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孕期营养性贫血与巨幼细胞贫血

Nutritional anemia and megaloblastosis in pregnancy.

作者信息

Lowenstein L, Brunton L, Hsieh Y S

出版信息

Can Med Assoc J. 1966 Mar 26;94(13):636-45.

Abstract

Macrogranulocytic and/or erythroid megaloblastic bone marrow changes which could not be accurately predicted from the hematologic findings in the blood were present in 25% of 305 mildly to moderately anemic pregnant women attending a public antepartum clinic in Montreal. Iron deficiency was the primary cause of anemia in most instances. Serum folate activity of less than 4.1 ng./ml. and/or serum vitamin B(12) levels of less than 100 pg./ml. were present in 90% of the 77 patients having these bone marrow changes, whereas approximately one-third of 228 patients with normoblastic marrow had these low values. Red cell folate did not correlate as well as serum folate activity with bone marrow changes. After treatment with oral folic acid in the range of 0.2 mg. to 0.8 mg., daily, for seven to 14 days, the megaloblastic and macrogranulocytic changes in patients with low serum folate activity and normal serum vitamin B(12) values disappeared in 15 of 21 patients. Of five women having both low folate and vitamin B(12) values, three failed to respond and two showed only partial improvement after 0.4 mg. of folic acid daily, per os, for 10 days. The average diet of these anemic women was suboptimal in folate and in iron.

摘要

在蒙特利尔一家公共产前诊所就诊的305名轻度至中度贫血孕妇中,25%存在血液学检查结果无法准确预测的巨粒细胞和/或红系巨幼样骨髓改变。大多数情况下,缺铁是贫血的主要原因。在有这些骨髓改变的77例患者中,90%的患者血清叶酸活性低于4.1 ng./ml和/或血清维生素B12水平低于100 pg./ml,而在228例正常幼红细胞骨髓患者中,约三分之一有这些低值。红细胞叶酸与骨髓改变的相关性不如血清叶酸活性。在用0.2 mg至0.8 mg的口服叶酸每日治疗7至14天后,血清叶酸活性低且血清维生素B12值正常的患者中,21例患者中有15例的巨幼样和巨粒细胞改变消失。在5例叶酸和维生素B12值均低的女性中,3例无反应,2例在每日口服0.4 mg叶酸10天后仅显示部分改善。这些贫血女性的平均饮食中叶酸和铁含量欠佳。

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本文引用的文献

2
Vitamin B12 in pregnancy and the puerperium.孕期及产褥期的维生素B12
Am J Clin Nutr. 1960 May-Jun;8:265-75. doi: 10.1093/ajcn/8.3.265.
10
Association of anaemia in pregnancy and folic acid deficiency.孕期贫血与叶酸缺乏的关联
J Obstet Gynaecol Br Emp. 1962 Oct;69:724-8. doi: 10.1111/j.1471-0528.1962.tb01270.x.

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