Kelishadi Roya, Poursafa Parinaz, Keramatian Kasra
Professor, Department of Paediatrics, Child Health Promotion Research Center, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran.
J Res Med Sci. 2011 Sep;16(9):1234-50.
Pediatric pre-hypertension (pre-HTN) has a complex multifactorial etiology. Although most cases are secondary to other disorders, a substantial number of children and adolescents have primary or essential HTN and pre-HTN. The gene-gene and gene-environment interactions should be considered in this context. The strong relationship of pre-HTN with environmental factors such as air pollution, noise pollution and passive smoking and obesity suggest that its prevalence will be escalating.Exposure to ambient particulate matters may increase blood pressure (BP) within hours to days. The underlying biologic pathways include autonomic nervous system imbalance and arterial vascular dysfunction or vasoconstriction because of systemic oxidative stress and inflammation. Likewise, tobacco smoke exposure of pregnant mothers increases systolic BP of their offspring in early infancy. Parental smoking also independently affects systolic BP among healthy preschool children. Noise exposure, notably in night, is associated with catecholamine secretion, increased BP and a pre-HTN state even in pre-school age children.Excess weight is associated with dysfunction of the adipose tissue, consisting of enlarged hypertrophied adipocytes, increased infiltration by macrophages and variations in secretion of adipokines and free fatty acids. These changes would result in chronic vascular inflammation, oxidative stress, activation of the renin-angiotensin-aldosterone system and sympathetic response, and ultimately to pre-HTN from childhood.Prevention and control of the modifiable risk factors of pre-HTN from prenatal period can have long-term health impact on primordial and primary prevention of chronic non-communicable diseases. This review presents a general view on the diagnosis, prevalence and etiology of pre-HTN along with practical measures for its prevention and control.
儿童高血压前期有复杂的多因素病因。虽然大多数病例继发于其他疾病，但相当数量的儿童和青少年患有原发性或特发性高血压及高血压前期。在这种情况下应考虑基因-基因和基因-环境相互作用。高血压前期与空气污染、噪音污染、被动吸烟和肥胖等环境因素的密切关系表明其患病率将会不断上升。接触环境颗粒物可能在数小时至数天内使血压升高。潜在的生物学途径包括自主神经系统失衡以及由于全身氧化应激和炎症导致的动脉血管功能障碍或血管收缩。同样，孕妇接触烟草烟雾会使其后代在婴儿早期收缩压升高。父母吸烟也会独立影响健康学龄前儿童的收缩压。噪音暴露，尤其是夜间暴露，即使在学龄前儿童中也与儿茶酚胺分泌增加、血压升高和高血压前期状态有关。超重与脂肪组织功能障碍有关，表现为肥大的脂肪细胞增大、巨噬细胞浸润增加以及脂肪因子和游离脂肪酸分泌的变化。这些变化会导致慢性血管炎症、氧化应激、肾素-血管紧张素-醛固酮系统激活和交感反应，最终导致儿童期高血压前期。从围生期预防和控制高血压前期的可改变风险因素对慢性非传染性疾病的初级预防和一级预防具有长期健康影响。本综述对高血压前期的诊断、患病率和病因以及预防和控制的实际措施进行了概述。
