Craigen W J, Lindsay E A, Bricker J T, Hawkins E P, Baldini A
Department of Molecular and Human Genetics, Baylor College of Medicine, Houston, Texas 77030, USA.
Am J Med Genet. 1997 Oct 3;72(1):63-5.
A newborn boy with complex congenital heart disease, unilateral renal agenesis, and hypocalcemia was found to have a submicroscopic deletion of 22q11.2 (DiGeorge anomaly). In evaluating the pathogenesis of the hypocalcemia, repeatedly elevated or normal levels of parathyroid hormone were found, consistent with a diagnosis of pseudohypoparathyroidism. Pseudohypoparathyroidism can be due to mutation of a GTP binding protein (Gs-alpha protein) located on chromosome 20. Since there is another G protein locus (Gz alpha) adjacent to the DiGeorge critical region of chromosome 22, we hypothesized that a more extensive deletion may lead to pseudohypoparathyroidism. Fluorescence in situ hybridization was performed using a probe containing the Gz alpha gene, but no deletion was detected. This patient emphasizes the importance of determining the pathogenesis of the hypocalcemia in cases of DiGeorge anomaly.
一名患有复杂先天性心脏病、单侧肾缺如和低钙血症的男婴被发现存在22q11.2亚微观缺失(迪格奥尔格综合征)。在评估低钙血症的发病机制时,发现甲状旁腺激素水平反复升高或正常,符合假性甲状旁腺功能减退的诊断。假性甲状旁腺功能减退可能是由于位于20号染色体上的一种GTP结合蛋白(Gs-α蛋白)发生突变所致。由于在22号染色体的迪格奥尔格关键区域附近还有另一个G蛋白基因座(Gzα),我们推测更广泛的缺失可能导致假性甲状旁腺功能减退。使用包含Gzα基因的探针进行了荧光原位杂交,但未检测到缺失。该患者强调了在迪格奥尔格综合征病例中确定低钙血症发病机制的重要性。