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Prevalence and Risk Factors Associated with Hyperuricemia in the Pearl River Delta, Guangdong Province, China
research-article
Author(s):
Weiqi Liu
1 ,
Weiling Liu
2 ,
Shaoling Wang
3 ,
Huichun Tong
4 ,
Jianmin Yuan
5 ,
Zhenning Zou
6 ,
Jianwen Liu
7 ,
Donghai Yang
8 ,
Zhongxing Xie
9
Publication date (Electronic):
16 February 2021
Publisher:
Dove
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Abstract
Background
In China, the prevalence of HUA in the Pearl River Delta (PRD) region of Guangdong Province has not been extensively investigated. Therefore, this study investigated the prevalence of HUA and its related factors among people aged 20–99 years in nine cities in the PRD.
Materials and Methods
We selected 6491 health check participants from 9 cities in the PRD and collected participants’ anthropometric and biochemical test results for a cross-sectional study. We included 6491 participants and assessed their blood pressure (BP), body mass index (BMI), total cholesterol (TC), triglycerides (TG), glucose (Glu) and serum uric acid (UA) to analyze the regional prevalence of HUA and its related factors. HUA was indicated when fasting serum UA level was >420 μmol/L in men and >360 μmol/L in women.
Results
Overall prevalence of HUA in our cohort was 34.05%; prevalence was higher in men than in women (41.53% vs 26.14%, P < 0.001). Characteristics associated with HUA were hypertension (odds ratio (OR), 5.506; 95% confidence interval (CI), 4.402–6.889), higher body mass index (BMI; OR: 1.746; 95% CI: 1.560–1.954), age 31–40 years (OR: 0.829; 95% CI: 0.706–0.973), age 61–70 years (OR: 1.434; 95% CI: 1.194–1.722) and age ≥71 years (OR: 1.742; 95% CI: 1.397–2.173). In all subjects, serum UA was positively correlated with Glu, TG and TC. After we adjusted for age, BMI and BP, multivariate logistic regression analysis showed that HUA risk factors were high TC (OR: 1.770; 95% CI: 1.459–2.147) and TG (OR: 1.961; 95% CI: 1.632–2.357) in men; and high Glu (OR: 1.508; 95% CI: 1.084–2.099), TC (OR: 1.341; 95% CI: 1.084–1.660) and TG (OR: 1.680; 95% CI: 1.290–2.187) in women.
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Most cited references51
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2018 Chinese Guidelines for Prevention and Treatment of Hypertension—A report of the Revision Committee of Chinese Guidelines for Prevention and Treatment of Hypertension
(2019)
Preamble Since 2010, as research evidence is ever-increasing regarding hypertension and related diseases worldwide, guidelines for hypertension have been successively developed or revised in many countries and regions. In China, new evidence from population studies and clinical trials are accumulating, including representative sampling survey on the population with hypertension in the 12th Five-Year Plan, FEVER study subgroup, Chinese Hypertension Intervention Efficacy study (CHIEF), China Stroke Primary Prevention Trial (CSPPT). These studies have provided further information and evidence for the revision of Chinese guidelines for hypertension. In September 2015, supported by the former Disease Control Bureau of National Health and Family Planning Commission of China, the Chinese Hypertension League, in partnership with Chinese Society of Cardiovascular Disease of the Chinese Medical Association, Hypertension Branch of the China International Exchange and Promotion Association for Medical and Healthcare, Hypertension Branch of the Chinese Geriatrics Society, and the Hypertension Committee of Chinese Medical Doctor Association organized a committee for revising the 2010 Chinese Guidelines for the Management of Hypertension. Over the past two years, discussions have been conducted for many times with respect to guiding ideas and plans of guideline revision. In the survey on major problems for revision of the guideline, 20 issues have been proposed including: goal of blood pressure (BP) control for treatment of hypertension, management of hypertension among special populations, role of β-blocker in treatment of hypertension. In response to these survey results, document retrieval has been extensively performed. Document database include China Biology Medicine (CBM), Wanfang Data Knowledge Service Platform, CNKI Platform, PubMed, Excerpta Medica Database (EMBASE), and platform of Institute of Medical Information & Library, CMAS&PUMC. After writing the first draft of the revised guideline, nearly 30 symposiums had been held by the committee for revision of guidelines, in which in-depth discussions were made regarding problems and development trends of management of hypertension. For those controversial issues, the consensuses were made with anonymous electronic voting by committee members. In early 2018, the newly revised guideline was reviewed and revised by a special group consisting 10 members of the committee, including five cardiologists, two epidemiologists, one endocrinologist, and one nephrologist. Subsequently, “the 2018 exposure draft for Chinese guidelines for the management of hypertension” was