警惕虚假 HbA1c:罕见的 alpha1-globin 基因突变。

IF 1.6 4区 医学 Q2 PEDIATRICS
Lucy Collins, Eleanor Angley, Joel Smith, Fergus Cameron, Phoebe Stewart
{"title":"警惕虚假 HbA1c:罕见的 alpha1-globin 基因突变。","authors":"Lucy Collins,&nbsp;Eleanor Angley,&nbsp;Joel Smith,&nbsp;Fergus Cameron,&nbsp;Phoebe Stewart","doi":"10.1111/jpc.16649","DOIUrl":null,"url":null,"abstract":"<p>An 11-year-old girl was investigated for impaired glucose tolerance. Her medical history included transient congenital hypothyroidism. Her family medical history was notable for type 2 diabetes mellitus affecting her mother, maternal grandmother, maternal uncle and paternal grandfather. She denied history of polyuria, polydipsia, weight loss and exogenous glucocorticoid administration. On examination, her weight was 72.3 kg (99.5 percentile, <i>Z</i> = 2.59), height 160.5 cm (98.9 percentile, <i>Z</i> = 2.30) and body mass index 28.1 kg/m<sup>2</sup> (98.0 percentile, <i>Z</i> = 2.06). Acanthosis nigricans was noted circumferentially around her neck. There was no clinical stigmata of endogenous hypercortisolism. Initial biochemistry (Table 1) demonstrated elevated glycosylated haemoglobin (HbA1c) at 14.9%. Antibodies associated with type 1 diabetes mellitus were negative. Full blood count, thyroid function, renal function and haematinics were unremarkable. C-peptide was elevated. Liver function, urinary albumin/creatinine ratio and lipid profile were unremarkable.</p><p>Repeat HbA1c (14.5%, Biorad D10 Ion exchange chromatography, Fig. 1) was elevated. A presumed diagnosis of type 2 diabetes was made. Metformin extended release and 18 units of basal insulin were commenced, in addition to life-style and dietary intervention. Blood glucose monitoring reflected excellent glycaemic control, with blood sugar levels between 4.7 and 6.3 mmol/L. Basal insulin was rapidly reduced, and eventually ceased after 4 weeks due to stable blood glucose levels. A spurious HbA1c result was suspected.</p><p>Fructosamine was low at 231 μmol/L (250–380) and oral glucose tolerance test (OGTT) was normal; fasting glucose 4.5 mmol/L (&lt;6.1 mmol), 60-min glucose 5.0 mmol/L (&lt;7.8 mmol/L) and 120-min glucose 4.6 mmol/L (&lt;7.8 mmol/L). A Freestyle Libre 2 Continuous Glucose Monitoring System displayed 99% of blood glucose readings in range (3.9–10.0 mmol/L). HbA1c was repeated on an alternative assay. HbA1c was normal at 5.4% (Trinity Biotech Boronate Affinity Chromatography). Metformin was ceased, and the diagnosis of type 2 diabetes was revised.</p><p>An underlying haemoglobinopathy was hypothesised to cause the discrepancy in HbA1c and OGTT results. A haemoglobinopathy screen detected an abnormal haemoglobin variant in zone 11 of 10.6%, suggestive of an uncommon alpha variant (Fig. 2). Genetic testing was undertaken. DNA sequencing found her to be compound heterozygous for the common single gene deletion (−alpha 3.7) alpha thalassaemia mutation and the HbA1:c382A&gt;G (Hb Shantou) variant in the alpha1-globin gene. The HbA1:c382A&gt;G (Hb Shantou) genetic variant is responsible for the haemoglobin variant.</p><p>Cascade testing in her family is underway.</p><p>The incidence of paediatric type 2 diabetes has increased, especially in high-risk ethnic groups (Indigenous Australians, Pacific Islanders and Maori people).<span><sup>1</sup></span> Close monitoring and intensive management of paediatric type 2 diabetes is crucial; glycaemic control typically deteriorates quickly, and complications occur earlier than in adults. Diagnosis is based on fasting glucose, or 2-h glucose concentration during an OGTT or HbA1c. In the absence of symptoms, testing should be confirmed with a repeat test on a different day.<span><sup>2</sup></span></p><p>HbA1c holds a central role in the diagnosis and management of diabetes mellitus. The rate of A1c formation is proportional to the concentration of glucose within the erythrocyte during its life-span, typically 120 days. It is important to be alert to clinical scenarios and interfering factors that may yield false results.<span><sup>3</sup></span> Falsely elevated HbA1c can be seen in any condition that prolongs the life of the erythrocyte or is associated with reduced red cell turnover, such as iron/B12/folate deficiency anaemia and asplenia. Severe hypertriglyceridaemia, hyperbilirubinaemia and uraemia may also falsely elevate HbA1c.<span><sup>3</sup></span> Falsely low HbA1c results can be seen in acute and chronic bone loss, haemolytic anaemia and splenomegaly. In addition, haemoglobin variants can lead to falsely elevated or lowered HbA1c. If the amino acid substitution causes a change in the net charge (as with HbS, C, D and E), ion-exchange high-performance liquid chromatography (HPLC) or electrophoresis may be affected. If a substitution occurs at a glycation site, the rate of glycation may be affected. If the variant causes a reduced erythrocyte life-span, the HbA1c would be falsely lowered, irrespective of method used.