Children with spinal muscular atrophy (SMA) frequently experience feeding intolerance and diminished growth. Although splicing modulators to prevent symptoms are available worldwide, adequate nutrition to support growth, development, and improved quality of life remains essential. We present a case study of a one-year-old malnourished male with SMA type I who achieved improved growth and feeding tolerance with a human milk (HM)-derived nutrition intervention. Despite feeding with appropriately balanced semielemental formula, he remained severely malnourished after two months of hospitalization. Feeds were partially replaced with HM-based diet plus a HM-based fat modular. Feeding tolerance, fecal calprotectin levels, and z scores for weight and length improved while receiving the HM-based intervention. We hypothesize that the HM-based feeding reduced intestinal inflammation by diminishing pathogenic elements of his microbiome. Owing to their aberrant fatty acid metabolism, patients with SMA are uniquely positioned to benefit from HM-based nutrient acquisition even while receiving splicing modulators to stabilize the disease process.
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http://dx.doi.org/10.1016/j.pediatrneurol.2023.08.007 | DOI Listing |
Neurol Int
January 2025
Kuwait Medical Genetics Center, Shuwaikh Industrial 70050, Kuwait.
In the published publication [...
View Article and Find Full Text PDFBrain Dev
January 2025
Department of Pediatrics, Aichi Medical University School of Medicine, Nagakute, Japan.
Background: Most cases of spinal muscular atrophy (SMA) can be diagnosed by copy number analysis of survival motor neuron (SMN) 1. However, a small number of cases of SMA can only be diagnosed by sequencing analysis. We present a case of SMA diagnosed 7 years after the onset of symptoms.
View Article and Find Full Text PDFInt J Neonatal Screen
January 2025
Cellular, Molecular and Genomics Biomedicine Group, La Fe Health Research Institute, 46026 Valencia, Spain.
Spinal muscular atrophy (SMA) is a degenerative neuromuscular condition resulting from a homozygous deletion of the survival motor neuron 1 () gene in 95% of patients. A timely diagnosis via newborn screening (NBS) and initiating treatment before the onset of symptoms are critical for improving health outcomes in affected individuals. We carried out a screening test by quantitative PCR (qPCR) to amplify the exon seven of using dried blood spot (DBS) samples.
View Article and Find Full Text PDFTher Adv Neurol Disord
January 2025
Department of Neurology, Ulm University, Ulm, Germany.
The advent of antisense oligonucleotide (ASO) therapies in neurodegenerative disorders is associated with enormous hope. Nusinersen treatment was a breakthrough intervention in the recessive disease spinal muscular atrophy, and superoxide dismutase 1 (SOD1) amyotrophic lateral sclerosis (ALS) seems to be the paradigm disease in dominant degenerative diseases. The results of treatment with the ASO tofersen in SOD1-ALS show that the drug has a convincing beneficial effect on ALS caused by SOD1 mutations, that preclinical studies in rodents predicted the therapeutic effect in the human disease, and that clinical efficacy is associated with a specific sequence of effects of the drug on mechanistic and degenerative biomarkers and, subsequently, functional outcomes such as weight stabilization and ALSFRS-R.
View Article and Find Full Text PDFFront Neurosci
January 2025
Hospital Pediátrico Dr. Hugo Mendoza, Santo Domingo, Dominican Republic.
Spinal muscular atrophy (SMA) is a progressive genetic neuromuscular condition affecting spinal motor neurons. The underlying cause of SMA is deletions or mutations in the SMN gene. It is classified into five variants based on age and clinical manifestations of the patient.
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