released to collect peers comments, based on which the final draft was completed. By referring to the guideline development processes of World Health Organization (WHO) and Chinese Medical Association (CMA), assessment had been performed regarding important content, level of evidence (Table 1), and class of recommendation in this revised Guidelines (Table 2), with considerations on recent scientific developments on related fields, and current reality of hypertension management in China, the 2018 guidelines provide guidance for prevention and intervention, diagnosis and evaluation, classification and stratification and treatment and management of hypertension. Revision Committee of 2018 Chinese Guidelines for Hypertension Table 1. Class of recommendation. Definition Recommended expression Class I Evidence and/or overall agreement that the treatment or method is beneficial, useful or effective Recommended/indication Class II Inconsistent evidence and/or disagreement about the use/effect of the treatment or method Class IIa Evidence/views tend to be useful/effective Should be considered Class IIb Evidence/views are not sufficient to establish useful/effective Can consider it Class III Evidence and/or expert agree that the treatment or method is useless/ineffective and may be harmful in some cases Not recommended Table 2. Level of evidence. Level A Data from multiple randomized controlled clinical trials or meta-analyses consisting of randomized controlled clinical trials Level B Data from a single randomized clinical trial or multiple large randomized controlled trials Level C Data from expert consensus and/or small-scale studies, retrospective studies or registration studies 1. Prevalence of hypertension in Chinese population Key point 1. Prevalence of hypertension in Chinese population The prevalence of hypertension is still increasing in China. There are two significant features of the population with hypertension in China: the prevalence of hypertension increases from the south to the north; the prevalence of hypertension varied among different ethnic groups. The awareness, treatment and control (crude rate) of hypertension patients in China have increased significantly in recent years, reaching 51.6%, 45.8% and 16.8% respectively, but is overall at a low level. The important risk factors for hypertension are high sodium intake, low potassium diet, overweight, and obesity in Chinese population. 1.1 Prevalence, incidence and epidemic trend of hypertension in Chinese population The 2012–2015 national hypertension survey,[1] showed the overall crude prevalence of hypertension was 27.9% (weighted rate 23.2%) in Chinese residents aged 18 and over. Compared with the previous national surveys of hypertension conducted in 1958–1959, 1979–1980, 1991, 2002 and 2012,[2] the trend keeps on increasing, although the total participants, age and diagnostic criteria for each survey are not completely consistent (Table 3). Table 3. Results of six prevalence rates surveys of hypertension in China. Year No. of surveyed province/city/autonomous region Age, yrs Diagnostic criteria No. of participants No. of hypertension Prevalence, % 1958–1959 13 ≥ 15 Disunity 739,204 37,773 5.1Δ 1979–1980 29 ≥ 15 Diagnosis of hypertension: ≥ 160/95 mmHg 4,012,128 310,202 7.7Δ Critical hypertension: 140–159/90–95 mmHg 1991 29 ≥ 15 ≥ 140/90 mmHg and (or) taking antihypertensive drugs within two weeks 950,356 129,039 13.6Δ 2002 29 ≥ 18 ≥ 140/90 mmHg and (or) taking antihypertensive drugs within two weeks 272,023 51,140 18.8Δ 2012 31 ≥ 18 ≥ 140/90 mmHg and (or) taking antihypertensive drugs within two weeks - - 25.2¶ 2015 31 ≥ 18 ≥ 140/90 mmHg and (or) taking antihypertensive drugs within two weeks 451,755 125,988 27.9Δ ΔRough rate; ¶Comprehensive adjustment of prevalence. The prevalence of hypertension increases significantly with age. According to the 2012–2015 national survey, the prevalence of hypertension in young people aged 18 to 24, 25 to 34, and 35 to 44 years old was 4.0%, 6.1%, and 15.0%, respectively.[1] It is higher in male than in female. The prevalence of hypertension in the north is still higher than that in the south. The pattern is gradually changing into a higher prevalence of hypertension in large and medium-sized cities, such as in Beijing (35.9%), Tianjin (34.5%) and Shanghai (29.1%),[1] respectively. The prevalence of hypertension in rural areas increased faster than that in urban areas. According to the national survey from 2012 to 2015, the prevalence rate in rural areas (crude rate 28.8%, standardized rate 23.4%) surpassed that of in urban areas (crude rate: 26.9%, standardized rate: 23.1%) for the first time. Compared with different ethnic groups, the prevalence of hypertension among Tibetans, Manchus and Mongolians is higher than that of Han, but is lower in Hui, Miao, Zhuang and Buyi.