{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,4,14]],"date-time":"2026-04-14T00:53:46Z","timestamp":1776128026178,"version":"3.50.1"},"reference-count":23,"publisher":"BMJ","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["J Clin Pathol"],"published-print":{"date-parts":[[1968,1]]},"abstract":"<jats:p>In a Chinese population 1,000 full-term male neonates and a further 117 jaundiced neonates of both sexes were studied in an investigation of the frequency of deficiency of erythrocyte glucose-6-phosphate dehydrogenase (G6PD). This enzyme was found to be deficient in 3\u00b76% of male neonates. Correlation of the results with the birthplace of the 602 mothers who were known to come from Kwangtung province showed no significant differences in the frequency of the deficiency between certain parts of the province.<\/jats:p>\n                  <jats:p>The deficiency of G6PD in hemizygous males is profound but it is not associated with erythrocyte acid monophosphoesterase deficiency in Chinese in Hong Kong. The G6PD deficiency accounts for 15\u00b74% of all the 117 cases of neonatal jaundice. The relative importance of G6PD deficiency as a cause of neonatal jaundice does not differ materially in male and female mutants. Neonatal jaundice can occur in all genotypes of G6PD mutation in Chinese.<\/jats:p>","DOI":"10.1136\/jcp.21.1.44","type":"journal-article","created":{"date-parts":[[2007,6,9]],"date-time":"2007-06-09T00:50:46Z","timestamp":1181350246000},"page":"44-47","source":"Crossref","is-referenced-by-count":13,"title":["Glucose-6-phosphate dehydrogenase deficiency in Chinese"],"prefix":"10.1136","volume":"21","author":[{"given":"H. C.","family":"Lai","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Michael P. Y.","family":"Lai","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Kevin S. 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