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Multivariate analysis on factors affecting suppression of thyroid-stimulating hormone in treated congenital
S M Ng1, S C Wong, D M Isherwood
1Endocrinology Department, Royal Liverpool Children's Hospital Alder Hey, Liverpool, UK. ngszemay@yahoo.com
Insights
Congenital hypothyroidism (CH) treatment aims to suppress thyroid-stimulating hormone (TSH). Early TSH suppression depends on thyroxine levels and CH cause, but by one year, only the CH cause matters.
Area of Science:
- Pediatric Endocrinology
- Neonatal Screening
- Thyroid Disorders
Background:
- Congenital hypothyroidism (CH) is a condition requiring lifelong thyroid hormone replacement.
- Effective treatment aims to normalize thyroid hormone levels and suppress elevated thyroid-stimulating hormone (TSH).
- Understanding factors influencing TSH suppression is crucial for optimizing CH management.
Purpose of the Study:
- To identify factors influencing thyroid-stimulating hormone (TSH) suppression in infants with congenital hypothyroidism (CH) after treatment initiation.
- To analyze the impact of etiology, initial thyroid function, and treatment parameters on TSH normalization.
- To determine the time-dependent changes in factors affecting TSH suppression.
Main Methods:
- Retrospective analysis of thyroid function tests in 140 infants with CH screened from birth to 3 years.
- Classification of CH etiology into athyreosis, ectopia, and dyshormonogenesis based on thyroid scans.
- Statistical analysis, including stepwise logistic regression, to identify independent predictors of TSH suppression at 6 months and 1 year.
Main Results:
- 58% of infants had persistently high TSH at 6 months; 31% at 1 year.
- Infants with athyreosis and ectopia showed delayed TSH normalization compared to dyshormonogenesis.
- At 6 months, plasma T4 levels and CH etiology independently predicted TSH suppression; at 1 year, only CH etiology was significant.
Conclusions:
- CH etiology and early plasma T4 levels are key to achieving TSH suppression by 6 months.
- By one year of age, the underlying cause of CH is the sole determinant of successful TSH suppression.
- These findings highlight the importance of etiology in long-term CH management and monitoring.
Aims:
To determine the factors which influence the suppression of thyroid-stimulating hormone (TSH) in infants with congenital hypothyroidism (CH) following treatment.
Methods:
We examined retrospectively the patterns of thyroid function tests from diagnosis to 3 years of age in 140 infants diagnosed with CH from screening. Patients were classified into 3 groups: athyreosis, ectopia and presumed dyshormonogenesis on the basis of thyroid scans. Adequate TSH suppression was defined as plasma TSH concentration <6 mU/l. The factors affecting the suppression of TSH at 6 months and 1 year of age which were evaluated were: initial confirmatory plasma TSH, initial plasma thyroxine (T4), mean age of starting treatment with L-T4, dose of L-T4 at diagnosis, 6 weeks, 3 months and 6 months, and aetiology of the congenital hypothyroidism. Variables were then entered in a stepwise logistic regression model for TSH suppression at 6 months and 1 year of age.
Results:
All infants had radionuclide scans prior to treatment: athyreosis (n = 39), ectopia (n = 78) and dyshormonogenesis (n = 23). 58% of patients had persistently raised TSH at 6 months of age while 31% of patients had a persistently raised TSH at 1 year of age. There was a significant delay in the normalisation of plasma TSH in athyreosis and ectopia groups compared with dyshormonogenesis. Multiple regression analysis for TSH suppression at 6 months of age found plasma T4 levels and aetiology of CH as independent factors affecting the timing of TSH suppression. Aetiology of CH was the only independent factor affecting TSH suppression at 1 year of age.
Conclusion:
At 6 months of age, plasma T4 levels at 6 weeks and 3 months, and aetiology of CH were independent factors affecting timing of TSH suppression. However, by 1 year of age, the aetiology of CH was the only independent factor affecting suppression of TSH.
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