[3] The research on the incidence of hypertension is relatively insufficient. One study with 10,525 non-hypertensive patients aged over 40 years of age showed: the cumulative incidence of hypertension in males and females was 28.9% and 26.9%, respectively, after follow up for an average of 8.2 years in 1991–2000,[4] the incidence increased with age (Figure 1). Figure 1. Cumulative incidence of hypertension in different genders and baseline age groups from 1991 to 2000 1.2 Awareness, treatment and control of hypertension in China Awareness, treatment and control of hypertension are important parameters for reflecting status of the treatment and prevention of hypertension. According to the 2015 survey, the awareness, treatment, and control of hypertension in people over 18 years of age were 51.6%, 45.8%, and 16.8%, respectively, which were significantly higher than those in 1991 and 2002 (Table 4).[1] The prospective study of chronic diseases in China[5] from 2004 to 2009 showed that the rate of hypertension control was lower than that of 2002, which may be related to the sample method. Table 4. Survey results of awareness, treatment and control (roughness rate) of hypertension in China. Year Age, yrs Awareness, % Treatment, % Control, % 1991 ≥ 15 26.3 12.1 2.8 2002 ≥ 18 30.2 24.7 6.1 2012 ≥ 18 46.5 41.1 13.8 2015 ≥ 18 51.5 46.1 16.9 The awareness, treatment and control rate were higher in female than in male, and the treatment was significantly higher in urban than that in rural areas.[6] At the same time, these rates of residents in the southern region are higher than the north.[7],[8] With respect to ethnic groups, the treatment and control of hypertension is lower among ethnic minority than that of Han nationality.[1],[9] 1.3 Important risk factors for hypertension in Chinese population Risk factors for hypertension include genetic factors, age, and unhealthy lifestyles. The clustering of risk factors is prevalent in the population. As the number and severity of hypertension risk factors increase, BP levels increase, and the risk of hypertension increases.[10]–[13] 1.3.1 High sodium, low potassium diet High sodium and low potassium diets are important risk factors for hypertension in Chinese population. The INTERSALT study found that the median 24-h urinary sodium excretion increased by 2.3 g (100 mmol/day), and the median systolic blood pressure (SBP)/diastolic blood pressure (DBP) increased by an average of 5–7/2–4 mmHg. A survey found that the average cooking salt intake of residents aged 18 and over in China was 10.5 g in 2012, although it was lower than 12.9 g in 1992 and 12.0 g in 2002, but was still 75.0% higher than the recommended salt intake level,[15] while the Chinese population was generally sensitive to sodium.[14],[16] 1.3.2 Overweight and obesity Overweight and obesity significantly increase the risk of all-cause mortality in the global population[17] and are also important risk factors for hypertension. For people aged 35–64, the overweight rate is 38.8%, and the obesity rate is 20.2%, which are higher in female than in male, in urban than in rural areas, and in north than south.[18] A follow-up study[19] on the relationship between overweight/obesity and hypertension in Chinese adults found that the risk of hypertension was 1.16 to 1.28 times higher in the overweight and obesity groups than in the normal weight group along with the increase of body mass index (BMI).[1] Visceral obesity is closely related to hypertension. With the increase of visceral fat index, the risk of hypertension increases.[20] In addition, visceral obesity is closely related to metabolic syndrome, which can lead to abnormal glucose and lipid metabolism.[21] 1.3.3 Excessive drinking Excessive drinking includes dangerous drinking (male: 41–60 g, female 21–40 g) and harmful drinking (more than 60 g for men and 40 g for women). Drinking is prevalent in China. The harmful drinking rate is 9.3%[15] among residents over 18 years old. Restricted drinking was significantly correlated with a drop in BP, with an average reduction in alcohol intake of 67%, a decrease in SBP of 3.31 mmHg and in DBP of 2.04 mmHg.[22] At present, there is insufficient evidence supports the correlation between cardiovascular health and less alcohol intake. However, some relevant research shows that even for people who drink a small amount of alcohol, reducing alcohol intake can improve cardiovascular health and reduce the risk of cardiovascular disease.[23] 1.3.4 Long-term nervousness Long-term nervousness is a risk factor for hypertension, and mental stress can activate sympathetic nerves and increase BP.[24],[25] A meta-analysis of 13 cross-sectional studies and eight prospective studies[26] showed that the risk of hypertension was 1.18 times (95% CI: 1.02–1.37) and 1.55 times (95% CI: 1.24–1.94) among people with mental stress (defined as anxiety, stress, anger, panic or fear) than the normal population. 1.3.5 Other risk factors In addition to the above risk factors for hypertension, other risk factors include age, family history of hypertension, lack of physical activity, and diabetes, etc. Studies have shown that exposure to PM2.5, PM10, SO2, and O3 is associated with increased risk of hypertension and increased mortality from cardiovascular disease.