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*Corresponding author: E-mail: hassanshora56@gmail.com;    
 
 
 

Asian Journal of Immunology 
 
2(1): 26-33, 2019; Article no.AJI.53002 
 

 
 

 

 

Asthma Severity and Serum Leptin Level in Obese 
Egyptian Children 

 
Enas F. Elngar1, Osama A. Zekry1, Mamdouh M. Ali1 and Hassan A. Shora1* 

 
1
Department of Pediatrics and Neonatology, Faculty of Medicine, Suez Canal University and  

Port-Said University, Egypt. 
 

Authors’ contributions  
 

This work was carried out in collaboration among all authors. Author EFE designed the study, 
performed the statistical analysis, wrote the protocol and wrote the first draft of the manuscript, 

Authors OAZ and MMA managed the analyses of the study. Author HAS managed the literature 
searches and contributed in writing the final manuscript. All authors read and approved the final 

manuscript. 
 

Article Information 
 

Editor(s): 
(1) Dr. Darko Nozic, Professor, Higher Medical School in Belgrade, University of Belgrade, Serbia. 

Reviewers: 
(1) Hanan Mohamed Hamed, National research Centre, Egypt. 

(2) Gayatri C. Gawade, Bharati Vidyapeeth Dental College and Hospital, India. 
Complete Peer review History: http://www.sdiarticle4.com/review-history/53002 

 
 
 
 

Received 22 September 2019  
Accepted 28 November 2019 
Published 04 December 2019 

 
 

ABSTRACT 
 

Background: The relation between leptin and asthma is still unclear especially in obese children. 
We hypothesized that high serum leptin concentrations would also be associated with asthma in 
obese Egyptian children. We aimed to evaluate serum leptin concentrations in asthmatic obese and 
none obese children to investigate their association with asthma and degree of asthma severity. 
Subjects and Methods: The study was carried out on 56 Children attended pediatric outpatient 
clinic of Suez Canal University hospital on Jan, 2016 to Dec 2016. They were divided into three 
groups (group 1) asthmatic obese children involved 16 child (group 2) asthmatic non- obese child; 
20 (group 3) 20 non asthmatic child as control. Diagnosis of asthma was done according to global 
initiative of asthma. Serum leptin level was assessed in all study groups by ELISA.  
Results: Serum leptin levels in obese asthmatic patients was 91.3±9.3 ng/ml ,while in non-obese 
asthmatics it was 87.8±5.6 ng/ml, finally in non-asthmatic control it was71.3±8.2  ng/ml (P value 
0.175). There was positive significant correlation between serum leptin levels and asthma severity 
(p = <0.001). There was also significant negative association of leptin with peak expiratory flow rate 
results; There was also significant relation between serum leptin levels and history of allergy as 

Original Research Article 



 
 
 
 

Elngar et al.; AJI, 2(1): 26-33, 2019; Article no.AJI.53002 
 

 

 
27 

 

well as family history of asthma (p = <0.001). There was significantly higher body mass index in 
asthmatics than non-asthmatics (p = 0.004).   
Conclusion: Leptin is playing an important role in assessment of asthma severity and is the most 
predictive factor for asthma severity when compared to body mass index, family history of asthma 
and history of allergy. 
 

 
Keywords: Asthma; leptin; asthma severity; body mass index. 
 

ABBREVIATIONS 
 
BMI : Body Mass Index; 
PEFR : Peak Expiratory Flow Rate test; 
ELISA : Enzyme-Linked Immunosorbent Assay; 
 

1. INTRODUCTION 
 
Asthma afflicts 339 million people worldwide and 
8.3% of US children and is considered the most 
common disease of children. The annual 
healthcare expenditures for asthma is estimated 
$ 81 billion in US and EUR72 billion in Europe 
since it is a major reason for pediatric emergency 
room visits, admissions in hospitals’ pediatric 
wards, Abstenance from schools in addition to 
the economic loss due to decreased parental 
work [1-3]. 
 
Bronchial Asthma is a chronic inflammation of 
the bronchial tree characterized, by completely or 
partially reversible airway obstruction, which may 
improve spontaneously or by specific therapy. 
Airway hyper-responsiveness is a narrowing of 
the airways due to a variety of stimuli, such as 
allergens and nonspecific triggers and infections 
[4]. 
 
