Essential hypertension in adolescen

Essential hypertension in adolescents and children: Recent advances in causative mechanisms
Abstract
Essential hypertension is the most common form of hypertension in adults, and it is recognized more often in adolescents than in younger children. It is well known that the probability of a diagnosis of essential hypertension increases with age from birth onward. The initiation of high blood pressure burden starts in childhood and continues through adolescence to persist in the remaining phases of life. The genesis of essential hypertension is likely to be multifactorial. Obesity, insulin resistance, activation of sympathetic nervous system, sodium homeostasis, renin-angiotensin system, vascular smooth muscle structure and reactivity, serum uric acid levels, genetic factors and fetal programming have been implicated in this disorder. In addition, erythrocyte sodium transport, the free calcium concentration in platelets and leukocytes, urine kallikrein excretion, and sympathetic nervous system receptors have also been investigated as other possible mechanisms. Obesity in children appears to be the lead contributor of essential hypertension prevalence in children and adolescents. Suggested mechanisms of obesity-related hypertension include insulin resistance, sodium retention, increased sympathetic nervous system activity, activation of renin-angiotensin-aldosterone, and altered vascular function. The etiopathogenesis of essential hypertension in children and adolescents appears to closely resemble that of adults. The minor variations seen could probably be due to the evolving nature of this condition. Many of the established mechanisms that are confirmed in adult population need to be replicated in the pediatric age group by means of definitive research for a better understanding of this condition in future.

Keywords: Adolescents, children, essential hypertension, etiology, pathogenesis
Introduction
Essential hypertension is the most common form of hypertension in adults and it is recognized more often in adolescents than in younger children.[1] Hypertension is a major contributor to the global burden of disease. Worldwide, 7.6 million premature deaths were attributed to high blood pressure in 2001.[2] Roughly half of stroke and ischemic heart disease events worldwide were attributable to high blood pressure during the same period.[2] Suboptimal blood pressure was reported to account for 10% of global health care expenditure in 2001 for population aged 30 years and more.[3] The global public health significance of high blood pressure in childhood and adolescence is based on observations that confirm a strong tracking of blood pressure levels from childhood to adulthood.[4] It is well known that the probability of a diagnosis of essential hypertension increases with age from birth onward.[1] Children and young adolescents with blood pressure greater than the 90th percentile for age have roughly threefold greater likelihood of becoming adults with hypertension compared to their peers with blood pressure at the 50th percentile.[1] These findings clearly suggest that the initiation of high blood pressure burden starts in childhood and continues through adolescence to persist in the remaining phases of life. The current review is an attempt to present recent research in basic etiopathogenesis of essential hypertension in children and adolescents.
Etiopathogenesis of Essential Hypertension
The genesis of essential hypertension is likely to be multifactorial. Obesity, insulin resistance, activation of sympathetic nervous system, sodium homeostasis, renin-angiotensin system (RAS), vascular smooth muscle structure and reactivity, serum uric acid levels, genetic factors and fetal programming have been implicated in this disorder.[1,5–8] In addition, erythrocyte sodium transport, the free calcium concentration in platelets and leukocytes, urine kallikrein excretion, and sympathetic nervous system receptors have also been investigated.[1]

Obesity and high blood pressure

Obesity in children is well known to be associated with hypertension. Data from a recent study covering 25,000 school children in the age group of 5–16 years reported increased prevalence of prehypertension and hypertension among overweight and obese children when compared to their non-overweight counterparts.[9] Hypertension (first instance) was seen in 10.10% of normal weight, 17.34% of overweight and 18.32% of obese children in this study. The corresponding figures for systolic hypertension were 5.38%, 12.31% and 14.66%, respectively. The same for diastolic hypertension were 6.45%, 8.86% and 8.90%, respectively.[9] Suggested mechanisms of obesity-related hypertension include insulin resistance, sodium retention, increased sympathetic nervous system activity, activation of renin-angiotensin-aldosterone system (RAAS), and altered vascular function.[10] Probable reasons for activation of the sympathetic nervous system in obesity include hyperinsulinemi

