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Biallelic loss-of-function variants in TRPV6 underlie transient neonatal hyperparathyroidism (TNHP), an autosomal recessive disorder of placental calcium transport. Eight probands have been reported to date, including a dizygous twin case harboring compound heterozygous variants c.1282G>C (p.Gly428Arg) and c.668T>C (p.Ile223Thr), who presented with severe skeletal undermineralization, elevated parathyroid hormone, vitamin D deficiency (HP:0100512), and respiratory distress (HP:0002098) while the co-twin lacking TRPV6 mutations remained asymptomatic (PMID:30820485).
Mechanistically, TRPV6-mediated placental Ca2+ uptake is modulated by PDZK2 binding to its C-terminal PDZ motif; disruption of this interaction or knockout of Trpv6 in mice reduces epithelial calcium currents and recapitulates impaired mineralization consistent with TNHP pathology (PMID:17645868). No conflicting reports have been identified. TRPV6 genetic testing should be considered in neonates with unexplained hyperparathyroidism to inform diagnosis and anticipate transient clinical course.
Gene–Disease AssociationLimitedEight probands with biallelic TRPV6 variants in AR inheritance; variant segregation in dizygous twin confirms association ([PMID:30820485]) Genetic EvidenceLimitedEight AR probands with compound heterozygous TRPV6 variants support recessive genetic mechanism ([PMID:30820485]) Functional EvidenceModerateIn vitro and mouse models demonstrate TRPV6 loss-of-function impairs epithelial Ca2+ transport and aligns with TNHP pathophysiology ([PMID:17645868]) |