The prevalence of asthma and allergies is 
increasing in both western and developing 
countries. Despite a large volume of clinical and 
epidemiological research within affected 
populations, the etiology and risk factors of these 
conditions remains poorly understood [5]. 
Several epidemiological studies have shown that 
the prevalence of bronchial asthma and obesity 
is increasing concomitantly worldwide among 
children and young adults [6]. Obesity may be 
associated with respiratory symptoms via cardio-
respiratory deconditioning, physiological 
restriction of the chest wall by excess adipose 
tissue, or comorbidities, including gastro 
esophageal reflux and sleep-disordered 
breathing [7]. Obesity is characterized by chronic 
low-grade systemic inflammation. Obese adipose 
tissue is infiltrated by macrophages that are a 
source of inflammatory cytokines [8], More than 
50 different adipocytokines are secreted by 

adipocytes. Adipocytokines are proteins that help 
regulate various body functions [9]. Serum leptin 
is pro inflammatory adipocytokine that affects 
both innate and adaptive immune responses, 
and its serum levels are markedly increased in 
obesity [10]. Leptin is one of the adipose tissue-
derived energy-regulating hormones and a 
product of the obesity gene. Circulating leptin is 
positively correlated with body fat percentage 
and body fat mass. In addition to its primary 
effects on energy regulation, which it exerts by 
inhibiting food intake and increasing energy 
expenditure, leptin has been found to play a 
regulatory role within the immune system [11]. 
The regulatory capacity of leptin is associated 
not only with adaptive immunity but also with the 
innate system [12]. Leptin promotes the 
production of nitric oxide and pro-inflammatory 
cytokines in macrophages and monocytes [10]. 
 
The aim of this study was to evaluate serum 
leptin concentrations in asthmatic obese and 
none obese children and its association with 
degree of asthma severity. 
 
What is known? 
 

 Serum leptin is pro inflammatory cytokine 
that affects both innate and adaptive 
immune responses, and serum levels are 
markedly increased in obesity. 

 Circulating leptin is positively correlated 
with body fat percentage and body fat 
mass. 
 

What is New? 
 

 Leptin is playing an important role in 
assessment of asthma severity. 

 There is a significant relation between 
serum leptin levels and history of allergy as 
well as family history of asthma.  

   

2. MATERIALS AND METHODS 
 
This study is observational cross-sectional case 
control. This study was conducted among 
asthmatic children in pediatric outpatients clinic 



 
 
 
 

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28 

 

in Suez Canal University hospital. Control group 
was normal healthy children. Fifty-six children 
were included; 20 non asthmatic children (control 
group) and 36 asthmatic children; 16 obese 
asthmatic and 20 non obese asthmatic, all aged 
above 3 years old. Diagnosis of asthma was 
done according to global initiative of asthma 
(GINA 2015).  
 
Obese children were identified as children with 
body mass index above 95th percentile for their 
age according to Egyptian growth charts. 
 
Inclusion criteria: Asthmatic children above 3 
years old who did not receive steroid treatment 
are included in the study without injury of vital 
organs including heart, liver and kidney. 
 

Exclusion criteria: children who receive 
treatment with steroid either by inhalation or 
systemic route or children with infection and 
severe allergic reactions are excluded from the 
study. The ethical committee of Suez Canal 
University hospital approved the study and 
signed informed consent of children’s guardians 
is obtained. 
 

Detailed history and full clinical examination was 
done. 
 

2.1 Pulmonary Function Test 
 

It was done by peak Expiratory Flow Rate test 
(PEFR) for children above five years old. 
 

2.2 Leptin Assessment  
 
Five ml blood samples was collected by a skilled 
and qualified technician at the outpatient clinic 
around 8 a.m. in the morning following an 
overnight fast. After collection, the blood samples 
was centrifuged for 10 minutes and serum leptin 

stored at −80 C. The materials used for collection 
was disposable, adequately labeled, and of 
recognized quality. Leptin levels measured using 
a commercially available enzyme-linked 
immunosorbent assay (ELISA) kit according to 
the manufacturer's instructions and standard 
guidelines. 
 

Statistical analysis was performed using SPSS 
for Windows statistical package, version 20. 
(SPSS, Inc., Chicago, Ill., USA). Data were 
expressed as mean ± SD. Student’s t test, Mann-
Whitney U test and χ

2
 test were used for 

comparing mean values. A p value <0.05 was 
considered statistically significant. 
 