[27],[28] 2 Hypertension and cardiovascular risk Key point 2. Hypertension and cardiovascular risk BP is continuously, independently, directly and positively associated with cardiovascular risk. Stroke is still the most important complication of hypertension in China by now, while the incidence of coronary events also increased evidently. Other complications include heart failure, left ventricular hypertrophy, atrial fibrillation and end-stage renal disease. 2.1 Relationship between BP and cardiovascular risk There is a close causal relationship between BP and cardiovascular morbidity and mortality. A global prospective observational study of 61 populations (about 1 million people aged 40–89 years with the baseline BP ranging from 115/75 mmHg to 185/115 mmHg and with an average follow-up of 12 years)[29] showed that clinic SBP or DBP was continuously, independently, directly and positively associated with the risk of stroke, coronary heart disease (CHD) events and cardiovascular mortality. Each 20 mmHg increase in SBP or 10 mmHg increase in DBP was associated with doubled risk of cardiovascular and cerebrovascular morbidity. In the Asia Pacific cohort study (APCSC) which consists of 13 Chinese populations,[30] clinic BP was closely associated with the risk of stroke and ischemic heart disease events, and the association between elevated BP and stroke or ischemic heart disease events in Asian populations was stronger than in Australia and New Zealand populations. For each 10 mmHg increase in SBP, the risk of stroke and fatal myocardial infarction increased by 53% and 31% respectively in Asian populations, while by 24% and 21% respectively in Australian and New Zealand populations. There is also a causal relationship between BP level and heart failure. Clinical follow-up data showed that the incidence of heart failure increased with BP level.[31] Heart failure and stroke were the two complications most closely related to BP level. Chronic hypertension, left ventricular hypertrophy, heart failure constitute of an important chain of events. Hypertension mainly leads to heart failure with preserved ejection fraction, while if combined with CHD or myocardial infarction, it can also lead to heart failure with reduced ejection fraction. Hypertension is an important cause of atrial fibrillation.[32] Hypertension-atrial fibrillation-cerebral embolism constitute of an important but easily overlooked chain of events. Long-term clinical follow-up studies revealed that the incidence of end-stage renal disease (ESRD) also increased significantly with clinic BP.[33] The incidence of ESRD was 11 times higher in severe hypertension, and even 1.9 times higher in subjects with high normal BP compared to that in normotensive subjects. The relationship between clinic BP and the above-mentioned complications and cardiovascular diseases has also been confirmed in studies on ambulatory or home BP monitoring.[34],[35] The 24-h ambulatory BP, nocturnal BP and morning BP were even more closely and significantly correlated with the risk of cardiovascular and cerebrovascular disease. Recent studies have also shown that long-term BP variation (BPV), which reflects BP fluctuations, may also be associated with cardiovascular risk.[35] 2.2 Cardiovascular risk characteristics of hypertension population in China According to the population-based surveillance data in China,[36] cardiovascular and cerebrovascular diseases account for more than 40% of the total number of deaths. The annual incidence of stroke is 250/100,000, and the annual incidence of CHD events is 50/100,000. The incidence of stroke is five times higher than that of CHD events. In recent years, despite the ascending trend of the incidence of CHD events, the incidence difference between stroke and CHD events is still significant. In clinical trials, the incidence ratio of stroke/myocardial infarction is about 5:1–8:1 in hypertensives in China, while about 1: 1[37]–[41] in hypertensives in the Western countries. Therefore, stroke is still the major cardiovascular risk threatening the Chinese hypertensive population, and stroke prevention is an important goal of hypertension treatment in China. 3 Diagnostic evaluation Diagnostic evaluation comprises the following three aspects: (1) to establish the diagnosis of hypertension, determine the stage of BP level; (2) to identify the etiology of hypertension, distinguish the primary or secondary hypertension; and (3) to search for other cardiovascular and cerebrovascular risk factors, target organ damage and their associated clinical conditions, so as to facilitate the differential diagnosis of hypertensive etiologies, assess the cardiovascular and cerebrovascular risk, and guide the diagnosis as well as the treatment. 