ArticleCureus2026
Thanatophoric Dysplasia Type I Confirmed by Fibroblast Growth Factor Receptor 3 (FGFR3) Mutation: Clinical Course and Ethical Considerations.
Article in Cureus, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Authors and funding
5 authors.
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Abstract
Thanatophoric dysplasia (TD) is the most common lethal skeletal dysplasia, caused by de novo fibroblast growth factor receptor 3 (FGFR3) mutations. Prenatal ultrasound may detect key features such as severe micromelia, narrow thorax, macrocephaly, and temporal lobe dysplasia, although molecular confirmation is essential. Type I TD (TD1), the most frequent subtype, shows "telephone-receiver" femur bowing, frontal bossing, and midface hypoplasia. Type II TD presents with a cloverleaf skull and straight femurs. TD is generally fatal due to pulmonary hypoplasia, narrow thorax, and brainstem compression, with survival beyond the early neonatal period being uncommon. We report a newborn with prenatal suspicion of skeletal dysplasia, confirmed postnatally as TD1 via FGFR3 p.Ter807Trp mutation, highlighting the importance of prenatal counseling, early genetic confirmation, and palliative care involvement.
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