Curr Hypertens Rep (2014) 16:495 DOI 10.1007/s11906-014-0495-z

PEDIATRIC HYPERTENSION (JT FLYNN, SECTION EDITOR)

The Emerging Epidemic of Hypertension in Asian Children and Adolescents Chong Guk Lee

Published online: 11 October 2014 # Springer Science+Business Media New York 2014

Abstract Hypertension has become a serious global public health burden because of its high incidence and concomitant risk of cardiovascular disease. Many studies have verified that risk factors, such as hypertension and obesity which are responsible for cardiovascular disease, start in early childhood. In Asian countries, the prevalence of hypertension in the pediatric age group has become more prevalent than ever before with the increasing obesity epidemic. To tackle the epidemic of cardiovascular disease, a leading cause of death and disability of non-communicable diseases in Asian countries, population-based measures aiming at reducing harmful environmental factors to blood pressure and body weight must be applied to individuals in their early childhood, as early as the fetal stage. This review focused on the prevalence of pediatric hypertension in Asian countries and outlined several considerations for accurate blood pressure (BP) measurement and evaluation, along with an overview of pathophysiology of fetal programming and obesity related with childhood hypertension.

Keywords Non-communicable disease . Pediatric hypertension . Asian children . Blood pressure measurement devices . Mercurial sphygmomanometer . Oscillometric device . Blood pressure reference tables . Secular trend . Tracking phenomenon . Low birth weight . Fetal programming . Obesity

This article is part of the Topical Collection on Pediatric Hypertension C. G. Lee (*) Division of Pediatric Nephrology, Department of Pediatrics, Ilsan Paik Hospital, Inje University, 2280, Ilsanseo-gu, Goyang-si, Gyeonggi-do 411-706, South Korea e-mail: [email protected]

Introduction The WHO global status report on non-communicable diseases (NCDs) shows that NCDs are the leading causes of death in the world, responsible for 63 % of deaths in 2008. The majority of these deaths are attributed to cardiovascular diseases (48 %), cancers (21 %), chronic respiratory diseases (12 %), and diabetes (2 %) [1, 2]. The leading risk factors for this mortality are hypertension (responsible for 13 % of deaths globally) and obesity (5 %), followed by tobacco use, high blood glucose, and physical inactivity [3]. Alarmingly, these risk factors are the major causes of death and disability burden in nearly all countries, regardless of the extent of economic development. In fact, NCD burden is increasing more rapidly in Asian countries [4]. The prevalence of hypertension in adults in various regions of the world has been widely reported [4, 5]. However, sufficient epidemiologic data on blood pressure (BP) in relation to prevalence and absolute burden in children and adolescents have not been compiled. Even though the prevalence, awareness, treatment, and control of hypertension in developing countries are coming closer to those in developed countries [6], their own accurate estimates of the prevalence of hypertension are essential for the rational planning of health services for their children and adolescents. Hypertension used to be regarded as an adult disease with no real relevance to children, because pediatric hypertension was thought to be mostly attributed to secondary causes [7•], and because the economic impact of pediatric hypertension was so trivial as compared to costs related to adult hypertension [8, 9]. If so, why should we be concerned about pediatric hypertension in Asian countries? Reasons that justify the recent increasing attention to pediatric hypertension can be summarized as follows: (i) epidemiologic shift to primary hypertension with increasing obesity epidemic [7•, 10•], (ii) tracking phenomenon of BP from childhood to adulthood [11,

495, Page 2 of 9

12•], (iii) target organ damage (TOD) related to primary hypertension in children [13–15], and (iv) high incidence of childhood obesity and low birth weight (LBW) infant in Asian countries [3, 16]. In this review, the uncertainty of BP reference tables for Asian children and adolescents in making diagnosis of pediatric hypertension, the prevalence of pediatric hypertension in Asian countries, and secular trends and tracking phenomenon of primary hypertension in children and adolescents are described. Furthermore, an overview of programming of hypertension in LBW infants and the pathophysiology of hypertension with obesity are presented.

Curr Hypertens Rep (2014) 16:495

a

male

mmHg 160 140 120

SBP

100 80

DBP

60 40 20

The Diagnostic Uncertainty of BP Reference Tables for Asian Children and Adolescents

0 8

BP is defined differently in children than in adults. As children and adolescents grow into adult size, their BP normally exhibits a gradual rise. A gender difference in adolescents in the normal range of BP, with lower levels in female than in male, is also noted. Therefore, children’s BP is categorized from thresholds based on gender, age, and height. The fourth report from National H igh B lood Pressure Edu cation P rogram (2004NHBPEP)’s Working Group on High Blood Pressure in Children and Adolescents defines hypertension as the average systolic BP (SBP) or diastolic BP (DBP) that is greater than or equal to the 95th percentile for gender, age, and height on at least three separate occasions [17]. This statistical definition based on the normative distribution of BP in healthy children lacks the evidence-based findings found in adult guidelines [18]. Another limitation to using this percentile definition is the need to account for the secular trend of body size and accompanying change in BP which may vary in children and adolescents from different countries, because the socioeconomic environment of human populations are substantially different among countries [5, 19•, 20]. Therefore, it is uncertain whether the 2004NHBPEP BP reference table is applicable to children and adolescents in other countries, who have different ethnic and biocultural backgrounds. High BP (prehypertension and hypertension) in Asian countries, namely China, Japan, and Korea, is defined by either the SBP, DBP, or both values exceeding the 90th and 95th percentiles of the recommended BP reference cutoffs for their own children. They are using their own BP reference tables [21, 22]. Figure 1 is showing the differences in BP levels of the 95th percentile in the BP reference tables of Korea [21], China [22], and the USA [17], respectively. Only the 95th BP levels of the 50th age-specific height percentile of each age group were compared. The SBP of males across different age groups was 5–8 mmHg greater in the Korean population than that in the US population, but there was little difference between SBP of the USA and China in the age group of 7–14 years, with a 4 mmHg greater BP after 15 years