3.1 Medical history Patient's medical history should be comprehensively and thoroughly understood, including the following contents: (1) family history: the patients should be asked whether they have a family history of hypertension, stroke, diabetes mellitus, dyslipidemia, CHD or kidney disease, including the age at which cardiovascular and cerebrovascular events occur in first-degree relatives. (2) Clinical course: the time and place where hypertension was first detected or diagnosed the highest level of BP. If having been treated with anti-hypertensive drugs, type, dose, efficacy and side effects of anti-hypertensive drugs used in the past and at present should be recorded. (3) Symptoms and past history: inquire about the present and past history, symptoms and treatment of stroke or transient ischemic attacks, CHD, heart failure, atrial fibrillation, peripheral vascular disease, diabetes, gout, dyslipidemia, sexual dysfunction and kidney disease, etc. (4) Secondary hypertension clues: such as nephritis history or anemia history; muscle weakness, paroxysmal soft paralysis, etc; paroxysmal headache, palpitation, sweating; snoring with apnea; whether long-term use of drugs which can result in BP elevation. (5) Lifestyle: the dietary intake of salt, alcohol and fat, smoking status, physical activity, weight change, sleep habits, etc. (6) Socio-psychological factors: including patient's family situation, work environment, education background and history of psychological trauma. 3.2 Physical examination Careful physical examinations are helpful in finding clues of secondary hypertension and target organ damages. Physical examinations include: BP measurement (see BP measurement section 3.5 for details), measurement of heart rate, BMI, and waist and hip circumference; observing whether there are features of Cushing's syndrome, skin stigmata of neurofibromatosis, eye signs suggestive of hyperthyroidism, or edema at the lower extremities; searching for murmurs via the auscultation at the carotid arteries, thoracic aorta, abdominal aorta and the femoral arteries; palpating the thyroid glands, examining thoroughly the heart and lungs, examining the abdomen to find out whether there is enlargement of kidneys (polycystic kidney) or masses, palpating the arterial pulses at the extremities, and performing neurological examinations. 3.3 Laboratory examinations Routine examinations: blood chemistry (potassium, sodium, fasting blood glucose, lipids, uric acid and creatinine), blood routine test, urinalysis (urine protein, sugar, sedimentary microscopic examination), electrocardiogram, etc. Recommended examinations include: echocardiography, carotid ultrasonography, oral glucose tolerance test, glycated hemoglobin, blood high-sensitivity C-reactive protein, urinary albumin/creatinine ratio, quantitative estimation of urinary protein, eye fundoscopy, chest X-ray, pulse wave velocity (PWV), and ankle-brachial BP index (ABI), etc. Optional examinations include: blood homocysteine, for patients suspected of secondary hypertension. The following examinations might be performed if indicated: plasma renin activity or renin concentration, blood and urine aldosterone, blood and urine cortisol, blood free metanephrine and normetanephrine, blood or urine catecholamine, renal artery ultrasound and angiography, echogram, computed tomography (CT) or magnetic resonance imaging (MRI) of kidneys and adrenal glands, adrenal venous sampling, and polysomnography, etc. Hypertensives with comorbidity should be examined for relevant cardiac function, renal function and cognitive function. 3.4 Genetic analysis Although genome-wide association studies (GWAS) of hypertension has reported a number of gene loci related to BP level or hypertension,[42] the current clinical genetic diagnosis is only applicable to Liddle syndrome,[43] glucocorticoid-remediable aldosteronism[44] and other monogenic inherited hypertension. 3.5 BP measurement Key point 3A. Procedures for clinic BP measurement Patient should be seated for at least 5 min in a quiet room before BP measurements, and keep the upper arm at the heart level. Validated upper arm medical electronic sphygmomanometer is recommended, and mercury sphygmomanometer will be deprecated gradually. Use a standard cuff (with a bladder of 12 cm wide and 22–26 cm long) for most patients, larger cuffs should be used for obese patients or those with large arm circumference (> 32 cm). Measure BP on both arms at the first visit. Use the arm with higher value as the reference. Two BP measurements should be taken 1–2 min apart and averaged for records. An additional measurement is required if the first two readings differ by > 5 mmHg, and the mean value of the three readings should be recorded. Measure BP 1 min and 3 min after standing from a seated position in case of elderly patients, diabetic patients, and patients suspected orthostatic hypotension. Heart rate should be measured together with BP. Key point 3B: evaluation of various BP measurement methods Clinic BP measurement is by now the common method to diagnose hypertension, grade the BP level category and observe the antihypertensive efficacy in China. If possible, out-of-office BP measurement should be performed to diagnose white-coat hypertension and masked hypertension, evaluate the efficacy of antihypertensive therapy, and assist the diagnosis and treatment of resistant hypertension.