<span><sup>4</sup></span> The presence of a haemoglobin variant should be suspected in patients with incongruent glucose monitoring and HbA1c results, markedly elevated HbA1c results&gt;15% and significantly different HbA1c results compared to a previous value.<span><sup>3</sup></span></p><p>Reports of Hb Shantou (HbA1:c382A&gt;G) are limited.<span><sup>5</sup></span> Hb Shantou reflects a nucleotide mutation at position c.382 A&gt;G on the α1-globin gene. A single published report describes a case of a falsely high HbA1c value in a pregnant woman of Chinese ethnicity due to this novel α1-globin gene mutation.<span><sup>5</sup></span></p><p>Fructosamine measurement, glycated albumin and continuous glucose monitoring may provide alternatives to HbA1c. Fructosamine, the product formed by a nonenzymatic reaction of glucose and serum proteins, reflects a shorter period of glycaemic control (typically 2–3 weeks) compared to HbA1c as the half-life of albumin is approximately 20 days.<span><sup>3</sup></span> The accuracy of fructosamine measurement is limited in situations of hypoproteinaemia/hypoalbuminaemia, such as nephrotic syndrome and chronic liver disease. In addition, boronate affinity HPLC, subsequently utilised in our case, is not typically affected by haemoglobin variant interference<span><sup>6</sup></span> and may provide a more accurate representation of glycaemic control.</p><p>In conclusion, as rates of type 2 diabetes increase in our paediatric population, clinicians should be alert to the limitations and inaccuracies of diagnostic and monitoring tests, most notably HbA1c. Haemoglobin variants may falsely elevate or lower HbA1c, and alternative diagnostic methods are required to improve accuracy.</p>","PeriodicalId":16648,"journal":{"name":"Journal of paediatrics and child health","volume":null,"pages":null},"PeriodicalIF":1.6000,"publicationDate":"2024-08-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/jpc.16649","citationCount":"0","resultStr":"{\"title\":\"Be alert to a spurious HbA1c: A rare alpha1-globin gene mutation\",\"authors\":\"Lucy Collins,&nbsp;Eleanor Angley,&nbsp;Joel Smith,&nbsp;Fergus Cameron,&nbsp;Phoebe Stewart\",\"doi\":\"10.1111/jpc.16649\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p>An 11-year-old girl was investigated for impaired glucose tolerance. Her medical history included transient congenital hypothyroidism. Her family medical history was notable for type 2 diabetes mellitus affecting her mother, maternal grandmother, maternal uncle and paternal grandfather. She denied history of polyuria, polydipsia, weight loss and exogenous glucocorticoid administration. On examination, her weight was 72.3 kg (99.5 percentile, <i>Z</i> = 2.59), height 160.5 cm (98.9 percentile, <i>Z</i> = 2.30) and body mass index 28.1 kg/m<sup>2</sup> (98.0 percentile, <i>Z</i> = 2.06). Acanthosis nigricans was noted circumferentially around her neck. There was no clinical stigmata of endogenous hypercortisolism. Initial biochemistry (Table 1) demonstrated elevated glycosylated haemoglobin (HbA1c) at 14.9%. Antibodies associated with type 1 diabetes mellitus were negative. Full blood count, thyroid function, renal function and haematinics were unremarkable. C-peptide was elevated. Liver function, urinary albumin/creatinine ratio and lipid profile were unremarkable.</p><p>Repeat HbA1c (14.5%, Biorad D10 Ion exchange chromatography, Fig. 1) was elevated. A presumed diagnosis of type 2 diabetes was made. Metformin extended release and 18 units of basal insulin were commenced, in addition to life-style and dietary intervention. Blood glucose monitoring reflected excellent glycaemic control, with blood sugar levels between 4.7 and 6.3 mmol/L. Basal insulin was rapidly reduced, and eventually ceased after 4 weeks due to stable blood glucose levels. A spurious HbA1c result was suspected.</p><p>Fructosamine was low at 231 μmol/L (250–380) and oral glucose tolerance test (OGTT) was normal; fasting glucose 4.5 mmol/L (&lt;6.1 mmol), 60-min glucose 5.0 mmol/L (&lt;7.8 mmol/L) and 120-min glucose 4.6 mmol/L (&lt;7.8 mmol/L). A Freestyle Libre 2 Continuous Glucose Monitoring System displayed 99% of blood glucose readings in range (3.9–10.0 mmol/L). HbA1c was repeated on an alternative assay. HbA1c was normal at 5.4% (Trinity Biotech Boronate Affinity Chromatography). Metformin was ceased, and the diagnosis of type 2 diabetes was revised.