9

10

Age(years)

b

11

12

13

2007 Korea

14

15

16

2010 China

17

2004 USA

female

mmHg 140

120

SBP 100

80

DBP

60

40

20

0 7 Age(years)

8

9

10 2007 Korea

11

12

13

2010 China

14

15

16

17

2004 USA

Fig. 1 Comparison of the systolic and diastolic BP 95th percentile in male (a) and female (b) between Korea (21), China (22), and the USA (17) blood pressure reference tables

of age in the US population. SBPs in females showed a slight difference of 1–5 mmHg among the three countries. However, DBP of the Korean population demonstrated a much lower level by 5–11 mmHg than that of the USA and by 2–6 mmHg than that of China. These differences could be explained by ethnic differences or differences in the BP measurement methodology. BP was measured using a mercury sphygmomanometer in China and the USA, but an oscillometric device (Dinamap ProCare 300) in Korea. Though the 2004NHBPEP recommends auscultation as the preferred method of measuring BP in children, not specifically a mercury sphygmomanometer [17], a mercury sphygmomanometer is mostly being used as the standard device for accurate BP measurement in children and adolescents.

Curr Hypertens Rep (2014) 16:495

However, because of environmental concerns about mercurial toxicity, alternate instruments are needed. Oscillometric devices, widely being used, have advantages of their ease of use and minimization of observer bias in BP measurements on young children [23]. However, a major disadvantage is that BP level measured by oscillometric devices does not always match BP level obtained by a mercury sphygmomanometer [24]. Oscillometric devices measure mean arterial BP and then calculate SBP and DBP through algorithms which are proprietary and differ depending on the maker and device [25]. Therefore, oscillometric devices must be validated on a regular basis. Protocols for validation have been developed, but the validation process is limited to adults of over 25 years old [26•]. BP measurement using oscillometric devices is based on the principle that pulsatile blood flow through an artery creates oscillations of the arterial wall, and these oscillations are sensed to determine BP. Oscillations of blood vessels can vary according to the state of their stiffness [27]. Therefore, validation studies of oscillometric devices in children and adolescents are needed. When the two devices were compared, a mercury sphygmomanometer (Baumanometer Mercury Gravity Sphygmomanometer, W.A. Baum Co., Copiague, NY, USA) vs. an oscillometric device (Dinamap ProCare 300, GE Medical Systems, Milwaukee, WI, USA), the oscillometric device showed a 1.85 ± 1.65 mmHg greater SBP and a 4.41 ± 3.53 mmHg lower DBP [28]. The difference of BP readings measured by the oscillometric device and the mercurial device in 290 children and adolescents in the clinical setting was 3.8 ±9.1 mmHg greater for SBP and 5.9±7.9 mmHg lower for DBP, respectively, in the oscillometric device [29]. In comparison with the Omron 705 IT (Omron Healthcare, Inc., Bannockburn, IL, USA), another oscillometric device, the mean SBP reading was 4.6±4.9 mmHg greater, and the mean DBP reading was 3.3±5.4 mmHg lower [30]. In general, oscillometric devices record slightly higher SBP levels, but lower DBP levels compared to those measured by mercurial devices in children and adolescents. Accordingly, when BP readings are evaluated in children and adolescents, the difference of BP level between the auscultation and oscillometric device is needed to be considered. The 2004NHBPEP recommends that an elevated BP reading obtained with an oscillometric device should be repeated by using auscultation [17]. Prevalence of Hypertension in Asian Pediatric Age Group The prevalence of pediatric hypertension vary greatly depending on the differences in the definition of high BP, normative BP reference tables, BP measurement devices, and the number of occasions on which BP is measured. Based on the use of ≥95th percentile to define hypertension, the prevalence of hypertension is expected to be approximately 5 %. However,

Page 3 of 9, 495

due to the effects of accommodation and regression to the mean with repeated measurements, the actual prevalence of hypertension is lower than 5 % and had been reported to be 1– 3 % after three separate BP measurements in children and adolescents with an initial BP measurement in the ≥95th percentile [31]. BP screening studies conducted in schools show that many children with an initially high BP have normal BP after repeated measurements [32]. This reduction in the prevalence of hypertension after repeated measurements emphasizes that a single elevated BP is insufficient to make the clinical diagnosis of hypertension in children and adolescents [33]. A recent survey in community-based practices in the USA showed that the prevalence of prehypertension and hypertension was 12.7 and 5.4 %, respectively, at the first visit, but it was 12.0 and 0.3 %, respectively, after two subsequent visits [34]. In view of those variables in determining the prevalence of pediatric hypertension in a certain area, it seems to be inappropriate to compare the prevalence rate in a country with others. A standardized method for BP measurement and evaluation should be uniformly applied to the surveillance study of childhood BP. The epidemiologic evidence to support an adverse impact of childhood obesity on BP levels has been suggested. In China, prevalence rates of prehypertension and hypertension accounted for 7.2 and 3.1 %, respectively, according to the criteria of recommended BP reference cutoffs for Chinese children [22] in Changsha City. Being overweight or obese was both markedly associated with an increased risk of hypertension and prehypertension. The proportions of adolescents with hypertension across the body mass index (BMI) categories were, respectively, 1.0, 3.3, and 11.5 % in normal weight, overweight, and obese girls and 2.6, 7.5, and 21.7 % in normal weight, overweight, and obese boys [10•]. Another Chinese national survey in 2010 showed that the prevalence of hypertension was 16.1 % for boys and 12.9 % for girls [35]. A perspective on the prevalence of hypertension in Korean children and adolescents can be made using the results of nationwide health examinations for school students aged 7 to 18 years. Hypertension was defined by BP over ≥95th percentile of the Korean BP reference table by gender, age, and height [21, 36]. Screening studies conducted in 7-, 10-, 13-, and 16-year-old children and adolescents of 87,253 in 2012 revealed the prevalence of hypertension after the first screening to be 2.8, 4.6, 7.1, and 8.2 %, respectively [37]. It surely does not represent the actual prevalence of hypertension in Korean children and adolescents. Repeated measurements, at least three times apart, will result in much lower rates. The prevalence of obesity (BMI ≥95th percentile of the 2007 Korean growth chart) was around 10 % before the age of 11 years but increased abruptly to 22 % at the age of 17 to 18 years in males; however, it was 8 % before the age of 12 years and then reached 13.2 % at the age of 18 years in females [37]. Another study showed that the overall

