To the Editor: Rice and colleagues (Oct. 25 issue)1 report asevere neonatal presentation of medium-chain acyl–coenzymeA dehydrogenase (MCAD) deficiency and suggest that newborn screeningresults should be communicated by 72 hours of age. In practice,it is unlikely that newborn screening, however timely, couldprevent such events. My colleagues and I documented fatal neonatalpresentations in 4 of the 81 patients with MCAD deficiency whowere born in Australia between 1994 and 2004.2 All died before72 hours. Five babies in the cohort with other fatty acid–oxidationdefects also died, between 22 and 65 hours of age.
Mollinedo, F., Gajate, C., Morales, A. I., del Canto-Janez, E., Justies, N., Collia, F., Rivas, J. V., Modolell, M., Iglesias, A.
(2009). Novel Anti-Inflammatory Action of Edelfosine Lacking Toxicity with Protective Effect in Experimental Colitis. J. Pharmacol. Exp. Ther.
329: 439-449
[Abstract][Full Text]
Yaldizli, O., Putzki, N.
(2009). Review: Natalizumab in the treatment of multiple sclerosis. Therapeutic Advances in Neurological Disorders
2: 115-128
[Abstract]
Norman, R., Haas, M., Chaplin, M., Joy, P., Wilcken, B.
(2009). Economic Evaluation of Tandem Mass Spectrometry Newborn Screening in Australia. Pediatrics
123: 451-457
[Abstract][Full Text]
Racke, M. K., Stuve, O.
(2008). Natalizumab: increased vigilance is required in treating patients with multiple sclerosis. Therapeutic Advances in Neurological Disorders
1: 155-156
Linker, R. A., Kieseier, B. C.
(2008). Review: Innovative monoclonal antibody therapies in multiple sclerosis. Therapeutic Advances in Neurological Disorders
1: 33-42
[Abstract]