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ORIGINAL ARTICLE
Year : 2014  |  Volume : 11  |  Issue : 2  |  Page : 45-48

Association of obesity and thyrotropinemia in children and adolescents


Department of Endocrinology and Metabolism, Narayana Medical College and Hospital, Nellore, Andhra Pradesh, India

Date of Web Publication31-Mar-2014

Correspondence Address:
Rajendra Prasad Namburi
Department of Endocrinology and Metabolism, Narayana Medical College and Hospital, Chinthareddy Palem, Nellore - 524 004, Andhra Pradesh
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0973-0354.129649

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  Abstract 

Introduction: Alteration in the hypothalamo-pituitary-axis results in elevated thyroid stimulating hormone (TSH) in obesity. Aim: The aim of our study is to compare serum TSH level among obese and overweight children with normal weight and also to assess the relation between body mass index (BMI) and TSH in these children. Materials and Methods: A total of 124 patients aged between 6 and 17 years attending our obesity clinic were recruited. The patients were subdivided into three groups; Group 1: Normal weight (n = 24), Group 2: Overweight (n = 30), and Group 3: Obese (n = 70). All subjects underwent thyroid profile along with other routine tests. Fisher's exact test and Mann-Whitney U test were done to compare between study groups. Pearson's correlation analysis was done to assess the relationship between BMI and TSH. P < 0.05 was considered significant. Results: Out of 124 obese children and adolescents, 72 were females and 52 were and males. The overall mean age of the children was 11.99 ± 2.7 years (range 6.2-17 years). Subclinical hypothyroidism (5.5-10 mIU/L) was present 0/24 in Group 1, 13.33% (4/30) in Group 2, and 15.71% (11/70) in Group 3. The mean TSH values in Groups 1, 2, and 3 are 2.33, 3.03, and 3.35 mIU/L, respectively. Overall, serum TSH did not show correlation with BMI (r = 0.078; P = 0.681). Discussion: In this study, higher BMI resulted in elevated TSH levels, but there was no significant relation between severity of obesity and TSH. Large scale data from population based studies are required to confirm our findings.

Keywords: Adolescents, body mass index, children, hypothyroidism, obesity


How to cite this article:
Namburi RP, Ponnala AR, Srikanth KT, Raviraj RM, Palanki RR. Association of obesity and thyrotropinemia in children and adolescents. Thyroid Res Pract 2014;11:45-8

How to cite this URL:
Namburi RP, Ponnala AR, Srikanth KT, Raviraj RM, Palanki RR. Association of obesity and thyrotropinemia in children and adolescents. Thyroid Res Pract [serial online] 2014 [cited 2019 Sep 20];11:45-8. Available from: http://www.thetrp.net/text.asp?2014/11/2/45/129649


  Introduction Top


Obesity is occurring in epidemic proportions, turns out to be a major issue of public health concern throughout the world. [1] It leads to increase in overall morbidity and mortality. [1] The secular trends of obesity in India indicate an increasing prevalence of obesity, diabetes, and related cardiovascular risk factors not only in adults but also in the children and adolescents. [2] The estimated prevalence of overweight is about 15-18% and obesity is about 2-4% among Indian children. [3],[4] Although the prevalence of obesity in India is lower than in Western countries, the body composition and higher amount of centrally located body fat make the Indians including children more prone to significant morbidity. [5]

In general practice, the commonest laboratory evaluation in obese children includes thyroid function tests. Obesity affects hypothalamic-pituitary-thyroid axis directly or indirectly leading to alterations in thyroid function tests. The commonest observed change is mild elevation in thyroid stimulating hormone (TSH) and normal triiodothyronine (T3) and thyroxine (T4) hormones. [6] Regarding thyroxine replacement guidelines exist for adult population in subclinical hypothyroidism, but it is controversial in children. [7],[8]

Though TSH elevation with obesity is widely accepted, the data is conflict in regarding the changes in TSH with weight loss in obese children. Few studies have reported decrease in TSH with weight loss, whereas others did not show this reversal. [9],[10] Thus, it appears that body weight is a major determinant of level of serum TSH and it is not apparent from existing literature about the linear correlation between these two variables. [11] In the present study, we compared serum TSH level among obese and overweight children with normal weight and also assessed the relation between body mass index (BMI) and TSH in these children.


  Materials and Methods Top


We recruited 124 children and adolescents aged between 6 and 17 years, attending the endocrinology outpatient department after obtaining informed consent. Detailed clinical examination was done including anthropometry, pubertal status assessment, presence of goiter, acanthosis nigricans and any systemic features suggestive of syndromic obesity. Thyroid hormones (TSH, free T4 (FT4), and free T3 (FT3)) were determined in all the children. Thyroid function tests were done by chemiluminescence assay and intra and inter assay variations were less than 4.5%. The reference values considered as normal as per our laboratory were as follows: TSH (0.35-5.5mIU/L), FT3 (2.5-3.9pg/mL), and FT4 (0.61-1.12ng/dL). BMI was calculated as the weight in kilograms divided by square of the height in meters. Obesity was defined as BMI more than 95 th centile according to the body mass index (BMI) specific for age and sex as per Centers for Disease Control and Prevention (CDC) charts. Overweight was defined as BMI between 85 th and 95 th centile on the same chart. Normal weight was defined as BMI less than 85 th centile. Patients with TSH between 5.5 and 10 mIU/L, along with normal total FT3 and FT4 were considered to have subclinical hypothyroidism and were included in the study. Patients with serum TSH more than 10 mIU/L were considered to have overt hypothyroidism and excluded from the study. Smokers and children taking any medication likely to affect the weight and thyroid hormones, glucocorticoids, estrogen preparations, and antiepileptic drugs were excluded. Children with other possible endocrine or metabolic disorders were excluded from the study.

