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ORIGINAL ARTICLE
Year : 2018  |  Volume : 131  |  Issue : 4  |  Page : 435-439

Increased Endogenous Sulfur Dioxide Involved in the Pathogenesis of Postural Tachycardia Syndrome in Children: A Case-Control Study


1 Department of Pediatrics, Peking University First Hospital, Beijing 100034, China
2 Department of Cardiac Surgery, Guangdong General Hospital, Guangzhou, Guangdong 510000, China
3 Department of Intensive Care, Kaifeng Children's Hospital, Kaifeng, Henan 475000, China
4 Department of Physiology and Pathophysiology, Peking University Health Science Center, and Key Laboratory of Molecular Cardiology of Ministry of Education, Beijing 100191, China

Correspondence Address:
Prof. Yong-Hong Chen
Department of Pediatrics, Peking University First Hospital, Beijing 100034
China
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0366-6999.225051

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Background: The pathogenesis of postural tachycardia syndrome (POTS) remains unclear. This study aimed to explore the changes and significance of sulfur dioxide (SO2) in patients with POTS. Methods: The study included 31 children with POTS and 27 healthy children from Peking University First Hospital between December 2013 and October 2015. A detailed medical history, physical examination results, and demographic characteristics were collected. Hemodynamics was recorded and the plasma SO2was determined. Results: The plasma SO2was significantly higher in POTS children compared to healthy children (64.0 ± 20.8 μmol/L vs. 27.2 ± 9.6 μmol/L, respectively, P < 0.05). The symptom scores in POTS were positively correlated with plasma SO2levels (r = 0.398, P < 0.05). In all the study participants, the maximum heart rate (HR) was positively correlated with plasma levels of SO2(r = 0.679, P < 0.01). The change in systolic blood pressure from the supine to upright (ΔSBP) in POTS group was smaller than that in the control group (P < 0.05). The ΔSBP was negatively correlated with baseline plasma SO2levels in all participants (r = −0.28, P < 0.05). In the control group, ΔSBP was positively correlated with the plasma levels of SO2(r = 0.487, P < 0.01). The change in HR from the supine to upright in POTS was obvious compared to that of the control group. The area under curve was 0.967 (95% confidence interval: 0.928–1.000), and the cutoff value of plasma SO2 level >38.17 μmol/L yielded a sensitivity of 90.3% and a specificity of 92.6% for predicting the diagnosis of POTS. Conclusions: Increased endogenous SO2levels might be involved in the pathogenesis of POTS.

 

 Abstract in Chinese

内源性二氧化硫含量升高可能与儿童体位性心动过速综合征的发病机制相关

摘要

目的: 体位性心动过速综合征 (postural tachycardia syndrome, POTS) 的发病机制尚不明确, 此研究的目的是为了探索血浆二氧化硫 (sulfur dioxide, SO2) 含量在POTS患儿中的变化及意义。

方法: 本研究共有31例POTS患儿和27例健康对照组儿童。31例POTS患儿均为于2013年12月到2015年10月期间在北京大学第一医院儿科以直立不耐受症状就诊的患儿。 病史询问, 体格检查, 人口学特征及血流动力学参数等信息数据进行了收集。 同时测定了POTS患儿和健康对照组儿童血浆SO2 含量。

结果: POTS患儿血浆SO2含量明显高于对照组 (64.0 ± 20.8 mmol/l vs. 27.2 ± 9.6 mmol/l, P < 0.05); POTS患儿血浆SO2含量与症状评分呈正相关 (n = 31, r = 0.398, P < 0.05); 血浆SO2含量与最大心率呈正相关 (n = 58, r = 0.679, P < 0.01); POTS组的平卧位到直立位的血压变化值 (D(平卧) 明显低于对照组 (P < 0.05); POTS组和对照组的D和对照与血浆SO2含量呈负相关 (n = 58, r = −0.28, P < 0.05); 对照组的D照组的与血浆SO2含量呈正相关 (n = 27, r = 0.487, P < 0.01); POTS组的平卧位到直立位的心率变化值 (D(平) 明显高于对照组; 采用ROC曲线分析血浆SO2含量诊断POTS的价值, 曲线下面积为0.967, 置信区间为 (95% CI 0.928-1.000), 以血浆SO2含量38.17 mmol/l 为界值, 敏感度为90.3%, 特异度为 92.6%。

结论: 内源性SO2含量升高可能与POTS的发病机制有关。



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