1], [Figure 2], [Figure 3], [Figure 4]
 
 
    Tables

  [Table 1], [Table 2], [Table 3], [Table 4]



 

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