3. RESULTS  
 

3.1 Demographic Data 
 

This study was carried out on fifty-six children 
divided as; 20 non asthmatic children (control 
group) and 36 asthmatic children; 16 obese 
asthmatic and 20 non obese asthmatic, all aged 
above 3 years old, the mean BMI in was 
21.3±5.8 and 16.6±2.4 in asthmatic and non-
asthmatic groups respectively. The mean age of 
asthmatic group was 7.3±3.3 while it was 8.5±3.6 
in non-asthmatic group, all these data are 
summarized in Table 1. 
 

Serum leptin was significantly higher in 
asthmatics than non-asthmatics (p=<0.001), but 
there was no significant relation between serum 
leptin in obese asthmatic and non-obese 
asthmatic (p=0.175) as shown in Table  2. 
 
Relation of serum Leptin and degree of 
asthma severity: Table 3 shows significantly 
higher serum leptin in severe asthmatics 
97.6±8.5, than moderate 89.3±4.6 and mild 
asthmatics 82.0±3.2 (p =<0.001) respectively. 

 

Table 1. Socio demographic parameters of study groups 
 

P value Non-obese 
asthmatics (20) 

Obese 
asthmatics (16) 

P value Non-
asthmatic (20) 

Asthmatic 
(36) 

 

   0.201 8.5±3.6 7.3±3.3 Age (years) 
   0.584 30.8±14.5 33.0±15.5 Body 

weight 
   0.081 132.3±21.4 122.0±19.8 Height  
   0.004* 16.6±2.4 21.3±5.8 BMI 
      Sex  
   0.577 11(55.0%) 17(47.2%) Males 
   0.201 9(45.0%) 19(52.8%) Females 
0.175 87.8±5.6 91.3±9.3 <0.001* 71.3±8.2 89.3±7.6 Serum 

leptin 
data was presented as means ± SD or No. and % 

* Statistically significant p <0.05; 
≠
 OR for sex (male/female) 



 
 
 
 

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29 

 

Table 2. Relation of serum leptin and degree of asthma severity 
 

P value 
 

Asthma severity  

Severe (8) Moderate (19) Mild (9) 

<0.001* 97.6±8.5 89.3±4.6 82.0±3.2 Serum leptin 
 

Table 3. Relation between serum leptin levels and history of allergy 
 

P value       Serum leptin (Mean ± SD)  

 Negative Positive  

010.0*  79.5±12.2 87.7±9.0 History of allergy 
<0100. .* 75.7±9.7 91.2±7.4 Family history of asthma 

 

Table 4. Comparison between serum leptin in study groups 
 

Serum leptin Group P value   P value 

Asthmatics 
 (36) 

Non-asthmatics 
(20)  

Obese 
asthmatics 
(16) 

Non-obese 
asthmatics 
(20) 

89.3±7.6 71.3±8.2 <0.001* 91.3±9.3 87.8±5.6 0.175 
* Statistically significant at p<0.05 

 

Table 5. Relation of clinical parameters of asthmatics and asthma severity 
 

 Asthma severity P value 

 Mild (9)  Moderate (19)  Severe (8)   

Age (years) 7.7±3.6 7.5±3.6 6.5±2.8 0.776 
Body weight 34.0±11.6 34.0±18.5 29.6±12.5 0.745 
Height  126.1±21.1 122.2±20.3 117.1±18.8 0.666 
BMI 21.3±6.0 21.5±6.2 20.9±5.5 0.995 
Sex      
Males 6(66.7%) 7(36.8%) 4(50.0%) 0.338 
Females  3(33.3%) 12(63.2%) 4(50.0%) 
History of allergy 3(33.3%) 8(42.1%) 5(62.5%) 0.503 
Family history of asthma 2(22.2%) 14(73.7%) 8(100.0%) 0.002* 
Serum leptin  82.0±3.2 89.3±4.6 97.6±8.5 <0.001* 
PEFR 146.1±50.9 140.2±67.9 151.1±62.9 0.824 

data was presented as means ± SD or No. and %; * Statistically significant p <0.05 

 
There was positive significant correlation 
between serum leptin levels and asthma severity 
(Correlation Coefficient was 0.862* and p value 
was <0.001) while it is demonstrated a significant 
negative association of leptin with PEFR results 
r=-0.468 and p<0.001. 
 

Relation between serum leptin levels and 
history of allergy: Table 2 shows a significant 
relation between serum leptin levels and history 
of allergy (p =0.019) as well as family history of 
asthma (p = <0.001). 
 

