Two families with spondylo-epi-metaphyseal dysplasia due to compound heterozygocity in the vWFA domain of MATN3

Heterozygous variants of MATN3 is one of the common causes of multiple epiphyseal dysplasia (MED). Here we report three individuals from two unrelated families who harbor compound heterozygous variants in MATN3 (p.Arg121Trp and p.Val220Ala). Contrary to the MED phenotype, these individuals exhibit spondyloepimetaphyseal dysplasia (SEMD) resembling the phenotypes caused by homozygous MATN3 variants. Clinical manifestations included short stature, aggravating genu varum, joint laxity, and spinal abnormalities. Radiographic findings were distinct from typical MED. These compound heterozygous variants in the von Willebrand factor A domain of MATN3 expand the phenotypic spectrum associated with MATN3, and suggest that extreme MATN3 dysfunction resulting from dual variants can lead to a specific pattern of SEMD.

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Publication Details

Journal
European Journal of Medical Genetics
Published
2024-09-16
DOI
https://doi.org/10.1016/j.ejmg.2024.104972
Citations
1
Primary Topic
Connective tissue disorders research
Type
article
Field-Weighted Citation Impact
0.55
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article

Two families with spondylo-epi-metaphyseal dysplasia due to compound heterozygocity in the vWFA domain of MATN3

Tae‐Joon Cho, Ok-Hwa Kim, Hyeran Lee, Jung Min Ko et al.
1 citations
European Journal of Medical Genetics
Connective tissue disorders research
0.55
article

Two families with spondylo-epi-metaphyseal dysplasia due to compound heterozygocity in the vWFA domain of MATN3

Tae‐Joon Cho, Ok-Hwa Kim, Hyeran Lee, Jung Min Ko, Chang-Ho Shin, Mihyun Song, Hae Ryong Song
article en
1 citations

Abstract

Heterozygous variants of MATN3 is one of the common causes of multiple epiphyseal dysplasia (MED). Here we report three individuals from two unrelated families who harbor compound heterozygous variants in MATN3 (p.Arg121Trp and p.Val220Ala). Contrary to the MED phenotype, these individuals exhibit spondyloepimetaphyseal dysplasia (SEMD) resembling the phenotypes caused by homozygous MATN3 variants. Clinical manifestations included short stature, aggravating genu varum, joint laxity, and spinal abnormalities. Radiographic findings were distinct from typical MED. These compound heterozygous variants in the von Willebrand factor A domain of MATN3 expand the phenotypic spectrum associated with MATN3, and suggest that extreme MATN3 dysfunction resulting from dual variants can lead to a specific pattern of SEMD.

European Journal of Medical GeneticsVol. 72
Korea University Medical Center (KR), Seoul National University Children's Hospital (KR), Incheon Medical Center (KR)
Zero hunger
Openalex Percentile: Top 26%
Connective tissue disorders research
0.55
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Two families with spondylo-epi-metaphyseal dysplasia due to compound heterozygocity in the vWFA domain of MATN3 — Tae‐Joon Cho, Ok-Hwa Kim, et al. · European Journal of Medical Genetics (2024) | TGRS Research Map | TGRS