Daily Ards Research Analysis
Analyzed 1 papers and selected 3 impactful papers.
Summary
A detailed case report describes neonatal hypothyroidism after maternal iohexol-enhanced imaging during lactation, ultimately linked to an underlying genetic disorder (RPS6KA3 deletion) rather than transient iodine exposure alone. It underscores gene–environment interplay, advises against reflexively interrupting breastfeeding, and highlights targeted thyroid monitoring in preterm infants after maternal iodinated contrast.
Research Themes
- Lactation safety after iodinated contrast
- Neonatal thyroid dysfunction and genetics
- Precision diagnostics in the NICU
Selected Articles
1. Case report of breastfeeding after maternal iodine contrast: neonatal hypothyroidism revealing an underlying congenital disorder.
A preterm neonate developed biochemical hypothyroidism after maternal iohexol-enhanced imaging and breastfeeding, with high urinary iodine suggesting exposure via milk. Persistent hormone abnormalities and the need for higher levothyroxine dosing prompted genetic testing, revealing an RPS6KA3 intragenic deletion (Coffin-Lowry syndrome) and IYD variants, indicating an underlying congenital etiology beyond transient iodine exposure.
Impact: This case refines clinical judgment on breastfeeding after iodinated contrast by demonstrating gene–environment interplay and the risk of misattributing neonatal hypothyroidism to transient iodine exposure. It supports thorough etiologic work-up before disrupting lactation, especially in preterm infants.
Clinical Implications: Do not automatically interrupt breastfeeding after maternal iohexol; instead, monitor thyroid function in at-risk neonates (especially preterm). If hypothyroidism persists or requires escalating levothyroxine, pursue genetic evaluation to rule out congenital etiologies.
Key Findings
- A 36+3 weeks small-for-gestation male neonate breastfed after maternal iohexol exposure (days 5–11) developed elevated TSH and low free T4 on day 11.
- Infant urinary iodine was elevated, indicating iodine exposure via breast milk, but persistent hypothyroidism required increasing levothyroxine dosing.
- Genetic testing identified a likely pathogenic intragenic deletion in RPS6KA3 (consistent with Coffin-Lowry syndrome) and two IYD variants of uncertain significance, supporting an underlying congenital etiology.
Methodological Strengths
- Temporal linkage of serial thyroid function tests and urinary iodine with breastfeeding exposure window.
- Integration of genomic testing (RPS6KA3, IYD) to investigate congenital etiologies.
Limitations
- Single-patient case report limits generalizability.
- No direct quantification of iodine concentration in expressed breast milk, and causal roles of IYD variants remain uncertain.
Future Directions: Prospective studies quantifying iodinated contrast transfer into breast milk and neonatal thyroid effects, particularly in preterm infants; standardized post-contrast thyroid monitoring protocols; functional studies on RPS6KA3 and IYD in thyroid development and hormone metabolism.
BACKGROUND: Iodine plays a critical role in producing thyroid hormones essential for brain development. An imbalance of iodine, whether deficiency or excess, can disrupt thyroid function. Iodine-induced hypothyroidism is rare but has been reported, particularly in premature infants exposed to excess iodine. Currently, iohexol, a nonionic radiocontrast agent, has limited data but is considered compatible with breastfeeding. CASE PRESENTATION: A small for gestation African American male neonate was born at 36 weeks and 3 days of gestation and admitted to the neonatal intensive care unit for respiratory distress and prematurity in the United States. Samples for Illinois newborn screens done at admission and repeated after 48 h of life were negative for thyroid abnormalities. On the infant's fifth day of life, the mother underwent a contrast-enhanced imaging study using iohexol, after which the infant received breast milk from days 5-11. On day 11, the neonate had an elevated thyroid-stimulating hormone (TSH) and low free thyroxine (T4) levels, consistent with hypothyroidism. Urine iodine level in the infant was checked and found to be elevated, prompting concern for the exposure to iodine in breastmilk. However, the need to increase the levothyroxine dose to achieve normal thyroid levels was not consistent with a transient effect such as iodine exposure. Genetic testing revealed a likely pathogenic intragenic deletion in the gene RPS6KA3, consistent with Coffin-Lowry syndrome, as well as two variants of unknown significance (VUS) in IYD. CONCLUSIONS: This case highlights the complex interplay between genetic factors and environmental influences in the development of neonatal hypothyroidism. While iodine contrast exposure through breast milk is generally considered safe, this case underscores the potential risks in preterm infants. Initially, iodine exposure through breastmilk was considered a likely contributor to thyroid dysfunction, but with further time and evaluation, congenital thyroid dysgenesis with underlying genetic findings complicated the diagnosis. This case demonstrates the importance of a comprehensive evaluation when working up thyroid dysfunction to exclude other potential etiologies before interrupting breastfeeding.
