Hydrops fetalis due to loss of function of hNav1.4 channel via compound heterozygous variants
2024

Hydrops fetalis and SCN4A gene variants

Sample size: 3 publication 10 minutes Evidence: high

Author Information

Author(s): Kubota Tomoya, Nagata Miho, Takagi Kazuko, Ishihara Yasuki, Kojima Kurumi, Uchikura Yuka, Yamamoto Reina, Yonei Ayumi, Ozaki Erina, Kira Natsuki, Takahashi Satoe, Homma Kazuaki, Miyashita Yohei, Eguchi-Ishimae Minenori, Sakai Norio, Asano Yohihiro, Sakata Yasushi, Ozono Keiichi, Eguchi Mariko, Takahashi Masanori

Primary Institution: Osaka University Graduate School of Medicine

Hypothesis

Can compound heterozygous variants of the SCN4A gene lead to hydrops fetalis and fetal death?

Conclusion

The study found that specific SCN4A gene variants are linked to hydrops fetalis and can result in fetal death.

Supporting Evidence

  • Whole-exome sequencing identified compound heterozygous variants in the SCN4A gene in all three infants.
  • Functional analysis showed that one variant caused a complete loss of ionic current.
  • The other variant exhibited reduced channel opening, indicating loss-of-function defects.

Takeaway

This study looked at three babies who died with a condition called hydrops fetalis and found that they had similar gene changes that might have caused their deaths.

Methodology

Whole-exome sequencing was used to identify gene variants, followed by functional analysis using whole-cell patch-clamp technique.

Limitations

The study did not include histological examinations of the skeletal muscle of the babies.

Participant Demographics

Three deceased infants from a nonconsanguineous family.

Statistical Information

P-Value

p<0.05

Statistical Significance

p<0.05

Digital Object Identifier (DOI)

10.1038/s10038-024-01284-z

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