Department of Pathology & Applied Neurobiology, Kyoto Prefectural University of Medicine, Graduate School of Medical Sciences, Kyoto, Japan.
Neuropathology. 2013 Dec;33(6):663-6. doi: 10.1111/neup.12036. Epub 2013 Apr 1.
Thanatophoric dysplasia is a lethal form of chondrodysplastic dwarfism in which the cerebral cortex displays a unique and complex malformation. We report a female case of thanatophoric dysplasia type I (TD1) with FGFR3 mutation. In this case, fetal ultrasonography at the 18th week of gestation led to a prenatal diagnosis of TD1 with characteristic bone features. The subject was stillborn at the 21st week of gestation, showing marked shortening of the long bones, small thorax and curved short femurs, but without a cloverleaf skull. The temporal lobe was enlarged and hyperconvoluted, appearing as broad gyri and deep sulci, which were composed of focal polymicrogyria-like shallow sulci and heterotopic neuroblastic nests in the intermediate zone and marginal zone. Abundant precursor cells, immunoreactive for nestin and Ki-67 were observed with scattered mitoses in the thickened inner intermediate and subventricular zones of the temporal and occipital lobes. The cytoarchitecture from the entorhinal cortex to Ammon's horn was disorganized with leptomeningeal glioneuronal heterotopia, immunoreactive for doublecortin and nestin. The expression of FGFR3 was virtually not discernible in the temporal and occipital lobes or in the hippocampus. Genetic analysis revealed a point mutation at C8526T (R248C) in the exon 7 of FGFR3. This is the first report that demonstrates that overproduction of intermediate progenitor cells might be induced by FGFR3 mutation in a human TD1 case.
致死性软骨发育不全型Thanatophoric 型(TD1)是一种致命的软骨发育不全侏儒症,其大脑皮层表现出独特而复杂的畸形。我们报告了一例 FGFR3 突变的 I 型致死性软骨发育不全(TD1)病例。在该病例中,妊娠 18 周的胎儿超声检查导致产前诊断为具有特征性骨骼特征的 TD1。该患者在妊娠 21 周时为死产,表现为长骨明显缩短、胸廓小、股骨弯曲短,但无三叶形颅骨。颞叶增大且过度卷曲,表现为宽脑回和深沟回,由局灶性多微脑回样浅沟和中间带及边缘带异位神经母巢组成。在颞叶和枕叶增厚的内中间带和室下区观察到大量巢蛋白和 Ki-67 免疫反应阳性的前体细胞,伴有散在的有丝分裂。从内嗅皮质到角回的细胞结构紊乱,软脑膜胶质神经元异位,对双皮质素和巢蛋白呈免疫反应阳性。FGFR3 在颞叶和枕叶或海马中几乎不可见。遗传分析显示 FGFR3 外显子 7 中的 C8526T(R248C)点突变。这是首例表明在人类 TD1 病例中,FGFR3 突变可能诱导中间祖细胞过度产生的报告。