Medical School, University of Birmingham, Birmingham, UK.
Clinical Laboratory Services, University Hospitals Birmingham NHS Foundation Trust, Birmingham, UK.
Diabet Med. 2019 Nov;36(11):1444-1452. doi: 10.1111/dme.13870. Epub 2019 Apr 30.
To investigate the relationship between HbA and glucose in people with co-existing liver disease and diabetes awaiting transplant, and in those with diabetes but no liver disease.
HbA and random plasma glucose data were collected for 125 people with diabetes without liver disease and for 29 people awaiting liver transplant with diabetes and cirrhosis. Cirrhosis was caused by non-alcoholic fatty liver disease, hepatitis C, alcoholic liver disease, hereditary haemochromatosis, polycystic liver/kidneys, cryptogenic/non-cirrhotic portal hypertension and α-1-antitrypsin-related disease.
The median (interquartile range) age of the diabetes with cirrhosis group was 55 (49-63) years compared to 60 (50-71) years (P=0.13) in the group without cirrhosis. In the diabetes with cirrhosis group there were 21 men (72%) compared with 86 men (69%) in the group with diabetes and no cirrhosis (P=0.82). Of the group with diabetes and cirrhosis, 27 people (93%) were of white European ethnicity, two (7%) were South Asian and none was of Afro-Caribbean/other ethnicity compared with 94 (75%), 16 (13%), 10 (8%)/5 (4%), respectively, in the group with diabetes and no cirrhosis (P=0.20). Median (interquartile range) HbA was 41 (32-56) mmol/mol [5.9 (5.1-7.3)%] vs 61 (52-70) mmol/mol [7.7 (6.9-8.6)%] (P<0.001), respectively, in the diabetes with cirrhosis group vs the diabetes without cirrhosis group. The glucose concentrations were 8.4 (7.0-11.2) mmol/l vs 7.3 (5.2-11.5) mmol/l (P=0.17). HbA was depressed by 20 mmol/mol (1.8%; P<0.001) in 28 participants with cirrhosis but elevated by 28 mmol/mol (2.6%) in the participant with α-1-antitrypsin disorder. Those with cirrhosis and depressed HbA had fewer larger erythrocytes, and higher red cell distribution width and reticulocyte count. This was reflected in the positive association of glucose with mean cell volume (r=0.39) and haemoglobin level (r=0.49) and the negative association for HbA (r=-0.28 and r=-0.26, respectively) in the diabetes group with cirrhosis.
HbA is not an appropriate test for blood glucose in people with cirrhosis and diabetes awaiting transplant as it reflects altered erythrocyte presentation.
研究同时患有肝病和糖尿病并等待移植的患者以及仅患有糖尿病而无肝病的患者的糖化血红蛋白(HbA)与血糖之间的关系。
我们收集了 125 名无肝病的糖尿病患者和 29 名患有糖尿病和肝硬化的等待肝移植的患者的 HbA 和随机血浆葡萄糖数据。肝硬化由非酒精性脂肪性肝病、丙型肝炎、酒精性肝病、遗传性血色素沉着症、多囊肝/肾、隐匿性/非肝硬化门静脉高压和α-1-抗胰蛋白酶相关疾病引起。
与无肝硬化的糖尿病组相比,肝硬化糖尿病组的中位(四分位间距)年龄为 55(49-63)岁,而 60(50-71)岁(P=0.13)。在肝硬化糖尿病组中,有 21 名男性(72%),而无肝硬化的糖尿病组中,有 86 名男性(69%)(P=0.82)。在肝硬化糖尿病组中,27 名患者(93%)为白种欧洲人,2 名(7%)为南亚人,没有非裔加勒比人/其他人种,而无肝硬化的糖尿病组中,94 名(75%)、16 名(13%)、10 名(8%)/5 名(4%)分别为白种欧洲人、南亚人、非裔加勒比人/其他人种(P=0.20)。肝硬化糖尿病组的中位(四分位间距)HbA 为 41(32-56)mmol/mol [5.9(5.1-7.3)%],无肝硬化的糖尿病组为 61(52-70)mmol/mol [7.7(6.9-8.6)%](P<0.001)。肝硬化糖尿病组的葡萄糖浓度为 8.4(7.0-11.2)mmol/l,无肝硬化的糖尿病组为 7.3(5.2-11.5)mmol/l(P=0.17)。28 名肝硬化患者的 HbA 降低了 20 mmol/mol(1.8%;P<0.001),而 1 名α-1-抗胰蛋白酶紊乱患者的 HbA 升高了 28 mmol/mol(2.6%)。肝硬化和 HbA 降低的患者具有较少的较大红细胞,并且具有更高的红细胞分布宽度和网织红细胞计数。这反映在肝硬化糖尿病组中,葡萄糖与平均红细胞体积(r=0.39)和血红蛋白水平(r=0.49)呈正相关,与 HbA 呈负相关(r=-0.28 和 r=-0.26)。
在等待移植的肝硬化和糖尿病患者中,HbA 不能作为血糖的适当检测手段,因为它反映了红细胞形态的改变。