</p><p>An underlying haemoglobinopathy was hypothesised to cause the discrepancy in HbA1c and OGTT results. A haemoglobinopathy screen detected an abnormal haemoglobin variant in zone 11 of 10.6%, suggestive of an uncommon alpha variant (Fig. 2). Genetic testing was undertaken. DNA sequencing found her to be compound heterozygous for the common single gene deletion (−alpha 3.7) alpha thalassaemia mutation and the HbA1:c382A&gt;G (Hb Shantou) variant in the alpha1-globin gene. The HbA1:c382A&gt;G (Hb Shantou) genetic variant is responsible for the haemoglobin variant.</p><p>Cascade testing in her family is underway.</p><p>The incidence of paediatric type 2 diabetes has increased, especially in high-risk ethnic groups (Indigenous Australians, Pacific Islanders and Maori people).<span><sup>1</sup></span> Close monitoring and intensive management of paediatric type 2 diabetes is crucial; glycaemic control typically deteriorates quickly, and complications occur earlier than in adults. Diagnosis is based on fasting glucose, or 2-h glucose concentration during an OGTT or HbA1c. In the absence of symptoms, testing should be confirmed with a repeat test on a different day.<span><sup>2</sup></span></p><p>HbA1c holds a central role in the diagnosis and management of diabetes mellitus. The rate of A1c formation is proportional to the concentration of glucose within the erythrocyte during its life-span, typically 120 days. It is important to be alert to clinical scenarios and interfering factors that may yield false results.<span><sup>3</sup></span> Falsely elevated HbA1c can be seen in any condition that prolongs the life of the erythrocyte or is associated with reduced red cell turnover, such as iron/B12/folate deficiency anaemia and asplenia. Severe hypertriglyceridaemia, hyperbilirubinaemia and uraemia may also falsely elevate HbA1c.<span><sup>3</sup></span> Falsely low HbA1c results can be seen in acute and chronic bone loss, haemolytic anaemia and splenomegaly. In addition, haemoglobin variants can lead to falsely elevated or lowered HbA1c. If the amino acid substitution causes a change in the net charge (as with HbS, C, D and E), ion-exchange high-performance liquid chromatography (HPLC) or electrophoresis may be affected. If a substitution occurs at a glycation site, the rate of glycation may be affected. If the variant causes a reduced erythrocyte life-span, the HbA1c would be falsely lowered, irrespective of method used.<span><sup>4</sup></span> The presence of a haemoglobin variant should be suspected in patients with incongruent glucose monitoring and HbA1c results, markedly elevated HbA1c results&gt;15% and significantly different HbA1c results compared to a previous value.<span><sup>3</sup></span></p><p>Reports of Hb Shantou (HbA1:c382A&gt;G) are limited.<span><sup>5</sup></span> Hb Shantou reflects a nucleotide mutation at position c.382 A&gt;G on the α1-globin gene. A single published report describes a case of a falsely high HbA1c value in a pregnant woman of Chinese ethnicity due to this novel α1-globin gene mutation.<span><sup>5</sup></span></p><p>Fructosamine measurement, glycated albumin and continuous glucose monitoring may provide alternatives to HbA1c. Fructosamine, the product formed by a nonenzymatic reaction of glucose and serum proteins, reflects a shorter period of glycaemic control (typically 2–3 weeks) compared to HbA1c as the half-life of albumin is approximately 20 days.<span><sup>3</sup></span> The accuracy of fructosamine measurement is limited in situations of hypoproteinaemia/hypoalbuminaemia, such as nephrotic syndrome and chronic liver disease. In addition, boronate affinity HPLC, subsequently utilised in our case, is not typically affected by haemoglobin variant interference<span><sup>6</sup></span> and may provide a more accurate representation of glycaemic control.</p><p>In conclusion, as rates of type 2 diabetes increase in our paediatric population, clinicians should be alert to the limitations and inaccuracies of diagnostic and monitoring tests, most notably HbA1c. Haemoglobin variants may falsely elevate or lower HbA1c, and alternative diagnostic methods are required to improve accuracy.</p>\",\"PeriodicalId\":16648,\"journal\":{\"name\":\"Journal of paediatrics and child health\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":1.6000,\"publicationDate\":\"2024-08-19\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://onlinelibrary.wiley.com/doi/epdf/10.1111/jpc.16649\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Journal of paediatrics and child health\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://onlinelibrary.wiley.com/doi/10.1111/jpc.16649\",\"RegionNum\":4,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q2\",\"JCRName\":\"PEDIATRICS\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of paediatrics and child health","FirstCategoryId":"3","ListUrlMain":"https://onlinelibrary.wiley.com/doi/10.1111/jpc.16649","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"PEDIATRICS","Score":null,"Total":0}
引用次数: 0