2. Case report of breastfeeding after maternal iodine contrast: neonatal hypothyroidism revealing an underlying congenital disorder.
Following maternal iohexol imaging, a preterm infant developed hypothyroidism with high TSH and low free T4 alongside elevated urinary iodine. The durable need for levothyroxine up-titration led to discovery of an RPS6KA3 deletion (Coffin-Lowry syndrome) and IYD VUS, suggesting congenital thyroid dysgenesis complicating the picture.
Impact: Provides a nuanced safety signal for breastfeeding after iodinated contrast in preterm infants and demonstrates the diagnostic value of integrating genetics when thyroid dysfunction persists.
Clinical Implications: Establish post-contrast thyroid screening pathways for high-risk neonates; reserve breastfeeding interruption for cases with compelling evidence, and broaden differential diagnoses to include congenital syndromes.
Key Findings
- Initial state newborn screens were normal; thyroid dysfunction emerged after maternal iohexol exposure and breastfeeding window.
- Elevated infant urinary iodine supported exposure, yet clinical course was inconsistent with transient iodine-induced hypothyroidism.
- Genomic testing revealed RPS6KA3 intragenic deletion (Coffin-Lowry) plus IYD VUS, indicating congenital contribution.
Methodological Strengths
- Clear temporal mapping of exposure, labs, and clinical decisions.
- Use of molecular diagnostics to refine the etiologic attribution.
Limitations
- Single case with limited external validity.
- Breast milk iodine content was not measured directly; functional impact of IYD variants remains unknown.
Future Directions: Develop risk-stratified guidance for lactation after contrast in preterm vs term infants; quantify iohexol-related iodine transfer; explore RPS6KA3’s role in thyroid development.
BACKGROUND: Iodine plays a critical role in producing thyroid hormones essential for brain development. An imbalance of iodine, whether deficiency or excess, can disrupt thyroid function. Iodine-induced hypothyroidism is rare but has been reported, particularly in premature infants exposed to excess iodine. Currently, iohexol, a nonionic radiocontrast agent, has limited data but is considered compatible with breastfeeding. CASE PRESENTATION: A small for gestation African American male neonate was born at 36 weeks and 3 days of gestation and admitted to the neonatal intensive care unit for respiratory distress and prematurity in the United States. Samples for Illinois newborn screens done at admission and repeated after 48 h of life were negative for thyroid abnormalities. On the infant's fifth day of life, the mother underwent a contrast-enhanced imaging study using iohexol, after which the infant received breast milk from days 5-11. On day 11, the neonate had an elevated thyroid-stimulating hormone (TSH) and low free thyroxine (T4) levels, consistent with hypothyroidism. Urine iodine level in the infant was checked and found to be elevated, prompting concern for the exposure to iodine in breastmilk. However, the need to increase the levothyroxine dose to achieve normal thyroid levels was not consistent with a transient effect such as iodine exposure. Genetic testing revealed a likely pathogenic intragenic deletion in the gene RPS6KA3, consistent with Coffin-Lowry syndrome, as well as two variants of unknown significance (VUS) in IYD. CONCLUSIONS: This case highlights the complex interplay between genetic factors and environmental influences in the development of neonatal hypothyroidism. While iodine contrast exposure through breast milk is generally considered safe, this case underscores the potential risks in preterm infants. Initially, iodine exposure through breastmilk was considered a likely contributor to thyroid dysfunction, but with further time and evaluation, congenital thyroid dysgenesis with underlying genetic findings complicated the diagnosis. This case demonstrates the importance of a comprehensive evaluation when working up thyroid dysfunction to exclude other potential etiologies before interrupting breastfeeding.
