Panichsillaphakit E.Laohathai P.Dhachpramuk D.Vatanavicharn N.Mahidol University2025-05-182025-05-182025-05-05BMJ case reports Vol.18 No.5 (2025)https://repository.li.mahidol.ac.th/handle/123456789/110199Riboflavin, a vital water-soluble vitamin, serves as a cofactor for numerous enzymes involved in cellular energy metabolism. Riboflavin deficiency can lead to diverse clinical manifestations and metabolic changes that mimic multiple acyl-CoA dehydrogenase deficiency (MADD). We report a case of a preterm female infant dependent on total parenteral nutrition (TPN) with insufficient riboflavin intake. The infant exhibited clinical and biochemical features resembling MADD; however, molecular analysis revealed no pathogenic or likely pathogenic variants associated with MADD or riboflavin transporter defects. Treatment with riboflavin, L-carnitine and multivitamin supplementation resulted in the resolution of clinical and biochemical abnormalities within 1 week. This case highlights that the transient MADD-like features were attributable to riboflavin deficiency induced by TPN.MedicineArticleSCOPUS10.1136/bcr-2025-2650892-s2.0-1050047099751757790X40324939