[45] Ambulatory BP monitoring can evaluate 24-h BP circadian rhythm, orthostatic hypotension, and postprandial hypotension, etc. Home BP monitoring may assist in adjusting treatment regimens. Remote real-time BP monitoring based on internet is a new mode of BP management. Patients with high psychological anxiety are not recommended to have their BP checked frequently. BP measurement is the fundamental means and method of evaluating BP level, diagnosing hypertension and observing antihypertensive efficacy. Clinic and out-of-office BP measurement are adopted frequently in clinical practice and population disease prevention and control, the latter refers to ambulatory BP monitoring (ABPM) and home BP monitoring (HBPM). Out-of-office BP measurement can provide large amount of BP data outside the medical environment, and its relationship with target organ damage is more significant than that of clinic BP, and it is better than clinic BP in predicting cardiovascular risk.[34],[46] 3.5.1 Clinic BP measurement The clinic BP measurement is carried out by doctors or nurses, under standard conditions and unified guidelines. It is the common method to diagnose hypertension, grade the BP level category and observe the antihypertensive efficacy. Upper arm medical electronic sphygmomanometer, which has been validated by international standardized protocols (ESH, BHS and AAMI) (electronic sphygmomanometer certification results are available in the following website: http://www.dableducational.org, http://www.bhsoc.org/default.stm), or mercury sphygmomanometer, which is up to the metrological standard (will be deprecated gradually), are used for the measurement. Automated office BP measurement (AOBP) can reduce the white-coat effect, which is worthy of further research and promotion.[47] See key point 3A for the measurement procedure. If mercury column sphygmomanometer is used for BP measurement, rapid inflation is required to let the inner pressure of the bladder go further up by 30 mmHg after the disappearance of the radial artery pulse downstream, and then deflate the bladder slowly at a speed of 2.0 mmHg per second. The deflation speed should be even slower if the heart rate is slow. Deflate the bladder quickly to zero after DBP reading is obtained; listen to the Korotkoff sound carefullly during the deflation of the bladder, watch the convex meniscus surface of the mercury column at its perpendicular height at the moment of Korotkoff phase I (the first sound) and phase V (the disappearance of the sound). Take the reading at Korotkoff phase I as SBP and the reading at Korotkoff phase V as DBP. In the case of children ( 55 years Woman > 65 years Smoking or passive smoking Left ventricular hypertrophy electrocardiogram: Sokolow-Lyon voltage > 3.8 mV or Cornell product > 244 mV·ms Echocardiogram: LVMI (man ≥ 115 g/m2, woman ≥ 95 g/m2) Cerebrovascular disease Cerebral hemorrhage Ischemic stroke Transient ischemic attack Impaired glucose tolerance (7.8–11.0 mmol/L for 2-h blood glucose) and/or impaired fasting glucose (6.1–6.9 mmol/L) Carotid ultrasonography (IMT ≥ 0.9 mm) or atherosclerotic plaque Heart disease History of myocardial infarction Angina pectoris Coronary revascularization Congestive heart failure Atrial fibrillation Dyslipidemia TC ≥ 6.2 mmol/L (240 mg/dL) or LDL-C ≥ 4.1 mmol/L (160 mg/dL) or HDL-C 75% bilateral carotid stenosis, central perfusion pressure is decreased, and intensive blood-pressure lowering may increase the risk of cerebral ischemia. Antihypertensive treatment should be based on the inhibition for the avoidance of cerebral ischemia symptoms. It is however, common to lose control of BP targets.[218] The BP of frail and elderly patients on medication to lower BP, should be regularly monitored. It is also advisable not to lower the BP excessively and at a high pace. 6.1.4 Drug application Drug selection for optimal treatment of hypertension in the elderly: current recommended drugs to be considered as initial therapy or combination therapy for BP lowering are diuretics, calcium channel blockers (CCB), angiotensin-converting-enzyme inhibitors (ACEI), and angiotensin II receptor blocking (ARB),[69],[70],[219]–[223] which should be initiated at a low dose and be increased gradually up to the maximum dose. β-blockers are usually not the first choice for the elderly hypertensive patients without commodity disease. Diuretics may reduce glucose tolerance, induce hypokalemia, hypeluricemia and dyslipidemia. Therefore, they should be used in small doses. Alpha-adrenergic receptor antagonists (α-blockers) are drugs of second line (adjuvant drugs) which can be used for patients with benign prostatic hyperplasia or refractory hypertension. When given to the very elderly patients with postural BP variations, α-blockers should be used with caution and they may cause postural hypotension. Drug therapy for elderly patients with isolated systolic hypertension (ISH): for patients with DBP 40 years old, BMI > 35, family history of preeclampsia, multifetation), low dose aspirin can be prescribed from the twelfth week of the gestation until one week before delivery.