3. Case report of breastfeeding after maternal iodine contrast: neonatal hypothyroidism revealing an underlying congenital disorder.
This report shows that neonatal hypothyroidism after maternal iodinated contrast may unmask a congenital disorder, rather than reflect a purely transient iodine effect. It advocates comprehensive evaluation and judicious monitoring rather than routine breastfeeding interruption.
Impact: By linking persistent hypothyroidism with a specific pathogenic genetic lesion (RPS6KA3 deletion), the paper challenges simplistic assumptions about iodine exposure in lactation and informs risk-aware counseling.
Clinical Implications: Provide lactation-compatible imaging guidance: reassure most dyads while instituting targeted thyroid testing in preterm infants after maternal iodinated contrast; escalate to genetics if biochemical abnormalities persist.
Key Findings
- Timing: maternal iohexol on day 5; breastfeeding days 5–11; thyroid dysfunction detected on day 11.
- Biochemistry: elevated TSH, low free T4, and high urinary iodine in the infant.
- Etiology: underlying RPS6KA3 deletion (Coffin-Lowry syndrome) plus IYD VUS suggested a congenital contribution beyond iodine exposure.
Methodological Strengths
- Detailed clinical chronology and serial laboratory data capture.
- Genetic confirmation of a likely pathogenic lesion refining diagnosis.
Limitations
- Case-level evidence; findings may not be broadly generalizable.
- Lack of direct breast milk iodine measurement limits exposure quantification.
Future Directions: Create evidence-based lactation recommendations post-contrast focusing on preterm infants; assess different iodinated agents; investigate mechanistic links between RPS6KA3 pathways and thyroid development.
BACKGROUND: Iodine plays a critical role in producing thyroid hormones essential for brain development. An imbalance of iodine, whether deficiency or excess, can disrupt thyroid function. Iodine-induced hypothyroidism is rare but has been reported, particularly in premature infants exposed to excess iodine. Currently, iohexol, a nonionic radiocontrast agent, has limited data but is considered compatible with breastfeeding. CASE PRESENTATION: A small for gestation African American male neonate was born at 36 weeks and 3 days of gestation and admitted to the neonatal intensive care unit for respiratory distress and prematurity in the United States. Samples for Illinois newborn screens done at admission and repeated after 48 h of life were negative for thyroid abnormalities. On the infant's fifth day of life, the mother underwent a contrast-enhanced imaging study using iohexol, after which the infant received breast milk from days 5-11. On day 11, the neonate had an elevated thyroid-stimulating hormone (TSH) and low free thyroxine (T4) levels, consistent with hypothyroidism. Urine iodine level in the infant was checked and found to be elevated, prompting concern for the exposure to iodine in breastmilk. However, the need to increase the levothyroxine dose to achieve normal thyroid levels was not consistent with a transient effect such as iodine exposure. Genetic testing revealed a likely pathogenic intragenic deletion in the gene RPS6KA3, consistent with Coffin-Lowry syndrome, as well as two variants of unknown significance (VUS) in IYD. CONCLUSIONS: This case highlights the complex interplay between genetic factors and environmental influences in the development of neonatal hypothyroidism. While iodine contrast exposure through breast milk is generally considered safe, this case underscores the potential risks in preterm infants. Initially, iodine exposure through breastmilk was considered a likely contributor to thyroid dysfunction, but with further time and evaluation, congenital thyroid dysgenesis with underlying genetic findings complicated the diagnosis. This case demonstrates the importance of a comprehensive evaluation when working up thyroid dysfunction to exclude other potential etiologies before interrupting breastfeeding.