495, Page 4 of 9

prevalence of hypertension among 46,024 children and adolescents between the ages of 7 and 18 years in 2005 Korea national survey was 10.6 % (12.9 % in male and 8.2 % in female, respectively). The survey was based on single BP measurements by using an oscillometric device and the 2004NHBPEP BP table. The proportions of hypertension across the BMI categories were, respectively, 7.5, 17.7, and 28.8 % in normal weight, overweight, and obese children and adolescents (unpublished data). The prevalence of obesity (BMI ≥95th percentile) increased from 5.5 to 9.7 % in the period of 10 years from 1995 to 2005 [38]. From numerous studies regarding the prevalence of childhood hypertension, it appears to have an overall prevalence of 2.5–3 % in children and adolescents and, of prehypertension, a prevalence of 9–12 % after repeated measurements. Recent studies have demonstrated that prevalence is generally similar in different countries irrespective of socioeconomic conditions in each country [7•]. Also, many analyses have verified that the population increase in BP among children and adolescents is largely due to the increase incidence of obesity [31]. Secular Trends and Tracking Phenomenon of Primary Hypertension in Children and Adolescents It is well established that hypertension in childhood is frequently associated with obesity. Increasing obesity epidemic all over the world, even in Asian countries, results in a high prevalence of hypertension [7•, 9, 10•]. The National Health and Nutrition Examination Survey (NHANES) in the USA showed that mean BP levels have increased in children over the past decade. SBP and DBP were found to increase by 1.4 and 3.3 mmHg from 1988–1994 to 1999–2000 [39]; also, during the same period, an overall increase in the prevalence of hypertension from 2.7 % in the 1988–1994 survey to 3.7 % in the 1999–2002 survey was reported [40]. A recent analysis of NHANES data revealed that the prevalence of elevated BP increased from NHANES III to NHANES 1999–2008 (boys, 15.8 to 19.2 %; girls, 8.2 % to 12.6 %). Increased prevalence of elevated BP was independently associated with BMI [41]. In the cohort study established in the USA, researchers tracked growth and BP for 27 years. They reported that the rate of hypertension was higher in children who were overweight or obese (14 and 26 %, respectively). Children classified as overweight or obese had double and quadruple the risk to have a diagnosis of hypertension in adulthood, respectively, as compared to normal weight children [42]. A Japanese group assessed the health report data between 1983 and 2007 to clarify the relationship between long-term changes in BMI and BP levels in children and adolescent. Through multiple regression analysis, they concluded that higher changes in BMI (ΔBMI) over the 6-year period were associated with higher SBP even in children whose BMI was in the lowest tertile at baseline. They

Curr Hypertens Rep (2014) 16:495

insisted that growth during childhood should be carefully monitored because steeper BMI increases during primary school lead to adolescent increases in BP even if baseline BMI is low [43]. A Chinese study showed a relationship between the prevalence of hypertension or prehypertension and BMI. Approximately 53.4 % of the hypertensive cases were attributed to excess body weight, and the prevalence of hypertension in obese females and males was more than 11and 8-fold greater, respectively, than that in normal weight subjects [10•]. A recent study in China also showed that BP among Chinese children and adolescents was on the rise from 2005 to 2010 by 1.2–1.5 mmHg of SBP and 1.0–1.1 mmHg of DBP, respectively, which were decreased by 40.5 and 26.9 %, respectively, after adjusting for the differences in BMI in 2005 and 2010 [44•]. A study of a school-based population in Shanghai revealed that BMI and waist circumference (WC) were positively correlated with SBP and DBP. Being overweight or obese greatly increased the risk of hypertension in Chinese children and adolescents, in which WC, denoting central obesity, was considered as a more sensitive indicator than BMI [45]. Even though a contradictory finding that neither the mean nor high BP levels increased during the period in which the prevalence of obesity increased almost threefold was reported [46••], in general, most studies have clearly showed that the increase in absolute mean BP levels and the prevalence of hypertension seem to be related to the obesity epidemic and that the secular trend of BP in children and adolescents is closely related to the increased prevalence of obesity. The recent upward trend of childhood obesity in Asian countries following the socioeconomic development attributes to the rising rates of childhood high BP. Meta-analysis of data from diverse populations showed that BP tracks from childhood to adulthood and that an elevated BP in childhood is likely to predict adult hypertension [12•]. Tracking of BP over time has been an intriguing subject as a way of identifying one of the high risk factors, hypertension, for cardiovascular disease. It is clear that hypertension begins in childhood, and high BP in the young predicts future high BP in the adult. Therefore, identifying children with elevated BP and hypertension and starting early treatment or prevention of hypertension may have an important impact on the long-term outcome of cardiovascular disease [47]. Low Birth Weight and Hypertension Many studies have identified various risk factors that are attributable to the development of hypertension in childhood, such as genes, dietary intake, physical activity, and environmental factors. Recent epidemiologic data showed that fetal and perinatal events appear to exert effects on certain chronic diseases, such as hypertension and chronic kidney disease later in adulthood. The term of the Developmental Origin of

