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埃及重型β地中海贫血儿童和青少年的葡萄糖稳态:与氧化应激的关系

Glucose homeostasis in Egyptian children and adolescents with β-Thalassemia major: Relationship to oxidative stress.

作者信息

Metwalley Kotb Abbass, El-Saied Abdel-Rahman Abdel-Hamed

机构信息

Department of Pediatrics, Assiut University, Assiut, Egypt.

Department of Clinical Pathology, South Valley University, Qena, Egypt.

出版信息

Indian J Endocrinol Metab. 2014 May;18(3):333-9. doi: 10.4103/2230-8210.131169.

DOI:10.4103/2230-8210.131169
PMID:24944927
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4056131/
Abstract

BACKGROUND

Oxidative stress in children with β-thalassemia may contribute to shortened life span of erythrocytes and endocrinal abnormalities.

AIM

This study was aimed to evaluate glucose homeostasis in Egyptian children and adolescents with β-thalassemia major and its relation to oxidative stress.

MATERIALS AND METHODS

Sixty children and adolescents with β-thalassemia major were studied in comparison to 30 healthy age and sex-matched subjects. Detailed medical history, thorough clinical examination, and laboratory assessment of oral glucose tolerance test (OGTT), serum ferritin, alanine transferase (ALT), fasting insulin levels, plasma malondialdehyde (MDA) as oxidant marker and serum total antioxidants capacity (TAC) were performed. Patients were divided into two groups according to the presence of abnormal OGTT.

RESULTS

The prevalence of diabetes was 5% (3 of 60) and impaired glucose tolerance test (IGT) was 8% (5 of 60). Fasting blood glucose, 2-hour post-load plasma glucose, serum ferritin, ALT, fasting insulin level, homeostatic model assessment for insulin resistance index (HOMA-IR) and MDA levels were significantly elevated while TAC level was significantly decreased in thalassemic patients compared with healthy controls (P < 0.001 for each). The difference was more evident in patients with abnormal OGTT than those with normal oral glucose tolerance (P < 0.001 for each). We also observed that thalassemic patients not receiving or on irregular chelation therapy had significantly higher fasting, 2-h post-load plasma glucose, serum ferritin, ALT, fasting insulin, HOMA-IR, oxidative stress markers OSI and MDA levels and significantly lower TAC compared with either those on regular chelation or controls. HOMA-IR was positively correlated with age, serum ferritin, ALT, MDA, and negatively correlated with TAC.

CONCLUSIONS

The development of abnormal glucose tolerance in Egyptian children and adolescents with β--thalassemia is associated with alteration in oxidant-antioxidant status and increase in insulin resistance.

RECOMMENDATION

1- Glucose tolerance tests, HOMA-IR, and MDA should be an integral part of the long-term follow-up of children and adolescents with β-thalassemia major. 2- Regular iron chelation and antioxidant therapy should be advised for thalassemic patients to improve glucose hemostasis.

摘要

背景

β地中海贫血患儿的氧化应激可能导致红细胞寿命缩短和内分泌异常。

目的

本研究旨在评估重度β地中海贫血埃及儿童和青少年的葡萄糖稳态及其与氧化应激的关系。

材料与方法

对60例重度β地中海贫血儿童和青少年进行研究,并与30例年龄和性别匹配的健康受试者作比较。记录详细病史,进行全面临床检查,并对口服葡萄糖耐量试验(OGTT)、血清铁蛋白、丙氨酸转氨酶(ALT)、空腹胰岛素水平、作为氧化标志物血浆丙二醛(MDA)和血清总抗氧化能力(TAC)进行实验室评估。根据OGTT结果异常与否将患者分为两组。

结果

糖尿病患病率为5%(60例中有3例),糖耐量受损(IGT)为8%(60例中有5例)。与健康对照组相比,地中海贫血患者的空腹血糖、负荷后2小时血浆葡萄糖、血清铁蛋白、ALT、空腹胰岛素水平、胰岛素抵抗指数稳态模型评估(HOMA-IR)和MDA水平显著升高,而TAC水平显著降低(每项P<0.001)。OGTT异常患者的差异比口服葡萄糖耐量正常患者更明显(每项P<0.001)。我们还观察到,未接受螯合治疗或接受不规则螯合治疗的地中海贫血患者,与接受常规螯合治疗的患者或对照组相比,空腹、负荷后2小时血浆葡萄糖、血清铁蛋白、ALT、空腹胰岛素、HOMA-IR、氧化应激标志物OSI和MDA水平显著更高,TAC显著更低。HOMA-IR与年龄、血清铁蛋白、ALT、MDA呈正相关,与TAC呈负相关。

结论

重度β地中海贫血埃及儿童和青少年葡萄糖耐量异常的发生与氧化还原状态改变及胰岛素抵抗增加有关。

建议

  1. 葡萄糖耐量试验、HOMA-IR和MDA应作为重度β地中海贫血儿童和青少年长期随访的组成部分。2. 建议对地中海贫血患者进行常规铁螯合和抗氧化治疗,以改善葡萄糖稳态。
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f924/4056131/7b5f1d692aea/IJEM-18-333-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f924/4056131/b9d78fe52041/IJEM-18-333-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f924/4056131/a76d0d8bbf1a/IJEM-18-333-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f924/4056131/458a0da12295/IJEM-18-333-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f924/4056131/e23aacef09a0/IJEM-18-333-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f924/4056131/7b5f1d692aea/IJEM-18-333-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f924/4056131/b9d78fe52041/IJEM-18-333-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f924/4056131/a76d0d8bbf1a/IJEM-18-333-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f924/4056131/458a0da12295/IJEM-18-333-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f924/4056131/e23aacef09a0/IJEM-18-333-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f924/4056131/7b5f1d692aea/IJEM-18-333-g009.jpg

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