TY - JOUR
T1 - FGF21 outperforms GDF15 as a diagnostic biomarker of mitochondrial disease in children
AU - Riley, Lisa G.
AU - Nafisinia, Michael
AU - Menezes, Minal J.
AU - Nambiar, Reta
AU - Williams, Andrew
AU - Barnes, Elizabeth H.
AU - Selvanathan, Arthavan
AU - Lichkus, Kate
AU - Bratkovic, Drago
AU - Yaplito-Lee, Joy
AU - Bhattacharya, Kaustuv
AU - Ellaway, Carolyn
AU - Kava, Maina
AU - Balasubramaniam, Shanti
AU - Christodoulou, John
N1 - Funding Information:
This work was supported by the United Mitochondrial Disease Foundation and the Mito Foundation [ PI-15-253 ]. The funding sources had no involvement in the study design; in the collection, analysis and interpretation of data; in the writing of the report; or in the decision to submit the article for publication.
Funding Information:
We thank the North American Mitochondrial Disease Consortium for supply of 11 MD patient samples. We thank the Department of Biochemistry, The Children's Hospital at Westmead for supplying control samples. We thank Dr. Richard Webster and Dr. Bindu Parayil Sankaran for supplying neuromuscular disease control samples. The research conducted at the Murdoch Children's Research Institute was supported by the Victorian Government ‘s Operational Infrastructure Support Program. The Chair in Genomic Medicine awarded to JC is generously supported by The Royal Children's Hospital Foundation . We are grateful to the Crane, Perkins and Miller families for their generous financial support.
Funding Information:
This work was supported by the United Mitochondrial Disease Foundation and the Mito Foundation [PI-15-253]. The funding sources had no involvement in the study design; in the collection, analysis and interpretation of data; in the writing of the report; or in the decision to submit the article for publication.We thank the North American Mitochondrial Disease Consortium for supply of 11 MD patient samples. We thank the Department of Biochemistry, The Children's Hospital at Westmead for supplying control samples. We thank Dr. Richard Webster and Dr. Bindu Parayil Sankaran for supplying neuromuscular disease control samples. The research conducted at the Murdoch Children's Research Institute was supported by the Victorian Government‘s Operational Infrastructure Support Program. The Chair in Genomic Medicine awarded to JC is generously supported by The Royal Children's Hospital Foundation. We are grateful to the Crane, Perkins and Miller families for their generous financial support.
Publisher Copyright:
© 2021 Elsevier Inc.
PY - 2022/1
Y1 - 2022/1
N2 - Several studies have shown serum fibroblast growth factor 21 (FGF21) and growth differentiation factor 15 (GDF15) levels are elevated in patients with mitochondrial disease (MD) where myopathy is a feature. In this study we investigated the utility of FGF21 and GDF15 as biomarkers for MD in a phenotypically and genotypically diverse pediatric cohort with suspected MD against a panel of healthy controls and non-mitochondrial disease controls with some overlapping clinical features. Serum was collected from 56 children with MD, 104 children with non-mitochondrial disease (27 neuromuscular, 26 cardiac, 21 hepatic, 30 renal) and 30 pediatric controls. Serum FGF21 and GDF15 concentrations were measured using ELISA, and their ability to detect MD was determined. Median FGF21 and GDF15 serum concentrations were elevated 17-fold and 3-fold respectively in pediatric MD patients compared to the healthy control group. Non-mitochondrial disease controls had elevated serum GDF15 concentrations while FGF21 concentrations were in the normal range. Elevation of GDF15 in a range of non-mitochondrial pediatric disorders limits its use as a MD biomarker. FGF21 was elevated in MD patients with a spectrum of clinical phenotypes, including those without myopathy. Serum FGF21 had an area under the receiver operating characteristic curve of 0.87, indicating good ability to discriminate between pediatric MD and healthy and non-mitochondrial disease controls. Triaging of pediatric MD patients by clinical phenotyping and serum FGF21 testing, followed by massively parallel sequencing, may enable more rapid diagnosis of pediatric MD.
AB - Several studies have shown serum fibroblast growth factor 21 (FGF21) and growth differentiation factor 15 (GDF15) levels are elevated in patients with mitochondrial disease (MD) where myopathy is a feature. In this study we investigated the utility of FGF21 and GDF15 as biomarkers for MD in a phenotypically and genotypically diverse pediatric cohort with suspected MD against a panel of healthy controls and non-mitochondrial disease controls with some overlapping clinical features. Serum was collected from 56 children with MD, 104 children with non-mitochondrial disease (27 neuromuscular, 26 cardiac, 21 hepatic, 30 renal) and 30 pediatric controls. Serum FGF21 and GDF15 concentrations were measured using ELISA, and their ability to detect MD was determined. Median FGF21 and GDF15 serum concentrations were elevated 17-fold and 3-fold respectively in pediatric MD patients compared to the healthy control group. Non-mitochondrial disease controls had elevated serum GDF15 concentrations while FGF21 concentrations were in the normal range. Elevation of GDF15 in a range of non-mitochondrial pediatric disorders limits its use as a MD biomarker. FGF21 was elevated in MD patients with a spectrum of clinical phenotypes, including those without myopathy. Serum FGF21 had an area under the receiver operating characteristic curve of 0.87, indicating good ability to discriminate between pediatric MD and healthy and non-mitochondrial disease controls. Triaging of pediatric MD patients by clinical phenotyping and serum FGF21 testing, followed by massively parallel sequencing, may enable more rapid diagnosis of pediatric MD.
KW - Biomarker
KW - Diagnosis
KW - FGF21
KW - GDF15
KW - Mitochondrial disease
KW - Pediatric
UR - https://www.scopus.com/pages/publications/85122244800
U2 - 10.1016/j.ymgme.2021.12.001
DO - 10.1016/j.ymgme.2021.12.001
M3 - Article
C2 - 34991945
AN - SCOPUS:85122244800
SN - 1096-7192
VL - 135
SP - 63
EP - 71
JO - Molecular Genetics and Metabolism
JF - Molecular Genetics and Metabolism
IS - 1
ER -