Curr Hypertens Rep (2014) 16:495

Health and Disease (DOHaD) emerged to describe the association between fetal and postnatal growth and, later, chronic adult diseases. DOHaD should be viewed as a part of a broader biological mechanism of plasticity by which organisms, in response to cues such as nutrition or hormones, adapt their phenotype to the environment [48, 49•]. Developmental plasticity, defined as the ability of an organism to develop in various ways, depending on the particular environment or setting [50••], provides a conceptual basis for DOHaD. This concept was first reported by Barker [51, 52], who showed a link between nutritional deficiency during fetal growth and adult diseases, hypertension and obesity. This Barker’s hypothesis was extended to an important paradigm, DOHaD, in a multidisciplinary field. Further extension of this idea developed into what became known as fetal origins of adult disease (FOAD). FOAD contends that environmental influences during fetal life can influence adult health and transgenerational inheritance of non-genomic information through various mechanisms, including epigenetics [50, 53, 54]. Birth weight is an indicator of nutrient availability in fetuses, and LBW is a marker of poor fetal growth. In the case of in utero stress caused by maternal undernutrition, the developing fetus senses the adverse environment and reprograms the genome, which favors immediate survival but results in predisposition to hypertension and obesity in adult life. When there is deprivation followed by plenty, catch-up growth occurs which predisposes the fetus to hypertension and obesity [55]. Fetal programming by maternal malnutrition results in LBW and reduction in nephron number, increasing the risk for hypertension and renal diseases [56]. A kidney with fewer nephrons was postulated to have a diminished filtration surface area, resulting in the limitation of sodium excretion, leading to raised BP and reduction of renal adaptive capacity in the setting of injury. A high prevalence of hypertension and renal disease in populations with an increased frequency of LBW (less than 2.5 kg) was recognized, whereby LBW and prematurity were shown as the most consistent clinical surrogates for a low nephron number and were associated with an increased risk of hypertension in later life [57••]. Globally, 15.5 % of live newborn babies born weigh less than 2.5 kg, as LBW infants, suggesting that they are at risk of hypertension and kidney disease in later life [58]. The incidence of LBW in Asian countries was reported to be around 18.3 %, with India contributing to 40 % of the developing world’s LBW population. In China, 1.1 million LBW infants were born in 2004 [58]; South Korea reported 25,900 LBW infants, which comprised 5 % of total live births in 2012 [59]. We, therefore, are sure that a quite large number of Asian children of LBW are vulnerable to hypertension and renal diseases. In fact, findings of a systematic review showed that, in preterm babies born at a mean gestational age of 30.2 weeks with a mean birth weight of 1.28 kg, BP in later life was

Page 5 of 9, 495

2.5 mmHg higher than in those born at term [60]. In another study, a 2.28 mmHg increase in SBP was recorded in individuals whose birth weight was less than 2.5 kg, compared with those heavier than 2.5 kg [61]. The precise mechanism for fetal programming of adult disease is still unclear. Accumulating evidence suggests that environmental factors during early life might also program the development of obesity and hypertension [62, 63], but these aspects are beyond the scope of this review. Pathophysiology of Hypertension in Obesity Although the mechanism of hypertension associated with obesity is still an area of research, inappropriate activation of the sympathetic nervous system life (SNS) and reninangiotensin system (RAS), the roles of adipokines and inflammatory cytokines, and endothelial dysfunction are suggested as main attributable factors [64]. White adipose tissue in visceral fat is regarded as the largest endocrine organ of the body that produce a variety of bioactive factors called adipokines and pro-inflammatory cytokines which are clearly risk factors for hypertension [65•]. Recent studies have shown that increased renal sympathetic nerve activity (RSNA) and RAS, which contribute to altered renal function, such as increased sodium reabsorption and impaired pressure natriuresis, play key roles in obesity hypertension. In fact, among several mediators of SNS activation, leptin functions as a promising mediator of obesityinduced SNS activation [66•]. It is well known that the level of leptin is increased in obesity and associated with elevated BP [67]. Normally, leptin binds to its receptors in the central nervous system (CNS), where it activates neural pathways that decrease appetite and increase SNS activity and energy expenditure. Increased leptin in obesity stimulates proopiomelanocortin (POMC) neurons in the hypothalamus and brain stem, and the subsequent activation of the melanocortin 4 receptor (MC4R) leads to SNS activation. Chronic activation of the CNS POMC-MC4R pathway induced by increased leptin is essential for SNS activation and hypertension in obesity [66•, 68]. In addition, leptin causes endothelial dysfunction and enhances the effects of angiotensin II on BP through SNS activation, which contributes to vascular stiffness and hypertension in obesity [69]. Adiponectin, another main adipokine, is mainly synthesized in adipose tissue and produces the beneficial effects on the vascular system. A recent clinical study demonstrated that the lowest serum levels of adiponectin were found in subjects who were both hypertensive and obese [70]. Some evidence suggests that the detrimental effects of increased SNS outflow in obesity lead to the downregulation of adiponectin levels [71]. Adiponectin has insulin-sensitizing anti-inflammatory and anti-atherogenic effects that protect against cardiovascular disease. Briefly, adiponectin inhibits TNF-α production and