摘要

一名 11 岁女孩因糖耐量受损接受了检查。她的病史包括一过性先天性甲状腺功能减退症。她的家族病史中,母亲、外祖母、舅舅和外祖父都患有 2 型糖尿病。她否认有多尿、多饮、体重减轻和外源性糖皮质激素用药史。经检查,她的体重为 72.3 千克(99.5 百分位数,Z = 2.59),身高 160.5 厘米(98.9 百分位数,Z = 2.30),体重指数为 28.1 千克/平方米(98.0 百分位数,Z = 2.06)。她的颈部周围有黑棘皮症。没有内源性皮质醇过多症的临床表现。初步生化检查(表 1)显示,糖化血红蛋白(HbA1c)升高至 14.9%。与 1 型糖尿病相关的抗体呈阴性。全血细胞计数、甲状腺功能、肾功能和血脂均无异常。C 肽升高。HbA1c(14.5%,Biorad D10 离子交换色谱法,图 1)升高。推测诊断为 2 型糖尿病。除了生活方式和饮食干预外,还开始使用二甲双胍缓释剂和 18 单位的基础胰岛素。血糖监测显示血糖控制良好,血糖水平在 4.7 至 6.3 毫摩尔/升之间。由于血糖水平稳定,基础胰岛素被迅速减少,最终在 4 周后停止使用。果糖胺较低,为 231 μmol/L (250-380),口服葡萄糖耐量试验(OGTT)正常;空腹血糖为 4.5 mmol/L (&lt;6.1 mmol),60 分钟血糖为 5.0 mmol/L (&lt;7.8 mmol/L),120 分钟血糖为 4.6 mmol/L (&lt;7.8 mmol/L)。Freestyle Libre 2 血糖连续监测系统显示 99% 的血糖读数在范围内(3.9-10.0 mmol/L)。用另一种检测方法复测了 HbA1c。HbA1c 正常,为 5.4%(三一生物技术公司硼酸盐亲和层析法)。假设潜在的血红蛋白病是导致 HbA1c 和 OGTT 结果不一致的原因。血红蛋白病筛查在第 11 区检测到 10.6% 的异常血红蛋白变异,提示为不常见的 alpha 变异(图 2)。进行了基因检测。DNA 测序发现,她是常见的单基因缺失(-α 3.7)α-地中海贫血突变和α1-球蛋白基因中的 HbA1:c382A&gt;G (汕头血红蛋白)变异的复合杂合子。HbA1:c382A&gt;G (Hb Shantou)基因变异是血红蛋白变异的原因。儿童 2 型糖尿病的发病率有所上升,尤其是在高危人群(澳大利亚土著居民、太平洋岛民和毛利人)1 中。诊断的依据是空腹血糖、OGTT 两小时血糖浓度或 HbA1c。在无症状的情况下,应在不同的日期重复检测以确认病情。2HbA1c 在糖尿病的诊断和管理中起着核心作用。A1c 的形成速度与红细胞寿命(通常为 120 天)内的葡萄糖浓度成正比。任何延长红细胞寿命或与红细胞新陈代谢减少有关的疾病,如铁/B12/叶酸缺乏性贫血和胰腺增生症,都可能导致 HbA1c 假性升高。严重的高甘油三酯血症、高胆红素血症和尿毒症也可能会使 HbA1c 假性升高3 。此外,血红蛋白变异也会导致 HbA1c 假性升高或降低。如果氨基酸取代导致净电荷发生变化(如 HbS、C、D 和 E),离子交换高效液相色谱法(HPLC)或电泳可能会受到影响。如果取代发生在糖化位点,糖化速率可能会受到影响。4 如果患者的血糖监测结果与 HbA1c 结果不一致、HbA1c 结果明显升高&gt;15%,以及 HbA1c 结果与之前的值有显著差异,则应怀疑患者存在血红蛋白变异体。关于汕头血红蛋白(HbA1:c382A&gt;G)的报道有限。5 汕头血红蛋白反映了α1-球蛋白基因上 c.382 A&gt;G 位点的核苷酸突变。5 Hb Shantou 反映了 α1-球蛋白基因上 c.382 A&gt;G 位点的核苷酸突变。一份已发表的报告描述了一例华裔孕妇因这种新型 α1-球蛋白基因突变而导致 HbA1c 值过高的病例。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Be alert to a spurious HbA1c: A rare alpha1-globin gene mutation