Relation between body mass index and 
asthma severity: Table 3 shows a significant 
moderate positive correlation between body 
mass index and asthma severity (rho=0.334, 
p=0.012). Table 4 Show Serum leptin was 
significantly higher in asthmatics than non-
asthmatics (p=<0.001) 

There was significant negative association 
between Peak Expiratory Flow Rate results and 
asthma severity.  r=-0.427and p=0.001. 
 

ROC curve of serum leptin for diagnosis of 
severe asthma showed serum leptin was 91.5% 
accurate in diagnosis of severe asthma 
(AUC=0.915, p<0.001). At cutoff value of 75.5, 
serum leptin was shown 100% Sensitivity        
and 75% Specificity for diagnosis of severe 
asthma. 
 

4. DISCUSSION  
 

Leptin is an obesity gene product derived from 
adipocytes and activates proinflammtory 
adipocytokines including tumor necrosis factor α, 
interleukine-6 and interferon-γ.   
 

This study showed no statistically significant 
difference between the two study groups in terms 



 
 
 
 

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30 

 

of socio demographic characteristics (age, body 
weight, height and sex) (p >0.05). 

 
In addition, the current study reported a 
significant difference between asthmatic and 
control groups in terms of BMI (21.3±5.8, 
16.6±2.4 respectively, p = 0.004). These findings 
are similar to those reported by Black et al who 
also found a significant difference between 
asthmatics and control groups in terms of BMI 
[13]. Furthermore, a recent meta-analytic study 
of 18 studies which included 73,252 children 
reported that overweight or obesity was a 
significant risk factor for asthma in obese 
children [14]. 
 
However our study revealed no statistically 
significant difference in BMI between obese and 
non-obese asthmatic children.  The present 
study showed that serum leptin levels of 
asthmatic children (89.3±7.6 ng/ml) were 
significantly higher than those of healthy control 
(71.3±8.2) p-value was <0.001. This coincides 
with the study done by About Yousif, et al.  who 
found a statistically significant difference in 
serum leptin values between asthmatics and 
controls being higher in asthmatics regardless to 
the body weight (p=0.034) [15] and also 
coincides with another two studies stated                   
that even after controlling of body mass index, 
leptin levels were increased in asthmatic children 
compared to non-asthmatic children [16,17] 
(Table 5).  

Our study showed that there was no significant 
difference between serum leptin in obese 
asthmatics and non-obese asthmatics p=0.175 
and this is consistent with results reported by 
Shore, et al. who also found no significant 
difference between the two groups (p > 0.05) 
[18]. It was also reported by another study which 
demonstrated that no differences in leptin or 
adiponectin levels in obese and non-obese 
children with asthma [19]. 

 
As regard to BMI, the present study showed a 
significant positive correlation of leptin and BMI 
(r= 0.434, p=0.001) (Table 6). This result is 
similar to the results reported by several 
researchers [20,21]. Yosif, et al. suggested that 
BMI is the main determinants for the variations of 
leptin [22]. As demonstrated by French 
Epidemiological Study on indirect effects of leptin 
on Genetics and Environment of Asthma EGEA 
revealed that leptin partially mediated the 
association between obesity and persistent 
asthma over time [23]. A recent longitudinal 
study used new mediation analysis to detect the 
direct and indirect effects mediated by leptin in 
asthma development confirmed the odds ratio of 
direct effect were 1.59 (95% CI: 0.95-2.97), 2.06 
(1.06-4.00) and 3.25 (1.01-9.41), respectively 
while the indirect effect mediated by leptin odds 
ratio were 1.68 (1.09-2.46), 1.55 (0.99-2.57) and              
1.99 (0.94-4.83), respectively [24]. Leptin 
mediated its effects by augmenting phagocytic 
function.  

 
Table 6. Socio demographic data of Asthmatic obese children 

 

Age in year Weight(kg) Height(cm) BMI sex Asthma severity 

10 47 130 27.8 female Mild 

5 34 14 26.2 Male Mild 

11 36.5 120 25.3 Female Moderate 

5 28 103 26.4 Female Moderate 

4 31 107 27.1 Male Mild 

13 66 152 28.6 Female Moderate 

8 45 126 28.3 Female Moderate 

7 37 117 27 Male severe 

6 37 112 29.5 female Moderate 

10 47 134 26.2 Male Moderate 

9 50 133 28.3 Female Severe 

4 25 97 26.6 Female Severe 

9 43 122 28.9 female Mild 

3.5 25 98 26 Male Moderate 

10.5 58 141 29.2 Female Moderate 

15 80 162 29.7 Female moderate 



 
 
 
 

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31 

 

 
 

Fig. 1. ROC curve of serum Leptin for diagnosis of asthma severity 
 

proliferation and alternation of macrophages and 
consequently led to increased secretion of 
proinflammatory cytokines. The latter include 
tumor necrosis factor α, reactive oxygen species 
and interleukin 6 [25]. 
 