495, Page 6 of 9

other inflammatory pathways in adipocytes and macrophages. It reduces oxidative stress by decreasing ROS production in endothelial cells and stimulates NO production in the vascular endothelium. All these effects protect the vascular system against endothelial dysfunction. Therefore, significant decreases in adiponectin levels in obesity contribute to the pathogenesis of obesity-related hypertension [72]. Many studies have confirmed that human adipose tissue synthesizes all the components of RAS: angiotensinogen, renin, angiotensin-converting enzymes (ACEs) 1 and 2, and Ang II receptors 1 and 2 [73]. Increased amount of these components in adipose tissue might contribute to obesityinduced hypertension. Indeed, circulating RAS components are elevated in human obesity, and weight loss reduces RAS levels in plasma and in adipose tissue [74]. Moreover, increased Ang II in obesity may exacerbate the hypertensive state via increased secretion of several proinflammatory cytokines (TNF-α and IL-6) and decreased adiponectin secretion and stimulation of leptin production in human adipocytes [65•]. All of these findings suggest that the adipose RAS has a significant physiological role in the regulation of blood pressure. There is growing evidence that elevated SNS activity in obesity contributes to the development and progression of target organ damage irrespective of the presence of hypertension. Several studies documented that sympathetic nerve traffic was the major determinant of early structural and functional cardiovascular abnormalities in human obesity. The studies showed that the association between adrenergic overdrive and vascular, cardiac, and renal organ damage was not limited to the hypertensive state but occurred in the obese normotensive state as well [75, 76•]. A recent study also showed that disturbed circadian BP and heart rate rhythmicity, conditions causing increased cardiovascular risk, in a group of obese adolescent boys with primary hypertension did not normalize after antihypertensive therapy despite BP lowering. These findings underline the importance of visceral adipose tissue for its role of SNS activation in the pathogenesis of hypertension and the establishment of treatment strategies. The therapy should focus not only on BP lowering but also on reducing visceral adipose tissue [77•, 78].

Curr Hypertens Rep (2014) 16:495

overnutrition) accompanying the rapid socioeconomic progress over the past few decades. Hypertension and obesity are major modifiable risk factors for cardiovascular disease in adulthood. Therefore, it is of considerable importance to assess BP and BMI of children and adolescents properly and adopt appropriate preventive strategies to obviate a future epidemic of adult cardiovascular disease before the development of obesity.

Compliance with Ethics Guidelines Conflict of Interest Chong Guk Lee declares no conflict of interest. Human and Animal Rights and Informed Consent This article does not contain any studies with human or animal subjects performed by any of the authors.

References Papers of particular interest, published recently, have been highlighted as: • Of importance •• Of major importance 1.

2.

3.

4.

5.

6.

7.•

Conclusions It should be clear that pediatric hypertension has emerged as an important public health problem in Asian countries with increasing obesity epidemic. The increasing prevalence of high BP among children and adolescents is closely related to increasing incidence of obesity. The causes of obesity epidemic in Asian countries are most frequently ascribed to a great change of lifestyle (i.e., decrease in physical activity and

8.

9.

WHO. Global status report on non-communicable diseases 2010. Geneva, World Health Organization, 2011. http://www.who.int/ nmh/publications/ncd_report_full_en.pdf. Accessed 10 Nov 2013 Alwan A, MacLean DR, Riley LM, d'Espaignet ET, Mathers CD, Stevens GA, et al. Monitoring and surveillance of chronic noncommunicable diseases: progress and capacity in high-burden countries. Lancet. 2010;376:1861–8. WHO. Global health risks: mortality and burden of disease attributable to selected major risks. Geneva, World Health Organization, 2009. http://www.who.int/healthinfo/global_burden_disease/ GlobalHealthRisks_report_full.pdf. Accessed 10 Nov 2013. WHO. Non-communicable diseases country profiles. Geneva, World Health Organization, 2011. http://www.who.int/nmh/ publications/ncd_profiles_report.pdf. Accessed 10 Nov 2013. Danaei G, Finucane MM, Lin JK, Singh GM, Paciorek CJ, Cowan MJ, et al. National, regional, and global trends in systolic blood pressure since 1980: systematic analysis of health examination surveys and epidemiological studies with 786 country-years and 5·4 million participants. Lancet. 2011;377:568–77. Pereira M, Lunet N, Azevedo A, Barros H. Differences in prevalence, awareness, treatment and control of hypertension between developing and developed countries. J Hypertens. 2009;27:963–75. Flynn J. The changing face of pediatric hypertension in the era of the childhood obesity epidemic. Pediatr Nephrol. 2013;28:1059– 66. This review presented updated data on the prevalence of hypertension in children and adolescents, the impact of the childhood obesity epidemic on hypertension prevalence, and epidemiologic shifts to primary hypertension in childhood. Tran CL, Ehrmann BJ, Messer KL, Herreshoff E, Kroeker A, Wickman L, et al. Recent trends in healthcare use among children and adolescents with hypertension in the United States. Hypertens. 2012;60:296–302. Samuels J. The increasing burden of pediatric hypertension. Hypertens. 2012;60:276–7.

