Hyperthyrotropinemia in obese children is reversible after weight loss and is not related to lipids
Thomas Reinehr1, Gideon de Sousa, Werner Andler
1Vestische Kinder- und Jugendklinik, University of Witten/Herdecke, Dr. F. Steiner Strasse 5, 45711 Datteln, Germany. T.Reinehr@kinderklinik-datteln.de
Insights
Hyperthyrotropinemia in obese children is likely a consequence of obesity, not a cause. Weight loss significantly reduced thyroid hormones, suggesting thyroxine treatment may not be necessary.
Area of Science:
- Pediatric Endocrinology
- Metabolic Disorders
- Thyroidology
Background:
- Controversy exists regarding thyroxine (T4) treatment for obese individuals with hyperthyrotropinemia.
- Understanding the relationship between obesity and thyroid function is crucial for appropriate clinical management.
Purpose of the Study:
- To investigate whether hyperthyrotropinemia is a cause or a consequence of obesity in children.
- To assess the impact of weight loss on thyroid hormone levels in obese children.
Main Methods:
- A cross-sectional study comparing 246 obese and 71 lean children, with a 1-year follow-up.
- Intervention involved exercise, behavior therapy, and nutrition education.
- Measured thyroid-stimulating hormone (TSH), free triiodothyronine (fT3), free thyroxine (fT4), and lipid profiles.
Main Results:
- Obese children had significantly higher TSH and fT3 levels compared to lean children; fT4 levels did not differ.
- Weight loss in a subset of obese children led to a significant reduction in TSH and fT3.
- Thyroid hormones and lipid profiles showed no significant correlations.
Conclusions:
- Elevated TSH and fT3 in obese children appear to be a consequence of obesity, particularly as weight loss normalized these levels.
- The findings suggest that thyroxine treatment may not be indicated in obese children with hyperthyrotropinemia, as thyroid dysfunction is secondary to obesity and not associated with adverse lipid profiles.
Context:
There is some controversy whether T(4) treatment is indicated in obese humans with hyperthyrotropinemia.
Objective:
The objective of this study was to examine whether hyperthyrotropinemia is a cause or a consequence of obesity.
Design:
The study was designed as a cross-sectional comparison between obese and lean children and includes a 1-yr follow-up study.
Setting:
The study was set in a primary care facility.
Patients:
The patients were 246 obese and 71 lean children.
Intervention:
The 1-yr intervention program was based on exercise, behavior therapy, and nutrition education.
Main Outcome Measures:
The main outcome measures were TSH, free T(3) (fT3), free T(4) (fT4), high-density lipoprotein, low-density lipoprotein, and total cholesterol at baseline and 1 yr later.
Results:
TSH (P = 0.009) and fT3 (P = 0.003) concentrations were significantly higher in obese children than in normal weight children, whereas there was no difference in fT4 levels (P = 0.804). Lipids did not correlate significantly to thyroid hormones in cross-sectional and longitudinal analyses. fT3, fT4, and lipids did not differ significantly in the 43 (17%) children with TSH levels above the normal range from the children with TSH levels within the normal range. Substantial weight loss in 49 obese children led to a significant reduction of TSH (P = 0.035) and fT3 (P = 0.036). The 197 obese children without substantial weight loss demonstrated no significant changes of thyroid hormones.
Conclusions:
Because fT3 and TSH were moderately increased in obese children and weight loss led to a reduction, the elevation of these hormones seems to be rather a consequence of obesity than a cause of obesity. Because fT3 and TSH were both increased in obesity and thyroid hormones were not associated to lipids, we put forward the hypothesis that there is no necessity for thyroxine treatment.
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