[257] 6.4 Hypertension with stroke Key point 6D For patients with stable stroke, antihypertensive therapy should be initiated if BP ≥ 140/90 mmHg, and the target of lowering BP is 220 mmHg. Intravenous antihypertensive agents are recommended if SBP > 180 mmHg. The reference goal for lowering BP is 160/90 mmHg (IIb, B). 6.4.1 BP management in stable stroke Systematic analysis showed that antihypertensive agents significantly reduced the risk of stroke recurrence by 22%.[131] For stable stroke patients, the goal for lowering BP should be 220 mmHg. Intravenous antihypertensive agents are recommended if SBP > 180 mmHg. The reference goal for lowering BP is 160/90 mmHg. Early aggressive antihypertension is safe, but the effectiveness of improving prognosis needs to be further investigated. The BP should be closely monitored during antihypertension therapy. BP should be monitored every 15 min. 6.5 Hypertension with coronary artery disease (CAD) Key point 6E In patients with CAD, it is recommended: the target BP is to 30 mL/min per 1.73 m2) (CKD stage 1–3), patients with GFR 2 g/kg per minute may induce cyanide poisoning. Nitroglycerine 5–100 µg/min, IV (hypertensive emergency with myocardial ischemia). 2–5 min 5–10 min Headache and vomiting. Phentolamine 2.5–5 mg, IV (used to diagnose pheochromocytoma and to treat hypertensive episodes caused by it, including hypertension occurred during surgical resection, and can also be used to assist in the diagnosis of pheochromocytoma based on the BP response to it). 1–2 min 10–30 min Tachycardia, headache and flushing. Nicardipine 0.5–10 µg/kg per minute, IV, (perioperative hypertension, hypertension emergencies).The initial dose is 5 mg/h, and is gradually increased to 15 mg/h according to blood pressure response (pregnancy-induced hypertension, safety level C). 5–10 min 1–4 h Tachycardia, headache, peripheral edema, angina pectoris, nausea, dizziness, inhibition of uterine contraction (combined with magnesium sulfate). Esmolol 0.15–0.3 mg/kg per minute, IVI (perioperative hypertension).250–500 µg/kg, IVFollowed by 50–300 µg/kg per minute, IV, (hypertension emergencies). 1–2 min 10–20 min Hypotension and nausea. Metoprolol 3–5 mg, IV, repeated every 5 min, the maximum dose is 15 mg (hypertension emergencies). 5–10 min 5–10 h Hypotension, heart failure, heart block, dizziness, fatigue, depression, bronchospasm. Labetalol 25–50 mg, IV, repeat every 15min is permitted, and the total dose can be used up to 200 mg. Intravenous infusion is also feasible, 1–4 mg/min, IV (perioperative hypertension).20–80 mg IV, 0.5–2.0 mg/min IVI (hypertensive emergency). 5–10 min 3–6 min Nausea, vomiting, cephalic anesthesia, bronchospasm, conduction block, orthostatic hypotension. Urapidil 10–50 mg IV6–24 mg/h 5 min 2–8 h Hypotension, dizziness, nausea, and fatigue. Enalaprilat 1.25–5 mg IV q6 h 15–30 min 6–12 h Blood pressure has a steep drop in high renin status, and the variation is high. Diltiazem 5–10 mg IV, or 5–15 µg/kg per minute IVI (perioperative hypertension, hypertension emergencies). 5 min 30 min Tachycardia, AV block, hypotension, cardiac failure, peripheral edema, headache, constipation, hepatotoxicity. Dralzine 10–20 mg IV10–40 mg IM 10–20 min20–30 min 1–4 h4–6 h Tachycardia, flushing, headache, vomiting and angina aggravated. Fenoldopam 0.03–1.6 µg/kg per minute, IV 110 mmHg, are prone to develop perioperative BP fluctuation. (3) Operations: perioperative hypertension often occurs in operation of carotid artery, abdominal aorta, peripheral blood vessels, abdominal cavity and thoracic cavity. Severe hypertension may occur in cardiac surgery, large artery operation including carotid endarterectomy and aortic surgery, nervous system operation, head and neck operation, kidney transplantation and severe trauma like empyrosis or head trauma. 6.13.2 Principles of perioperative hypertensive control and BP targets[296] (1) Principles: basic principle is to ensure perfusion of important organs, reduce cardiac afterload and protect cardiac function. Continuation of β-blockers or CCB is recommended in hypertensive patients, while ACEI and ARB should be discontinued. (2) BP targets: BP should be controlled 180/110 mmHg when entering operation room, deferring the intervention is recommended. If operation is necessary, such as tumor with hemorrhage, the operation could be performed with family members' approval. Considering possible ischemia of important target organ and side effect of antihypertensive pharmacological therapy, it is not recommended to lower blood pressure in few hours for patients with preoperative SBP/DBP > 180/110 mmHg. In patients with mild to moderate hypertension (SBP/DBP 70%), for example: if BP is poorly controlled, kidney atrophy or renal dysfunction occurred, revascularization is recommended.[309] Endovascular therapy is the first choice for vascular reconstruction. Open surgery is recommended for failed lesions. 