Povidine–iodine within disconnect caps of peritoneal dialysis (PD) sets have been reported to potentially contribute to hypothyroidism1–3. The Medicines and Healthcare Products Regulatory Agency (UK) alert (2006) for PD caps, suggests this is more likely to affect infants and children with smaller peritoneal fill volumes, where higher dialysate iodine concentrations can result. We report two infants with end–stage renal failure (ESRF) receiving continuous cycling peritoneal dialysis (CCPD) who developed hypothyroidism. Both infants had normal newborn blood spot screening (TSH <6 mu/L), indicating an acquired cause.
Case 1, a male infant with ESRF secondary to posterior urethral valves, commenced PD on day 6. He received manual PD for 6 weeks, followed by automated CCPD when minimum fill volumes were achieved. Case 2, a male infant with ESRF secondary to congenital obstructive uropathy commenced manual PD, from day 7 to 9 and subsequently aged 7 weeks. Manual PD was continued for 4 weeks followed by automated CCPD. Manual PD potentially allows for increased iodine exposure from both long–line connexion shields and PD caps.
Profound primary hypothyroidism was identified in both individuals, with free T4 levels <2.6pmol/L and TSH >100mu/L (day 54, case 1; day 85, case 2), necessitating levothyroxine treatment. Symptoms were masked by significant comorbidity. Both patients had negative thyroid peroxidase antibodies and were noted to have bulky thyroid glands on ultrasound, consistent with iodine toxicity. They remain on levothyroxine treatment, aged 4 and 5 months respectively.
These cases highlight the potential role of povidine–iodine in PD caps and long–line connexion shields in the development of primary hypothyroidism. Given the significant morbidity associated with hypothyroidism in this age group, increased awareness of the associated risk is essential, with regular screening of this at–risk group to ensure early detection and treatment.
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