Key result
Whole exome sequencing and environmental profiling of 5 HPAH families without known PAH mutations revealed new candidate variants in CYBA, FKBP1A, and PTGR2 in three families, and occupational toxin exposure in two families.
Observational (n=47)
Yes
This research identifies genetic causes and environmental triggers for heritable pulmonary arterial hypertension, suggesting a multifactorial approach for patients.
Our goal was to identify new environmental or genetic causes in heritable pulmonary arterial hypertension (HPAH) families outside the 18 known diagnostics PAH genes. PAH gene panel sequencing was performed for 47 HPAH families which revealed pathogenic variants in 39 families. Five of the remaining families agreed to whole exome sequencing and to fill in a drug and toxin exposure questionnaire. In Family 1 and 2, mother and daughter with HPAH carried a likely pathogenic variant in the CYBA gene and a variant of uncertain significance in the FKBP1A gene, respectively, following ACMG guidelines. In Family 3, we detected a likely pathogenic variant in the PTGR2 gene. These genes could play part in PAH pathogenesis but further functional analyses are required to corroborate these findings. In the remaining two families, we could not identify any plausible genetic cause. However, a father and son with PAH reported exposure to trichloroethylene, asbestos and tramadol in Family 4. In Family 5, two brothers with pulmonary veno-occlusive disease showed occupational toxin exposure. Thus, our findings indicate that not only a genetic predisposition but also environmental triggers should be investigated for HPAH patients.
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Shaukat et al. (2026) conducted an observational in Heritable pulmonary arterial hypertension (n=47). Genetic variants and environmental triggers was evaluated on Identification of new environmental or genetic causes. Whole exome sequencing and environmental profiling of 5 HPAH families without known PAH mutations revealed new candidate variants in CYBA, FKBP1A, and PTGR2 in three families, and occupational toxin exposure in two families.
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