Curr Hypertens Rep (2014) 16:495 10.• Cao ZQ, Zhu L, Zhang T, Wu L, Wang Y. Blood pressure and obesity among adolescents: a school-based population study in China. Am J Hypertens. 2012;25:576–82. Informations regarding the prevalence of hypertension and prehypertension as well as the epidemical situation of the associated risk factor, obesity, in adolescents in China are available. Also, characteristics of the Chinese blood pressure reference standards for children and adolescents are described. 11. Bao W, Threefoot T, Srinivasan SR, Berenson GS. Essential hypertension predicted by tracking of elevated blood pressure from childhood to adulthood: the Bogalusa Heart Study. Am J Hypertens. 1995;8:657–65. 12.• Chen X, Wang Y. Tracking of blood pressure from childhood to adulthood: a systematic review and meta-regression analysis. Circulation. 2008;117:3171–80. A meta-analysis conducted on 50 cohort studies. Data from diverse populations revealed the strong evidence for BP tracking from childhood into adulthood. 13. Seeman T, Pohl M, Palyzova D, John U. Microalbuminuria in children with primary and white-coat hypertension. Pediatr Nephrol. 2012;27:461–7. 14. Kupferman JC, Lande MB, Adams HR, Pavlakis SG. Primary hypertension and neurocognitive and executive functioning in school-age children. Pediatr Nephrol. 2013;28:401–8. doi:10. 1007/s00467-012-2215-8. 15. McNiece KL, Gupta-Malhotra M, Samuels J, Bell C, Garcia K, Poffenbarger T, et al. Left ventricular hypertrophy in hypertensive adolescents: analysis of risk by 2004 national high blood pressure education program working group staging criteria. Hypertens. 2007;50:392–5. 16. de Gusma˜o Correia ML, Volpato AM, Aguila MA, Mandarim-deLacerda CA. Developmental origins of health and disease: experimental and human evidence of fetal programming for metabolic syndrome. J Hum Hypertens. 2012;26:405–19. doi:10.1038/jhh. 2011.61. 17. National High Blood Pressure Education Program Working Group on High Blood Pressure in Children and Adolescents. The fourth report on the diagnosis, evaluation, and treatment of high blood pressure in children and adolescents. Pediatr. 2004;114:555–76. 18. Chobanian AV, Bakris GL, Black HR, Cushman WC, Green LA, Izzo Jr JL, et al. Seventh report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure. Hypertens. 2003;42:1206–52. 19.• Cole TJ. Secular trends in growth. Proc Nutr Soc. 2000;59:317–24. This paper aimed to consider the basic concept of secular trend in child height, weight, birth weight, and growth tempo over the last two centuries and to discuss its causation. The author insisted that the secular change reflects the varying health and affluence of populations over time, and it also highlights inequalities of health and wealth within populations. 20. Berg GVD, Eijsden MV, Galindo-Garre F, Vrijkotte TGM, Gemke RJBJ. Explaining socioeconomic inequalities in childhood blood pressure and prehypertension. ABCD Study Hypertens. 2013;61: 35–41. 21. Lee CG, Moon JS, Choi JM, Nam JM, Lee SY, Oh KW, et al. Normative blood pressure references for Korean children and adolescents. Korean J Pediatr. 2008;51:33–41. 22. Jie MI, Tian-you W, Ling-hui M, Guang-jin Z, Shao-mei H, Yan Z, et al. Development of blood pressure reference standards for Chinese children. Chin J Evid Based Pediatr. 2010;5:4–14. 23. Pickering TG. What will replace the mercury sphygmomanometer? Blood Press Monit. 2003;8:23–5. 24. Park MK, Menard SW, Yuan C. Comparison of auscultatory and oscillometric blood pressures. Arch Pediatr Adolesc Med. 2001;155:50–3. 25. O'Brien E, Waeber B, Parati G, Staessen J, Myers MG, on behalf of the European Society of Hypertension Working Group on Blood

Page 7 of 9, 495

26.•

27. 28.

29.

30.

31. 32.

33.

34.

35.

36.

37.

38.

39.

40.

41.

42.

Pressure Monitoring. Blood pressure measuring devices: recommendations of the European Society of Hypertension. BMJ. 2001;322:531–6. O’Brien E, Atkins N, Stergiou G, Karpettas N, Parati G, Asmar R, et al. European Society of Hypertension International Protocol revision 2010 for the validation of blood pressure measuring devices in adults. Blood Press Monit. 2010;15:23–38. Because of the increasing ban on the use of mercury-containing sphygmomanometers, there is a need for an equivalent standard device that does not contain mercury. This paper is giving an introduction of the recently revised protocol of validation study by the European Society of Hypertension. van Montfrans GA. Oscillometric blood pressure measurement: progress and problems. Blood Press Monit. 2001;6:287–90. Lee CG, Park HM, Shin HJ, Moon JS, Hong YM, Kim NS, et al. Validation study of the Dinamap ProCare 200 upper arm blood pressure monitor in children and adolescents. Korean J Pediatr. 2011;54:463–9. Lee CG. A comparison study between blood pressure measurement devices to evaluate cut-off values of hypertension in Korean children and adolescents. The report of Korea Center for Disease Control & Prevention, Oct. 2010 Van den Berg G, Van Eijsden M, Galindo-Garre F, Gemke R. Explaining socioeconomic inequalities in childhood blood pressure and prehypertension: the ABCD study. Hypertens. 2013;61:35–41. Falkner B. Hypertension in children and adolescents: epidemiology and natural history. Pediatr Nephrol. 2010;25:1219–24. Moore WE, Eichner JE, Cohn EM, Thompson DM, Kobza CE, Abbott KE. Blood pressure screening of school children in a multiracial school district: the Healthy Kids Project. Am J Hypertens. 2009;22:351–6. Sorof JM, Lai D, Turner J, Poffenbarger T, Portman RJ. Overweight, ethnicity, and the prevalence of hypertension in school-aged children. Pediatr . 2004;113:475–82. Lo JC, Sinaiko A, Chandra M, Daley MF, Greenspan LC, Parker ED, et al. Prehypertension and hypertension in community-based pediatric practice. Pediatr. 2013;131:e415–24. Dong B, Ma J, Wang HJ, Wang ZQ. The association of overweight and obesity with blood pressure among Chinese children and adolescents. Biomed Environ Sci. 2013;26:437–44. doi:10.3967/08953988.2013.06.004. Moon JS, Lee SY, Nam JM, Choi JM, Choe BK, Seo JW, et al. 2007 Korean national growth charts: review of developmental process and an outlook. Korean J Pediatr. 2008;51:1–25. Park SW, Park JH, Kim JH. The result of nationwide health examination for school students in primary, middle school and high school. Korea Educational Development Institute. 2012. https:// www.kedi.re.kr/khome/main/research/selectPubForm.do. Accessed 14 Nov 2013 Oh KW, Jang MJ, Lee NY, Moon JS, Lee CG, Yoo MH, et al. Prevalence and trends in obesity among Korean children and adolescents in 1997 and 2005. Korean J Pediatr. 2008;51:950–5. Munter P, He J, Cutler JA, Wildman RP, Whelton PK. Trends in blood pressure among children and adolescents. JAMA. 2004;291: 2107–13. Din-Dzietham R, Liu Y, Bielo M-V, Shamsa F. High blood pressure trends in children and adolescents in national surveys, 1963 to 2002. Circulation. 2007;116:1488–96. Rosner B, Cook NR, Daniels S, Falkner B. Childhood blood pressure trends and risk factors for high blood pressure: the NHANES Experience 1988–2008. Hyperten. 2013;62:247–54. Watson SE, Hannon TS, Eckert GJ, Pratt JH, Rosenman M, Tu W. Adult hypertension risk is more than quadrupled in obese children. Abstract No. 36 of High Blood Pressure Research 2013 Scientific Sessions, American Heart Association. 2013. http://my. americanheart.org/idc/groups/ahamah- public/@wcm/@sop/@

