Toro A H, Soto Allande R, Bello González A
Bol Med Hosp Infant Mex. 1975 Mar-Apr;32(2):211-25.
Five families with DG6F deficiency were studied. Out of the first family, neinatal hyperbilirubinemia was evident in 3 children. Exchange transfusion was given to the first two. Possibly, the hemolytic crisis was subsequent to the application of vitamin K. In the next family group, there is a history of 6 children dead from jaundice and deep dark urine. Partial deficiency was found in the wife and 3 children from the third family. Fortunately, the father who is the brother of a deficient patient, shows normal levels. In family number four, both the father and the mother show below normal levels of DG6F. They have a sick son and daughter with subnormal levels. In the last family, the mother carried and the father shows abnormal levels of the enzyme; consequently, a son and their 2 daughters complain from the diseases. It is pointed out that some drugs, infections and several foods may precipitate the hemolytic crisis and brief comments are made on diagnostic and therapeutic resources.
对五个患有DG6F缺乏症的家庭进行了研究。在第一个家庭中,3名儿童出现新生儿高胆红素血症。前两名儿童接受了换血治疗。溶血危机可能是在使用维生素K之后发生的。在下一个家庭组中,有6名儿童死于黄疸和深色尿液的病史。在第三个家庭的妻子和3名儿童中发现了部分缺乏症。幸运的是,作为一名缺乏症患者兄弟的父亲,其水平正常。在第四个家庭中,父亲和母亲的DG6F水平均低于正常水平。他们有一个患病的儿子和女儿,其水平也低于正常水平。在最后一个家庭中,母亲携带该酶异常,父亲的酶水平也异常;因此,他们的一个儿子和两个女儿患有这些疾病。指出一些药物、感染和几种食物可能会引发溶血危机,并对诊断和治疗资源进行了简要评论。