Our study results showed that there was 
significantly negative correlation between leptin 
and PEFR results in total asthmatic patients (r=-
0.468 and p=0.001). This result agreed with the 
result of Sin and Man work who also reported a 
negative correlation between serum leptin levels 
and PEFR in asthmatic patients (r=-0.521and 
p=0.001) [26]. 
 

Our study also showed significant relation 
between serum leptin levels and history of allergy 
(p=0.019) as well as family history of asthma (p= 
<0.001). The positive correlation between history 
of allergy and serum leptin level is consistent 
with these results reported by Samra, et al. as 
there was a positive correlation between leptin 
levels and history of allergy (p=0.0058) [27]. 
 

Concerning the severity of asthma, this study 
showed that the mean ± SD of serum leptin in 
moderate asthmatics (89.3±4.6 ng/ml) was 
significantly higher than that of mild asthmatics 
(82.0±3.2 ng/ml) p< 0.001. These results were in 
accordance with those reported by the American 
College of Allergy, asthma and immunology 
study [28], that linked serum concentration of 
leptin to disease activity and severity, patients 
with intermittent asthma had value of 8.9 ng/dl, 
those with mild persistent asthma had levels of 
14.5 ng/dl and moderately persistent asthma 

patients had 18.9 ng/dl with P-value less than 
0.05. Shore et al. suggested that increase serum 
leptin can increase airway hyperresponsivness 
and exacerbate asthma [29]. 
 

Our results showed that the sensitivity of serum 
leptin for diagnosis of severe asthma showed 
serum leptin was 91.5% accurate (P <0.001). At 
cutoff value of 75.5, serum leptin was shown 
100% Sensitivity and 75% Specificity for 
diagnosis of severe asthma. These findings were 
similar to those reported by Tanju et al who 
reported 89% accuracy of serum leptin levels in 
severe asthma (P <0.001). Our results suggest 
that leptin is playing an important role in 
diagnosis and determining the severity of 
asthma. 
 

The study showed also that leptin is the most 
predictive factor for severity of asthma when 
compared to body mass index, family history of 
asthma and history of allergy which has low 
significant prediction for severity of asthma. 
 

5. CONCLUSION 
 
Asthma in obese children is significantly 
correlated with serum leptin levels and BMI. So, 
high leptin levels and BMI may serve as markers 
of asthma severity in obese children as well as 
potential future therapeutic targets in the era of 
advanced bionanotechnology.This approach can 
be possible via targeting vital cell signaling 
pathways by novel ligands that act as agonists or 
antagonists for crucial adaptor molecules in 
asthma pathogenesis mediated by leptin such as 



 
 
 
 

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32 

 

Parathyroid-hormone-related protein (PTHrP) 
and prostaglandin E2 (PTHrP/PPARγ) signaling 
pathway inhibitors. 
 

6. FUTURE RESEARCH DIRECTIONS 
 

Due to heterogeneity of obesity related asthma in 
children and its multifactorial nature of the 
disease with genetic-environmental interactions, 
it is difficult to find out precise markers. However, 
emerging novel biomarkers for severe asthma 
using multi-omics technologies such as 
proteomics, epigenetics, transcriptomics, 
metagenomics, gut microbiome and untargeted 
metabolomics is a promising approach. Novel 
innovative advances in quantum computational 
sciences, biostatistics and molecular 
bioinformatics of asthma are needed for 
appropriate phenotypic subclassification and 
searching for more precise future digital 
biomarkers and enabling progress of precision 
medicine for asthma. 
 

CONSENT  
 

Informed consent was obtained from all 
individual participants included in the study. 
 

ETHICAL APPROVAL  
 

All procedures performed in this study were in 
accordance with the ethical standards of the 
institutional and national research committee and 
with the 1964 Helsinki Declaration and its later 
amendments. 
 

COMPETING INTERESTS 
 

Authors have declared that no competing 
interests exist. 
 

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© 2019 Elngar et al.; This is an Open Access article distributed under the terms of the Creative Commons Attribution License 
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