The patients were subdivided into three groups for analysis; Group 1: Normal weight (n = 24), Group 2: Overweight (n = 30), and Group 3: Obese (n = 70). Statistical analysis was done using Statistical Package for Social Sciences (SPSS) 17.0. Data were expressed as mean ± SD and comparison between groups was done by Mann-Whitney U test and Fisher's exact test. Relationship between BMI and TSH in an overall study population was done by Pearson's correlation analysis. A P < 0.05 was considered to be statistically significant.


  Results Top


Among 124 children and adolescents, 72 were females and 52 were males. The overall mean age of the children was 11.99 ± 2.7 years (range 6.2-17 years). [Table 1] shows the clinical and biochemical data of the study population.
Table 1: Clinical and biochemical characteristics of study population

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Females were more in obese and overweight group; whereas in normal weight group, males were more in number. Subclinical hypothyroidism was present 0/24 in Group 1, 13.33% (4/30) in Group 2, and 15.71% (11/70) in Group 3. The mean TSH values in Groups 1, 2, and 3 are 2.33, 3.03, and 3.35 mIU/L, respectively.

[Figure 1] depicts the TSH values of the study subjects. Mean TSH was not significantly different between the Groups 1 and 2 (2.33 ± 1.29 vs 3.03 ± 2.14 mIU/L; P = 0.121) and Groups 2 and 3 (3.03 ± 2.14 vs 3.35 ± 1.83 mIU/L; P = 0.197). However, there was significant difference in TSH levels between Groups 1 and 3 (2.33 ± 1.29 vs 3.35 ± 1.83 mIU/L; P = 0.027). Also, serum TSH did not show correlation with BMI in the entire study population.
Figure 1: Mean serum TSH values in the study subjects. Group 1: Normal weight (BMI < 85th centile), Group 2: (BMI: 85-95th centile) and Group 3: (BMI > 95th centil)

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  Discussion Top


In the present study, we studied TSH levels in normal weight, overweight, and obese children and adolescents (based on BMI percentile) and assessed the relation between BMI and TSH in these groups. The clinical profile was similar at presentation in both overweight and obese groups. Previous observational studies showed the prevalence of elevated TSH was seen in about 1-21% of obese children and adolescents. [12],[13] In one study by Hari Kumar et al., [14] showed the prevalence of subclinical hypothyroidism was more in obese children 30% (9/30) than overweight children 20% (4/20), but the observed difference was not statistically significant (P = 0.5219). Similarly, in our study the prevalence of subclinical hypothyroidism was more in obese children (15.71%, 11/70) than overweight children (13.33%, 4/30). Also, the observed difference was not statistically significant between obese and overweight groups (P = 0.228). The total prevalence of subclinical hypothyroidism in our study (15%) is quite lower than the study done by Hari Kumar et al., (26%) in obese children and this difference could be due to small sample size. [14]

Many studies have demonstrated elevation in serum TSH value in obese children when compared with normal weight children. [6],[12],[13] Similarly in the present study, TSH values were elevated and showed significant difference between obese children compared with normal weight children. Although, there is elevation in TSH levels in overweight and obese children compared to normal weight children; there exists no significant difference between normal weight vs overweight groups and overweight vs obese groups.

The adiopocytokine leptin is the most important link between obesity and hyperthyrotropinemia. Obese individuals have more adipose tissue and increased leptin production. The putative mechanism for elevated TSH in obese children involves leptin production which is known to stimulate thyrotropin releasing hormone (TRH) neurons in paraventicular nucleus. [15],[16],[17] The postulated etiology is an adaptive mechanism in expenditure of energy to avoid additional weight gain. Obesity also has indirect effects on hypothalamic-pituitary-thyroid axis resulting in elevation of TSH levels. [17] Neurotransmitters like neuropeptide Y (NPY) and agouti related peptide (AgRP) and hormones such as melanocyte stimulating regulate (MSH) which regulate body weight and satiation also have influence on leptin. [18],[19]

In one study done by Reinehr et al., [9] showed that elevated TSH concentrations in obese children were significantly reduced with substantial loss of weight. The probable mechanism could be due to lowering of leptin levels. However, it must be emphasized that this relation between TSH and leptin is not supported by all studies. Thus, it is suggested that the elevation of TSH seems to be rather a consequence of obesity than a cause of obesity. In another study done by Eliakim et al., [8] showed no beneficial effects with thyroxine replacement in obese children with thyrotropinemia. The limitations of the present study were: (1) Nonavailability of thyroid peroxisomal antibody, (2) limited size of controls, and (3) leptin levels were not measured. Also, we did not exclude patients with family history of obesity or thyroid illness and did not consider the influence of socioeconomic status on obesity.