495, Page 8 of 9 scon/documents/downloadable/ucm_455971.pdf. Accessed 16 Nov 2013 43. Kuwahara E, Asakura K, Nishiwaki Y, Komatsu H, Nakazawa A, Ushiku H, Maejima F, Nishigaki Y, Hasegawa T, Okamura T, Takebayashi T. Steeper increases in body mass index during childhood correlate with blood pressure elevation in adolescence: a longterm follow-up study in a Japanese community. Hypertens Res. 2013. doi: 10.1038/hr.2013.109. http://www.ncbi.nlm.nih.gov/ pubmed/24026043. Accessed 16 Nov 2013 44.• Dong B, Wang HJ, Wang Z, Liu JS, Ma J. Trends in blood pressure and body mass index among Chinese children and adolescents from 2005 to 2010. Am J Hypertens. 2013;26:997–1004. doi:10.1093/ ajh/hpt050. This paper is showing the association between obesity and high blood pressure in Chinese children and adolescents. 45. Lu X, Shi P, Luo CY, Zhou YF, Yu HT, Guo CY, et al. Prevalence of hypertension in overweight and obese children from a large schoolbased population in Shanghai. China BMC Publ Health. 2013;13: 24. doi:10.1186/1471-2458-13-24. http://www.ncbi.nlm.nih.gov/ pubmed/?term=BMC+Public+Health+2013%3B13%3A24. Accessed 18 Dec 2013. 46.•• Freedman DS, Goodman A, Contreras OA, Das Mahapatra P, Srinivasan SR, Berenson GS. Secular trends in BMI and blood pressure among children and adolescents: the Bogalusa Heart Study. Pediatr. 2012;130:e159–66. Contrary to the results of other studies, there was no increase in systolic or diastolic blood pressure levels despite increases in obesity in Bogalusa cohort study. Authors insisted that it should not be assumed that trends in high blood pressure have paralleled those for obesity. 47. Flynn JT. Pediatric hypertension update. Curr Opin Nephrol Hypertens. 2010;19:292–7. 4 8 . H a n s on M , G l uc k m a n P. D e v e l o p m e n t a l or i g i n s o f noncommunicable disease: population and public health implications. Am J Clin Nutr. 2011;94(6 Suppl):1754S–8S. 49.• Lakshmy R. Metabolic syndrome: role of maternal undernutrition and fetal programming. Rev Endocr Metab Disord. 2013;14:229– 40. The concept of developmental origins of health and disease is provided through the review of recent experimental and epidemiological studies providing evidence for the fetal programming associated with the development of metabolic syndrome and related diseases. Roles of maternal macro- and micronutrients on fetal programming during pregnancy are explained. 50.•• Gluckman PD, Hanson MA, Cooper C, Thornburg K. Effect of in utero and early-life conditions on adult health and disease. N Engl J Med. 2008;359:61–73. In this review, they explained that the developmental plasticity requires stable modulation of gene expression, which is mediated by epigenetic processes such as DNA methylation and histone modification. Thus, both the genome and the epigenome interactively influence the mature phenotype and determine sensitivity to later environmental factors and the subsequent risk of disease. 51. Barker DJ, Osmond C. Low birth weight and hypertension. Br Med J. 1988;297:134–5. 52. Barker DJP. Maternal and fetal nutrition and disease in later life. Nutrition. 1997;13:807–13. 53. Gluckman P, Hanson M, Beedle AS. Non-genomic transgenerational inheritance of disease risk. Bioessays. 2007;29: 145–54. 54. Patti ME. Intergenerational programming of metabolic diseases: evidence from human populations and experimental animal models. Cell Mol Life Sci. 2013;70:1597–608. 55. Gluckman PD, Hanson MA, Beedle AS, Spencer HG. Predictive adaptive responses in perspective. Trends Endocrinol Metab. 2008;19:109–10. 56. Vaccari B, Mesquita FF, Gontijo J AR, Boer PA. Fetal kidney programming by severe food restriction: effects on structure, hormonal receptor expression and urinary sodium excretion in rats. J

