Ovaert C, Bachy A
Service de Pédiatrie, Clinique Notre-Dame, Belgique.
Arch Fr Pediatr. 1993 Oct;50(8):697-9.
Malabsorption of oraliron is rare, and more frequently suspected than proved. It could be due to prolonged iron deficiency.
Case no. 1: A boy was admitted at the age of 5 months for recurrent bronchitis. His hemoglobin was 8.2 g/dl, mean corpuscular volume (MCV) 60 micron3, mean corpuscular hemoglobin (MCH) 15 ng and mean corpuscular hemoglobin concentration (MCHC) 25 gHb/dl. The serum iron was 1 microgram/dl, iron binding capacity (IBC) was 284 micrograms/dl and ferritin was 14.9 ng/ml. Dietary iron was inadequate. The patient was given ferrous sulfate but iron deficiency persisted at the ages of 11 months and 3 years, probably due to poor compliance. Similar hematologic data (Hb: 6.4 g/dl, MCV 55 micrograms/m3, MCH 13.9 ng, MCHC 24 gHb/dl) were found at the age of 9 years. The patient was then given ferrous sulfate orally as test but the serum iron levels were unchanged during the 4 hours following ingestion. A parenteral iron preparation (iron-dextran, 500 mg) improved the hematologic data. 6 months later, a new oral test with ferrous sulfate improved the serum iron level. Case no. 2: A boy with complex congenital cardiopathy was operated on in the neonatal period and given oral iron at the age of 9 months because of anemia with microcytosis and hypochromia. This anemia was still present at 17 months and was associated with normal or high serum ferritin. Electrophoresis of hemoglobin was normal. At the age of 4 yr 5 mo, Hb was 9.7 g/dl, MCV 62.8 micrograms/m3, MCH 18.4 ng, iron 16 micrograms/dl and ferritin 94.1 ng/ml. An oral test with ferrous sulfate failed to increase the serum iron. The patient was then given parenteral iron-dextran without benefit, and a second oral test remained ineffective. After a second course of parenteral iron-dextran, Hb was 11.5 g/dl, MCV 74.1 micrograms/m3, MCH 23.7 ng while the serum iron remained low (23 micrograms/dl) and ferritin increased to 587 ng/ml. A third oral test with ferrous sulfate was still ineffective, as was a test using 4 mg/kg iron.
The first patient suffered from iron malabsorption, presumably due to iron deficiency. The second patient could have abnormal metabolism and/or abnormal ferritin.
口服铁吸收不良较为罕见，更多时候是被怀疑而非得到证实。这可能是由于长期缺铁所致。
病例1：一名5个月大的男孩因反复支气管炎入院。其血红蛋白为8.2 g/dl，平均红细胞体积（MCV）为60立方微米，平均红细胞血红蛋白（MCH）为15纳克，平均红细胞血红蛋白浓度（MCHC）为25 gHb/dl。血清铁为1微克/分升，铁结合能力（IBC）为284微克/分升，铁蛋白为14.9纳克/毫升。饮食中铁摄入不足。给予该患者硫酸亚铁，但在11个月和3岁时仍存在缺铁情况，可能是由于依从性差。9岁时发现类似的血液学数据（血红蛋白：6.4 g/dl，MCV 55立方微米/立方米，MCH 13.9纳克，MCHC 24 gHb/dl）。随后口服硫酸亚铁进行试验，但摄入后4小时内血清铁水平未变。一种胃肠外铁制剂（右旋糖酐铁，500毫克）改善了血液学数据情况。6个月后，再次口服硫酸亚铁试验使血清铁水平有所改善。病例2：一名患有复杂先天性心脏病的男孩在新生儿期接受了手术，9个月大时因贫血伴小红细胞症和低色素血症而给予口服铁剂。17个月时这种贫血仍存在，且血清铁蛋白正常或升高。血红蛋白电泳正常。在4岁5个月时，血红蛋白为9.7 g/dl，MCV 62.8立方微米/立方米，MCH 18.4纳克，铁16微克/分升，铁蛋白9化，随后口服硫酸亚铁进行试验，但摄入后4小时内血清铁水平未变。一种胃肠外铁制剂（右旋糖酐铁，500毫克）改善了血液学数据情况。6个月后，再次口服硫酸亚铁试验使血清铁水平有所改善。病例2：一名患有复杂先天性心脏病的男孩在新生儿期接受了手术，9个月大时因贫血伴小红细胞症和低色素血症而给予口服铁剂。17个月时这种贫血仍存在，且血清铁蛋白正常或升高。血红蛋白电泳正常。在4岁5个月时，血红蛋白为9.7 g/dl，MCV 62.8立方微米/立方米，MCH 18.4纳克，铁16微克/分升，铁蛋白94.1纳克/毫升。口服硫酸亚铁试验未能提高血清铁水平。随后给予胃肠外右旋糖酐铁但无效果，再次口服试验仍无效。在第二个胃肠外右旋糖酐铁疗程后，血红蛋白为11.5 g/dl，MCV 74.1立方微米/立方米，MCH 23.7纳克，而血清铁仍低（23微克/分升），铁蛋白升至587纳克/毫升。第三次口服硫酸亚铁试验仍无效，使用4毫克/千克铁进行的试验也无效。
第一名患者患有铁吸收不良，可能是由于缺铁所致。第二名患者可能存在代谢异常和/或铁蛋白异常。
