Yaish Hassan M, Nussenzveig Roberto H, Agarwal Archana M, Siddiqui Abdul H, Christensen Robert D
Department of Pediatrics, Division of Hematology/Oncology, University of Utah School of Medicine, Salt Lake City, Utah, USA.
Neonatology. 2014;106(2):140-2. doi: 10.1159/000363219. Epub 2014 Jun 24.
We report a neonate with early and severe hemolytic jaundice and low erythrocyte pyruvate kinase enzymatic activity (<2 U/g hemoglobin, reference interval 9-22). We found her asymptomatic mother to be heterozygous for a novel PKLR mutation (c.1573delT) with an erythrocyte PK activity of 6.2 U/g hemoglobin. Her asymptomatic father was heterozygous for the common Northern European PKLR mutation (c.1529A) with an erythrocyte PK activity of 3.6 U/g. The neonate was a compound heterozygote with both mutations, but with no other mutations identified by sequencing a panel of 27 genes involved in severe neonatal jaundice.
我们报告了一名患有早期严重溶血性黄疸且红细胞丙酮酸激酶酶活性较低(<2 U/g血红蛋白,参考区间为9 - 22)的新生儿。我们发现其无症状的母亲为一种新型PKLR突变(c.1573delT)的杂合子,红细胞PK活性为6.2 U/g血红蛋白。其无症状的父亲为常见的北欧PKLR突变(c.1529A)的杂合子,红细胞PK活性为3.6 U/g。该新生儿为这两种突变的复合杂合子,但通过对一组涉及严重新生儿黄疸的27个基因进行测序,未发现其他突变。