Curr Hypertens Rep (2014) 16:495 RAAS 2013. doi: 10.1177/1470320313481081. http://jra.sagepub. com/content/early/2013/03/12/1470320313481081. Accessed 25 Nov 2013. 57.•• Luyckx VA, Bertram JF, Brenner BM, Fall C, Hoy WE, Ozanne SE, et al. Effect of fetal and child health on kidney development and long-term risk of hypertension and kidney disease. Lancet. 2013;382:273–83. They described how low birth weight and prematurity affect kidney development and risk of disease, hypertension, and kidney disease. 58. UNICEF and WHO. Low birthweight: country, regional and global estimates. UNICEF; 2004. p. 27. 59. Korean Statistical Information Service (KOSIS). Statistical database/vital statistics. http://kosis.kr/wnsearch/totalSearch.jsp 60. de Jong F, Monuteaux MC, van Elburg RM, Gillman MW, Belfort MB. Systematic review and meta-analysis of preterm birth and later systolic blood pressure. Hypertens. 2012;59:226–34. 61. Mu M, Wang SF, Sheng J, Zhao Y, Li HZ, Hu CL, et al. Birth weight and subsequent blood pressure: a meta-analysis. Arch Cardiovasc Dis. 2012;105:99–113. 62. Gluckman PD, Hanson MA, Buklijas P. A conceptual framework for the developmental origins of health and disease. J DOHaD. 2010;1:6–18. doi:10.1017/S2040174409990171. 63. Demicheva E, Crispi F. Long-term follow-up of intrauterine growth restriction: cardiovascular disorders. Fetal Diagn Ther. 2013;36: 143–53. doi:10.1159/000353633. 64. Bucher BS, Ferrarini A, Weber N, Bullo M, Bianchetti MG, Simonetti GD. Primary hypertension in childhood. Curr Hypertens Rep. 2013;15:444–52. 65.• Vlasova M, Purhonen AK AK, Jarvelin MR, Rodilla E, Pascual J, Herzig KH. Role of adipokines in obesity-associated hypertension. Acta Physiol. 2010;200:107–27. It is well known that increased amounts of most of the adipokines and the decreased adiponectin levels in obesity affect the regulation of vascular tone. This article is showing major effects of different adipokines on structural and functional changes in the cardiovascular system. 66.• Hall JE, da Silva AA, do Carmo JM, Dubinion J, Hamza S, Munusamy Smith SG, et al. Obesity-induced hypertension: role of sympathetic nervous system, leptin, and melanocortins. J Biol Chem. 2010;285:17271–6. Role of CNS melanocortins and the POMC-MC3/4R pathway in mediating obesity-induced SNS activation and blood pressure effects of leptin is reviewed. 67. Grontved A, Steene-Johannessen J, Kynde I, Franks PW, Helge JW, Froberg K, et al. Association between plasma leptin and blood pressure in two population-based samples of children and adolescents. J Hypertens. 2011;29:1093–100. 68. Harlan SM, Rahmouni K. Neuroanatomical determinants of the sympathetic nerve responses evoked by leptin. Clin Auton Res. 2013;23:1–7. 69. Wang J, Wang H, Luo W, Guo C, Wang J, Chen YE, et al. Leptininduced endothelial dysfunction is mediated by sympathetic nervous system activity. J Am Heart Assoc. 2013;2:e000299. doi:10. 1161/JAHA.113.000299. 70. Brambilla P, Antolini L, Street ME, Giussani M, Galbiati S, Valsecchi MG, et al. Adiponectin and hypertension in normal-weight and obese children. Am J Hypertens. 2013;26: 257–64. 71. Delporte ML, Funahashi T, Takahashi M, Matsuzawa Y, Brichard SM. Pre- and post-translational negative effect of beta-adrenoceptor agonists on adiponectin secretion: in vitro and in vivo studies. Biochem J. 2002;367:677–85. 72. Zhu W, Cheng KK, Vanhoutte PM, Lam KS, Xu A. Vascular effects of adiponectin: molecular mechanisms and potential therapeutic intervention. Clin Sci. 2008;114:361–74. 73. Achard V, Boullu-Ciocca S, Desbriere R, Nguyen G, Grino M. Renin receptor expression in human adipose tissue. Am J Physiol Regul Integr Comp Physiol. 2007;292:R274–82.

Curr Hypertens Rep (2014) 16:495 74.

Engeli S, Bohnke J, Gorzelniak K, Janke J, Schling P, Bader M, et al. Weight loss and the renin-angiotensin-aldosterone system. Hypertens. 2005;45:356–62. 75. Grassi G, Seravalle G, D’llOro R. Sympathetic activation in obesity: a noninnocent bystander. Hypertens. 2010;56:338–40. 76.• Lambert E, Sari CI, Dawood T, Nguyen J, McGrane M, Eikelis N, et al. Sympathetic nervous system activity is associated with obesity-induced subclinical organ damage in young adults. Hypertens. 2010;56:351–8. They evaluated the early signs of organ damage associated with hypertension in obese young adults to document their possible relationship to sympathetic nervous activity. They found that excess weight in young individuals was associated with subclinical alterations in renal and endothelial function as well as in the structure of the heart, even in the absence of

Page 9 of 9, 495 hypertension. Sympathetic activity seemed to be closely associated with cardiovascular and renal alterations observed in subjects with obesity. 77.• Niemirska A, Litwin M, Feber J, Jurkiewicz E. Blood pressure rhythmicity and visceral fat in children with hypertension. Hypertens. 2013;62:782–8. Their findings support the central role of the sympathetic nervous system in the pathophysiology of childhood hypertension and underscore the importance of visceral adiposity as not only an influence on sympathetic nervous system activity but also as a potential target for prevention of adult cardiovascular disease. 78. Grassi G, Quarti-Trevano F, D’llOro R, Mancia G. Essential hypertension and the sympathetic nervous system. Neurol Sci. 2008;29: S33–6.

The emerging epidemic of hypertension in Asian children and adolescents.

Hypertension has become a serious global public health burden because of its high incidence and concomitant risk of cardiovascular disease. Many studi...
520KB Sizes 1 Downloads 5 Views