  Conclusion Top


The present data suggests that moderately elevated TSH levels with normal T3 and T4 are frequently noted in obese children and adolescents. Obesity is associated with elevated TSH, but there is no significant association between serum TSH and severity of obesity. Elevation of TSH in obesity seems to be a consequence rather than a cause of obesity. Further, large scale population based studies are required to strengthen our findings.

 
  References Top

1.Adams KF, Schatzkin A, Haris TB, Kipnis V, Mouw T, Ballard-Barbash R, et al. Overweight, obesity and mortality in a large prospective cohort of persons 50 to 71 year old. N Engl J Med 2006;355:763-78.  Back to cited text no. 1
    
2.Marwaha RK, Tandon N, Singh Y, Aggarwal R, Grewal K, Mani K. A study of growth parameters and prevalence of overweight and obesity in school children from Delhi. Indian Pediatr 2006;43:943-52.  Back to cited text no. 2
    
3.Misra A, Vikram NK. Insulin resistance syndrome (metabolic syndrome) and obesity in Asian Indians: Evidence and implications. Nutrition 2004;20:482-91.  Back to cited text no. 3
    
4.Mehta M, Bhasin SK, Agrawal K, Dwivedi S. Obesity amongst affluent adolescent girls. Indian J Pediatr 2007;74:619-22.  Back to cited text no. 4
    
5.Kelishadi R. Childhood obesity today's and tomorrow's health challenge. Indian Pediatr 2008;45:451-2.  Back to cited text no. 5
[PUBMED]    
6.Michalaki MA, Vagenakis AG, Leonardou AS, Argentou MN, Habeos IG, Makri MG, et al. Thyroid function in humans with morbid obesity. Thyroid 2006;16:73-8.  Back to cited text no. 6
    
7.Biondi B, Cooper DS. The clinical significance of subclinical thyroid dysfunction. Endocr Rev 2008;29:76-131.  Back to cited text no. 7
    
8.Eliakim A, Barzilai M, Wolach B, Nemet D. Should we treatelevated thyroid stimulating hormone levels in obese childrenand adolescents? Int Pediatric Obes 2006;1:217-21.  Back to cited text no. 8
    
9.Reinehr T, de Sousa G, Andler W. Hyperthyrotropinemiainobese children is reversible after weight loss and is not related to lipids. J Clin Endocrinol Metab 2006;91:3088-91.  Back to cited text no. 9
    
10.Reinehr T, Andler W. Thyroid hormones before and after weight loss in obesity. Arch Dis Child 2002;87:320-3.  Back to cited text no. 10
    
11.Nyrnes A, Jorde R, Sundsfjord J. Serum TSH is positively associated with BMI. Int J Obes (Lond) 2006;30:100-5.  Back to cited text no. 11
    
12.Bhowmick SK, Dasari G, Levens KL, Rettig KR. The prevalence of elevated serum thyroid stimulating hormone in childhood/adolescent obesity and of autoimmune thyroid diseases in a subgroup. J Natl Med Assoc 2007;99:773-6.  Back to cited text no. 12
    
13.Stichel H, l'Allemand D, Grüters A. Thyroid function and obesity in children and adolescents. Horm Res 2000;54:14-9.  Back to cited text no. 13
    
14.Hari Kumar KV, Verma A, Muthukrishnan J, Modi KD. Obesity and thyrotropinemia. Indian J Pediatr 2008;76:933-5.  Back to cited text no. 14
    
15.Ortiga-Carvalho TM, Oliveira KJ, Soares BA, Pazos-Maura CC. The role of leptin in the regulation of TSH secretion in the fed state: In vivo and in vitro studies. J Endocrinol 2002;174:121-5.  Back to cited text no. 15
    
16.Feldt-Rasmussen U. Thyroid and leptin. Thyroid 2007;17:413-9.  Back to cited text no. 16
[PUBMED]    
17.Pinkney JH, Goodrick SJ, Katz J, Johnson AB, Lightman SL, Coppack SW, et al. Leptin and the pituitary thyroid axis: A comparative study in lean, obese, hypothyroid and hyperthyroid subjects. Clin Endocrinol (Oxf) 1998;49:583-8.  Back to cited text no. 17
    
18.Mihaly E, Fekete C, Tatro JB, Liposits Z, Stopa EG, Lechan RM. Hypophysio-tropic thyrotropin-releasing hormone-synthesizing neurons in the human hypo-thalamus are innervated by neuropeptide Y, agouti-related protein, and alpha-melanocyte-stimulating hormone. J Clin Endocrinol Metab 2000;85:2596-603.  Back to cited text no. 18
    
19.Rohner-Jeanraud F, Jeanraud B. The discovery of leptin and its impact in the understanding of obesity. Eur J Endocrinol 1996;135:649-50.  Back to cited text no. 19
    


    Figures

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    Tables

  [Table 1]


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