P10 Think zinc: nutritional deficiency in a breastfed infant associated with antenatal proton-pump inhibitor exposure

Abstract

Abstract A 5-month-old infant presented with a 3-month history of a dramatic periorofacial and acral dermatitis associated with recurrent infections, increasing lethargy and poor feeding. He was born at full term, breastfed exclusively, and had no family history of skin disease. Serum alkaline phosphatase was 41 (range 82–383) and zinc levels were undetectably low (< 3 mg mol–1; normal 10–25). Maternal breastmilk zinc levels were low (3.15, control mean 12.7), and maternal serum zinc was normal. A rapid improvement was noted within days of zinc sulfate supplementation. Zinc supplementation was stopped after 3 months, with normal follow-up zinc levels. The mother had taken omeprazole from 30 weeks’ gestation to birth. In her previous pregnancy there was no proton-pump inhibitor (PPI) ingestion, and no manifestation of zinc deficiency in the older sibling, who had also been breastfed exclusively. Maternal genetic testing for defects in SLC30A2, a zinc transporter in mammary tissue, was negative. Acrodermatitis enteropathica involves recessive mutations in the SLC39A4 gene, and secondary transient infantile zinc deficiency can be due to prematurity, low zinc intake, or malabsorptive processes such as cystic fibrosis. It is rare in breastfed infants due to enhanced bioavailability of zinc. PPIs can decrease serum zinc due to intestinal chelation, although little is known regarding their effect on transplacental or transmammary zinc transmission. To our knowledge this is the first report of zinc deficiency in a breastfed infant associated with maternal PPI use, potentially due to diminished transmammary and/or transplacental zinc transmission.