Fasting plasma glucose is an independent predictor for severity of H1N1 pneumonia.
Fasting plasma glucose is an independent predictor for severity of H1N1 pneumonia.
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DOI：
10.1186/1471-2334-11-104
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发表时间：
2011-04-21
影响因子：
3.7
通讯作者：
Zhang J
中科院分区：
文献类型：
--
作者：
Wang W;Chen H;Li Q;Qiu B;Wang J;Sun X;Xiang Y;Zhang J
甲型H1N1流感病毒于2009年出现，并在全球范围内蔓延。这种病毒会对肺、肝和心脏造成伤害。然而，关于这种流感病毒是否会影响胰岛的数据有限。我们研究了甲型H1N1流感肺炎对空腹血糖（FPG）和胰岛功能的影响，并评估了生化检测结果与H1N1肺炎严重程度之间可能的相关性。我们对2009年收治的确诊或疑似H1N1肺炎患者进行了回顾性分析。FPG水平和H1N1病毒感染之间的可能关联通过logistic回归进行评估。相关和回归分析用于评估FPG和生化检测结果之间的关系。通过单因素线性回归评估入院天数与重要数据之间的关系。为了评估H1N1对胰腺β细胞功能的影响，通过t检验比较H1N1组和非H1N1组之间的抵抗指数（homa-IR）、胰岛素功能指数（β-胰岛素）和胰岛素敏感性指数（IAI）的结果。FPG与H1N1病毒感染显著正相关（OR = 1.377，95%CI：1.062-1.786; p = 0.016）。在H1N1组中，FPG与AST（r = 0.215; p = 0.039）、LDH（r = 0.400; p = 0.000）、BUN（r = 0.28; p = 0.005）和动脉血氧饱和度（SaO 2; r = -0.416; p = 0.000）显著相关。低氧血症（SaO 2 <93%）的H1N1患者的FPG水平高于无低氧血症的患者（9.82 ± 4.14 vs. 6.64 ± 1.78; p < 0.05）。H1N1缺氧组FPG与SaO 2呈负相关（SaO 2 <93; r = -0.497; p = 0.041）。高FPG（≥7 mmol/L）患者SaO 2水平显著低于低FPG（<5.6 mmol/L）的H1N1患者。在调整年龄、性别和BMI后，H1N1和非H1N1组之间的homa-IR、β-淀粉样蛋白或IAI没有显著差异。入院时FPG可作为H1N1肺炎严重程度的独立预测因子。H1N1肺炎引起的FPG升高不是直接损伤胰岛β细胞的结果，而是H1N1病毒感染引起的多种因素综合作用的结果。
The pandemic influenza A (H1N1) virus emerged during 2009 and has spread worldwide. This virus can cause injuries to the lungs, liver, and heart. However, data regarding whether this influenza virus can affect pancreatic islets are limited. We investigated the effects of influenza A (H1N1) pneumonia on fasting plasma glucose (FPG) and islet function, and evaluated possible correlations between biochemical test results and the severity of H1N1 pneumonia. We performed a retrospective analysis of patients either diagnosed with or suspected of having H1N1 pneumonia who were admitted to our hospital in 2009. Possible associations between FPG levels and H1N1 virus infection were assessed by logistic regression. Correlation and regression analyses were used to assess relationships between FPG and biochemical test results. Associations between admission days and significant data were assessed by single factor linear regression. To evaluate effects of H1N1 on pancreatic β-cell function, results of a resistance index (homa-IR), insulin function index (homa-β), and insulin sensitivity index (IAI) were compared between a H1N1 group and a non-H1N1 group by t-tests. FPG was significantly positively associated with H1N1 virus infection (OR = 1.377, 95%CI: 1.062-1.786; p = 0.016). FPG was significantly correlated with AST (r = 0.215; p = 0.039), LDH (r = 0.400; p = 0.000), BUN (r = 0.28; p = 0.005), and arterial Oxygen Saturation (SaO2; r = -0.416; p = 0.000) in the H1N1 group. H1N1 patients who were hypoxemic (SaO2<93%) had higher FPG levels than those who were not hypoxic (9.82 ± 4.14 vs. 6.64 ± 1.78; p < 0.05). FPG was negatively correlated with SaO2 in the H1N1 group with hypoxia (SaO2<93; r = -0.497; p = 0.041). SaO2 levels in patients with high FPG levels (≥7 mmol/L) were significantly lower than those of H1N1 patients with low FPG levels (<5.6 mmol/L). There were no significant differences in homa-IR, homa-β, or IAI between the H1N1 and non-H1N1 groups after adjusting for age, sex, and BMI. FPG on admission could be an independent predictor for the severity of H1N1 pneumonia. Elevated FPG induced by H1N1 pneumonia is not a result of direct damage to pancreatic β-cells, but arises from various factors' combinations caused by H1N1 virus infection.
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