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Immunoskeletal dysplasia with neurodevelopmental abnormalities (ISDNA) is an ultra-rare autosomal recessive disorder caused by biallelic variants in EXTL3. To date, 17 cases have been described in unrelated families, including the 15th case reported in an Indian patient homozygous for c.953C>T (p.Pro318Leu) ([PMID:35114981]), the 16th lethal phenotype case ([PMID:38010729]), and the 17th novel Chinese family harboring c.2015G>A (p.Arg672Gln) ([PMID:38010033]). Affected individuals present with short stature (HP:0004322), coarse facial features (HP:0000280), global developmental delay (HP:0001263), hypotonia (HP:0001252), neurodevelopmental delay (HP:0012758), skeletal dysplasia (HP:0002652), immunodeficiency (HP:0002721), and hepatic cysts (HP:0001407).
Genetic evidence is limited: all reported probands carry homozygous missense variants with no additional segregation data. Functional studies of EXTL3 demonstrate its role in heparan sulfate chain elongation—siRNA knockdown alters chain length in HEK293 cells, consistent with a loss-of-function mechanism—but variant-specific assays are lacking (The Journal of Biological Chemistry, 2007 [PMID:17761672]). No conflicting evidence has been reported. Further functional characterization and larger cohorts are needed to advance clinical validity. Key Take-home: Biallelic EXTL3 missense variants cause ISDNA; early molecular diagnosis via WES enables precise genetic counseling and management.
Gene–Disease AssociationLimited17 probands in unrelated families with biallelic EXTL3 missense variants; no segregation data; limited cohort size Genetic EvidenceLimitedHomozygous pathogenic variants identified in three unrelated families (total 17 cases); no additional affected relatives segregating Functional EvidenceLimitedEXTL3 knockdown alters heparan sulfate chain elongation in vitro, consistent with LoF, but lacks variant-specific functional assays |