Be alert to a spurious HbA1c: A rare alpha1-globin gene mutation

An 11-year-old girl was investigated for impaired glucose tolerance. Her medical history included transient congenital hypothyroidism. Her family medical history was notable for type 2 diabetes mellitus affecting her mother, maternal grandmother, maternal uncle and paternal grandfather. She denied history of polyuria, polydipsia, weight loss and exogenous glucocorticoid administration. On examination, her weight was 72.3 kg (99.5 percentile, Z = 2.59), height 160.5 cm (98.9 percentile, Z = 2.30) and body mass index 28.1 kg/m2 (98.0 percentile, Z = 2.06). Acanthosis nigricans was noted circumferentially around her neck. There was no clinical stigmata of endogenous hypercortisolism. Initial biochemistry (Table 1) demonstrated elevated glycosylated haemoglobin (HbA1c) at 14.9%. Antibodies associated with type 1 diabetes mellitus were negative. Full blood count, thyroid function, renal function and haematinics were unremarkable. C-peptide was elevated. Liver function, urinary albumin/creatinine ratio and lipid profile were unremarkable.

Repeat HbA1c (14.5%, Biorad D10 Ion exchange chromatography, Fig. 1) was elevated. A presumed diagnosis of type 2 diabetes was made. Metformin extended release and 18 units of basal insulin were commenced, in addition to life-style and dietary intervention. Blood glucose monitoring reflected excellent glycaemic control, with blood sugar levels between 4.7 and 6.3 mmol/L. Basal insulin was rapidly reduced, and eventually ceased after 4 weeks due to stable blood glucose levels. A spurious HbA1c result was suspected.

Fructosamine was low at 231 μmol/L (250–380) and oral glucose tolerance test (OGTT) was normal; fasting glucose 4.5 mmol/L (<6.1 mmol), 60-min glucose 5.0 mmol/L (<7.8 mmol/L) and 120-min glucose 4.6 mmol/L (<7.8 mmol/L). A Freestyle Libre 2 Continuous Glucose Monitoring System displayed 99% of blood glucose readings in range (3.9–10.0 mmol/L). HbA1c was repeated on an alternative assay. HbA1c was normal at 5.4% (Trinity Biotech Boronate Affinity Chromatography). Metformin was ceased, and the diagnosis of type 2 diabetes was revised.

