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长期输血的重型地中海贫血患儿的白细胞介素-1β、肿瘤坏死因子-α、胰岛细胞抗体及胰岛素分泌

Interleukin-1-beta, tumour necrosis factor-alpha, islet-cell antibody, and insulin secretion in children with thalassemia major on long-term blood transfusion.

作者信息

el Nawawy A, Soliman A T, el Azzouni O, Abbassy A A, Massoud M N, Marzouk S, Ibrahim F, Helal L

机构信息

Department of Pediatrics, College of Medicine, University of Alexandria, Egypt.

出版信息

J Trop Pediatr. 1996 Dec;42(6):362-4. doi: 10.1093/tropej/42.6.362.

DOI:10.1093/tropej/42.6.362
PMID:9009565
Abstract

In vitro, cytokines like interleukin-1-beta (IL-1-B) and tumour necrosis factor-alpha (TNF-A) inhibit insulin release and can destroy islet B-cells. We measured blood levels of IL-1-B, TNF-A, and islet cell antibody (ICA) in 20 children with IDDM, 20 of their non-diabetic siblings, 20 children with thalassemia major on long-term hypertransfusion therapy and iron chelation, and 10 normal age-matched children. In the non-diabetic and thalassemic children we investigated the early phase of insulin release after i.v. glucose (0.5 g/kg, 30 per cent solution) and evaluated tolerance to oral glucose (1.75 g/ kg). Circulating IL-1-B and TNF-A concentrations were significantly higher in IDDM-siblings (33.7 +/- 12.7 pg/ml and 655 +/- 165 pg/ml, respectively) v. normal children (21.1 +/- 6.4 pg/ml and 383 +/- 122 pg/ml, respectively). Thalassemic children had no detectable circulating ICA. The prevalence of ICA was 30 per cent in children with IDDM and 60 per cent of their siblings. Impaired oral glucose tolerance was detected in five children with thalassemia (25 per cent), but in none of the IDDM-siblings. The early phase of insulin release was significantly depressed in thalassemic children (peak insulin = 29.2 +/- 5.1 mIU/ml) v. normal children (52.3 +/- 9.5 mIU/ml) and IDDM-siblings (45.3 +/- 12.4 mIU/ml). It appears that thalassemic children had significantly decreased insulin secretion and impaired glucose tolerance, however, the mechanism of B-cell dysfunction is not mediated by ICA nor by cytokines.

摘要

在体外,白细胞介素 -1β(IL -1 -B)和肿瘤坏死因子 -α(TNF -A)等细胞因子会抑制胰岛素释放,并能破坏胰岛B细胞。我们检测了20名患有胰岛素依赖型糖尿病(IDDM)的儿童、他们20名非糖尿病的兄弟姐妹、20名接受长期强化输血治疗和铁螯合治疗的重型地中海贫血患儿以及10名年龄匹配的正常儿童的血液中IL -1 -B、TNF -A和胰岛细胞抗体(ICA)的水平。在非糖尿病和地中海贫血患儿中,我们静脉注射葡萄糖(0.5 g/kg,30%溶液)后研究胰岛素释放的早期阶段,并评估口服葡萄糖(1.75 g/kg)的耐受性。IDDM患儿的兄弟姐妹中循环IL -1 -B和TNF -A浓度(分别为33.7±12.7 pg/ml和655±165 pg/ml)显著高于正常儿童(分别为21.1±6.4 pg/ml和383±122 pg/ml)。地中海贫血患儿未检测到循环ICA。IDDM患儿中ICA的患病率为30%,其兄弟姐妹中为60%。在5名地中海贫血患儿(25%)中检测到口服葡萄糖耐量受损,但在IDDM患儿的兄弟姐妹中未检测到。与正常儿童(峰值胰岛素 = 52.3±9.5 mIU/ml)和IDDM患儿的兄弟姐妹(45.3±12.4 mIU/ml)相比,地中海贫血患儿胰岛素释放的早期阶段显著降低(峰值胰岛素 = 29.2±5.1 mIU/ml)。似乎地中海贫血患儿胰岛素分泌显著减少且葡萄糖耐量受损,然而,B细胞功能障碍的机制既不是由ICA介导,也不是由细胞因子介导。

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