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Parafollicular C-cells of the thyroid are decreased in patients with congenital diaphragmatic hernia
A L Luis1, F Pederiva, J L Encinas
1Hospital Infantil La Paz, Pediatric Surgery, Madrid, Spain.
Insights
Thyroid C-cells are deficient in babies with congenital diaphragmatic hernia (CDH), indicating neural crest developmental issues. This finding supports using animal models to study human CDH pathogenesis.
Area of Science:
- Developmental biology
- Endocrinology
- Pediatric pathology
Background:
- Congenital diaphragmatic hernia (CDH) is associated with parathyroid and thymic anomalies linked to neural crest dysfunction.
- Affected individuals exhibit neurocristal defects, including conotruncal and facial anomalies.
Purpose of the Study:
- To investigate potential abnormalities in parafollicular C-cells (CC) of the thyroid in infants with CDH.
- To explore the relationship between CC embryogenesis and that of the parathyroids and thymus in CDH.
Main Methods:
- Autopsy thyroid sections from 12 infants with CDH and 11 controls were analyzed.
- Immunohistochemistry using anti-calcitonin antibodies was performed to assess CC.
- Quantitative analysis of calcitonin-stained areas and CC distribution was conducted.
Main Results:
- A significantly smaller proportion of calcitonin-stained surface area was observed in the thyroids of CDH infants compared to controls (p<0.05).
- The histological distribution of CC within the thyroid gland was found to be normal in both groups.
Conclusions:
- Infants with CDH exhibit a deficiency in parafollicular thyroid C-cells.
- These results reinforce the role of neural crest dysregulation in CDH pathogenesis.
- The study validates the use of this experimental model for investigating human CDH.
Background:
Parathyroid and thymic anomalies related to embryonic neural crest dysfunction have been demonstrated in rats with congenital diaphragmatic hernia (CDH). These rats, like infants with CDH, have conotruncal, facial, and other neurocristal defects. The present study examines whether parafollicular C-cells (CC) of the thyroid, whose embryogenesis is related to that of the parathyroids and thymus, might also be abnormal in babies with CDH.
Material And Methods:
Autopsy sections of the thyroids of 12 babies dead from CDH and of 11 controls were stained with anti-calcitonin antibodies. Calcitonin-stained areas and the histological distribution of CC within the thyroid gland were assessed. Mann-Whitney tests were used for comparison, with p<0.05 considered significant.
Results:
The proportion of stained surface to total thyroid surface was significantly smaller in CDH babies than in controls (0.035±0.030% vs. 0.072±0.052%, p<0.05). A normal central CC location was demonstrated in both groups.
Conclusions:
Parafollicular thyroid C-cells are deficient in patients with CDH. These findings further support the involvement of neural crest dysregulation in the pathogenesis of CDH and the pertinence of using this experimental model to investigate the human condition. The clinical effects of this anomaly are unknown and probably irrelevant, but they are currently under scrutiny.
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