An underlying haemoglobinopathy was hypothesised to cause the discrepancy in HbA1c and OGTT results. A haemoglobinopathy screen detected an abnormal haemoglobin variant in zone 11 of 10.6%, suggestive of an uncommon alpha variant (Fig. 2). Genetic testing was undertaken. DNA sequencing found her to be compound heterozygous for the common single gene deletion (−alpha 3.7) alpha thalassaemia mutation and the HbA1:c382A>G (Hb Shantou) variant in the alpha1-globin gene. The HbA1:c382A>G (Hb Shantou) genetic variant is responsible for the haemoglobin variant.

Cascade testing in her family is underway.

The incidence of paediatric type 2 diabetes has increased, especially in high-risk ethnic groups (Indigenous Australians, Pacific Islanders and Maori people).1 Close monitoring and intensive management of paediatric type 2 diabetes is crucial; glycaemic control typically deteriorates quickly, and complications occur earlier than in adults. Diagnosis is based on fasting glucose, or 2-h glucose concentration during an OGTT or HbA1c. In the absence of symptoms, testing should be confirmed with a repeat test on a different day.2

HbA1c holds a central role in the diagnosis and management of diabetes mellitus. The rate of A1c formation is proportional to the concentration of glucose within the erythrocyte during its life-span, typically 120 days. It is important to be alert to clinical scenarios and interfering factors that may yield false results.3 Falsely elevated HbA1c can be seen in any condition that prolongs the life of the erythrocyte or is associated with reduced red cell turnover, such as iron/B12/folate deficiency anaemia and asplenia. Severe hypertriglyceridaemia, hyperbilirubinaemia and uraemia may also falsely elevate HbA1c.3 Falsely low HbA1c results can be seen in acute and chronic bone loss, haemolytic anaemia and splenomegaly. In addition, haemoglobin variants can lead to falsely elevated or lowered HbA1c. If the amino acid substitution causes a change in the net charge (as with HbS, C, D and E), ion-exchange high-performance liquid chromatography (HPLC) or electrophoresis may be affected. If a substitution occurs at a glycation site, the rate of glycation may be affected. If the variant causes a reduced erythrocyte life-span, the HbA1c would be falsely lowered, irrespective of method used.4 The presence of a haemoglobin variant should be suspected in patients with incongruent glucose monitoring and HbA1c results, markedly elevated HbA1c results>15% and significantly different HbA1c results compared to a previous value.3

Reports of Hb Shantou (HbA1:c382A>G) are limited.5 Hb Shantou reflects a nucleotide mutation at position c.382 A>G on the α1-globin gene. A single published report describes a case of a falsely high HbA1c value in a pregnant woman of Chinese ethnicity due to this novel α1-globin gene mutation.5

Fructosamine measurement, glycated albumin and continuous glucose monitoring may provide alternatives to HbA1c. Fructosamine, the product formed by a nonenzymatic reaction of glucose and serum proteins, reflects a shorter period of glycaemic control (typically 2–3 weeks) compared to HbA1c as the half-life of albumin is approximately 20 days.3 The accuracy of fructosamine measurement is limited in situations of hypoproteinaemia/hypoalbuminaemia, such as nephrotic syndrome and chronic liver disease. In addition, boronate affinity HPLC, subsequently utilised in our case, is not typically affected by haemoglobin variant interference6 and may provide a more accurate representation of glycaemic control.

In conclusion, as rates of type 2 diabetes increase in our paediatric population, clinicians should be alert to the limitations and inaccuracies of diagnostic and monitoring tests, most notably HbA1c. Haemoglobin variants may falsely elevate or lower HbA1c, and alternative diagnostic methods are required to improve accuracy.

求助全文
通过发布文献求助,成功后即可免费获取论文全文。 去求助
来源期刊
CiteScore
2.90
自引率
5.90%
发文量
487
审稿时长
3-6 weeks
期刊介绍: The Journal of Paediatrics and Child Health publishes original research articles of scientific excellence in paediatrics and child health. Research Articles, Case Reports and Letters to the Editor are published, together with invited Reviews, Annotations, Editorial Comments and manuscripts of educational interest.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术官方微信