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เป็นความดันโลหิตสูงในเด็กและวัยรุ่น: ก้าวล่าสุดในกลไกสาเหตุบทคัดย่อความดันโลหิตสูงที่สำคัญเป็นแบบที่พบมากที่สุดของความดันโลหิตสูงในผู้ใหญ่ และรู้จักบ่อยขึ้นในวัยรุ่นมากกว่าในเด็ก เป็นที่ทราบกันดีว่า ความน่าเป็นวินิจฉัยของความดันโลหิตสูงจำเป็นเพิ่มขึ้นตามอายุตั้งแต่แรกเกิดเป็นต้นไป การเริ่มต้นของภาระความดันโลหิตสูงเริ่มในวัยเด็ก และเรื่อยไปจนถึงวัยรุ่นที่ยังคงอยู่ในขั้นตอนที่เหลือของชีวิต แหล่งกำเนิดของความดันโลหิตสูงจำเป็นจะเป็น multifactorial โรคอ้วน ความต้านทานต่ออินซูลิน เปิดใช้งานของระบบประสาท ภาวะธำรงดุลโซเดียม angiotensin กิจกรรมระบบ โครงสร้างและปฏิกิริยา ซีรั่มระดับกรดยูริก ปัจจัยทางพันธุกรรมของกล้ามเนื้อเรียบของหลอดเลือด และทารกในครรภ์การเขียนโปรแกรมที่มีการเกี่ยวข้องในโรคนี้ นอกจากนี้ เม็ดเลือดแดงขนส่งโซเดียม ความเข้มข้นของแคลเซียมฟรีในเกล็ดเลือด และเม็ดเลือดขาว ขับถ่ายปัสสาวะ kallikrein และระบบประสาทตัวรับมียังถูกตรวจสอบเป็นกลไกที่เป็นไปได้อื่น ๆ โรคอ้วนในเด็กจะ เป็นผู้นำของความชุกของความดันโลหิตสูงที่จำเป็นในเด็กและวัยรุ่น แนะนำกลไกของโรคอ้วนความดันโลหิตสูงได้แก่อินซูลินต้านทาน กักเก็บโซเดียม เพิ่มระบบประสาทกิจกรรม กิจกรรม angiotensin aldosterone การเปิดใช้งาน และเปลี่ยนแปลงฟังก์ชันของหลอดเลือด Etiopathogenesis ความจำเป็นความดันโลหิตสูงในเด็กและวัยรุ่นจะ คล้ายของผู้ใหญ่อย่างใกล้ชิด รูปแบบเล็กน้อยที่เห็นอาจจะเนื่องจากการพัฒนาสภาพนี้ หลายกลไกขึ้นที่ยืนยันในประชากรวัยผู้ใหญ่ต้องถูกจำลองแบบในเด็กกลุ่มอายุโดยใช้วิธีการวิจัยที่ชัดเจนสำหรับความเข้าใจของเงื่อนไขนี้ในอนาคตKeywords: Adolescents, children, essential hypertension, etiology, pathogenesisIntroductionEssential hypertension is the most common form of hypertension in adults and it is recognized more often in adolescents than in younger children.[1] Hypertension is a major contributor to the global burden of disease. Worldwide, 7.6 million premature deaths were attributed to high blood pressure in 2001.[2] Roughly half of stroke and ischemic heart disease events worldwide were attributable to high blood pressure during the same period.[2] Suboptimal blood pressure was reported to account for 10% of global health care expenditure in 2001 for population aged 30 years and more.[3] The global public health significance of high blood pressure in childhood and adolescence is based on observations that confirm a strong tracking of blood pressure levels from childhood to adulthood.[4] It is well known that the probability of a diagnosis of essential hypertension increases with age from birth onward.[1] Children and young adolescents with blood pressure greater than the 90th percentile for age have roughly threefold greater likelihood of becoming adults with hypertension compared to their peers with blood pressure at the 50th percentile.[1] These findings clearly suggest that the initiation of high blood pressure burden starts in childhood and continues through adolescence to persist in the remaining phases of life. The current review is an attempt to present recent research in basic etiopathogenesis of essential hypertension in children and adolescents.Etiopathogenesis of Essential Hypertension
The genesis of essential hypertension is likely to be multifactorial. Obesity, insulin resistance, activation of sympathetic nervous system, sodium homeostasis, renin-angiotensin system (RAS), vascular smooth muscle structure and reactivity, serum uric acid levels, genetic factors and fetal programming have been implicated in this disorder.[1,5–8] In addition, erythrocyte sodium transport, the free calcium concentration in platelets and leukocytes, urine kallikrein excretion, and sympathetic nervous system receptors have also been investigated.[1]

Obesity and high blood pressure

Obesity in children is well known to be associated with hypertension. Data from a recent study covering 25,000 school children in the age group of 5–16 years reported increased prevalence of prehypertension and hypertension among overweight and obese children when compared to their non-overweight counterparts.[9] Hypertension (first instance) was seen in 10.10% of normal weight, 17.34% of overweight and 18.32% of obese children in this study. The corresponding figures for systolic hypertension were 5.38%, 12.31% and 14.66%, respectively. The same for diastolic hypertension were 6.45%, 8.86% and 8.90%, respectively.[9] Suggested mechanisms of obesity-related hypertension include insulin resistance, sodium retention, increased sympathetic nervous system activity, activation of renin-angiotensin-aldosterone system (RAAS), and altered vascular function.[10] Probable reasons for activation of the sympathetic nervous system in obesity include hyperinsulinemi