9.2.2 Stenosis of aorta Aortic stenosis includes congenital and acquired aortic stenosis. Congenital aortic stenosis manifests as limited stenosis or atresia at the aorta, the onset site is usually near the orifice of the original ductus arteriosus in the isthmus of the aorta, while some of which may occur in other parts of the aorta. Acquired aortic stenosis includes Takayasu arteritis, atherosclerosis, and aortostenosis causes by Aortic dissection. The basic pathophysiological changes of the disease are blood flow redistribution caused by stenosis, water and sodium retention and RAS activation caused by renal ischemia, which results in left ventricular hypertrophy, heart failure, cerebral hemorrhage and other important organ damages. Aortic stenosis manifests as hypertension in upper limbs, weak or no arteries in lower limbs. The BP of both lower limbs was significantly lower than that of upper limbs (ABI 15 times/h), non-invasive ventilation (CPAP) is recommended. 9.4 Primary aldosteronism and other endocrine hypertension 9.4.1 Primary aldosteronism Primary aldosteronism is a clinical syndrome characterized by hyperaldosterone secretion in the globular zone of the adrenal cortex, which leads to hypertension, hypokalemia and renin activity inhibition. Common types of primary aldosteronism include aldosteronism (35%) and idiopathic aldosteronism (60%). Other rare types are adrenal cortical carcinoma and familial aldosteronism, such as glucocorticoid-inhibiting aldosteronism (GRA). Primary aldosteronism accounts for about 5%–10% of hypertensive patients and only a small percentage of them have hypokalemia, which accounts for about 20% of refractory hypertension. It can increase the risk of metabolic syndrome, arteriosclerosis and cardiovascular and cerebrovascular diseases.[311],[312] The clinical diagnosis process of primary aldosteronism includes three steps: screening, diagnosis and classification. Serum aldosterone/renin ratio (ARR) was used for screening.[301] The screening subjects were refractory hypertension, hypertension with spontaneous or diuretic-induced hypokalemia, or adrenal accidental tumors, primary aldosteronism in first-degree relatives, sleep apnea syndrome, early onset hypertension or family history of cardiovascular events ( 1 cm) or unilateral dominant secretory adenomas or nodules confirmed by AVS were should take surgical treatment. Drug therapy should be taken for those who have no surgical indication, intention or intolerance. The first-line drug is salt corticosteroid receptor antagonist, and spironolactone is recommended as the first choice. 9.4.2 Pheochromocytoma/paraganglioma Pheochromocytoma is a neoplasm originating from adrenal medulla or pheochromocyte of extra adrenal nerve chain. Tumor can secrete excessive catecholamine (CA), which can cause persistent or paroxysmal hypertension, functional and metabolic disorders on some organs. It is a clinically curable secondary hypertension. The clinical features of pheochromocytoma appeared to be paroxysmal, persistent or paroxysmal severe hypertension. Hypertension is often accompanied by headache, palpitation and hyperhidrosis, also abnormal glucose and lipid metabolism. The main method of qualitative diagnosis of pheochromocytoma is determination of catecholamines and its metabolites. Enhanced CT is recommended as the preferred locational method for thoracic, abdominal and pelvic lesions. MRI is recommended as the preferred locational method for skull base and neck lesions. Besides, metaiodobenzylguanidine (MIBG), 18F-FDG PET and somatostatin imaging can be used to make function and image localization for metastatic and extraadrenal tumors. Surgical treatment is important for patients with pheochromocytoma. Alpha-receptor blockers can be administered before surgery. Using beta-blockers before using alpha-blockers is not recommended. Lifelong follow-up should be taken after surgery. 9.4.3 Cushing's syndrome Cushing's syndrome (CS) that is hypercortisolism. Hypercortisolism can be accompanied by various complications, leading to the syndrome with typical manifestations like centripetal obesity, hypertension, abnormal glucose metabolism, hypokalemia and osteoporosis. As Qualitative and locational diagnosis of CS and its treatment is more complicated, it is suggested to communicate and cooperate with doctors in hypertension specialty or endocrinology department actively. ACEI or ARB antihypertensive drugs are preferred to use in the initial treatment of Cushing's syndrome-related hypertension. If BP is still higher than 130/80 mmHg, they can be combined with mineralocorticoids receptor antagonists or CCB according to the severity of the disease and the presence or absence of hypokalemia. If BP is still higher than 130/80 mmHg, the alpha-receptor blocker or nitric acid can be added. If BP still cannot reach the standard, beta-blocker and diuretic can be carefully selected and used. 9.5 Other rare types of secondary hypertension According to the present epidemiological data, there are still some rare causes of elevated BP, which account for less than 1% of the causes of hypertension, mainly includes thyroid dysfunction, hyperparathyroidism, renin tumors and so on. 9.6 Drug-induced hypertension Drug-induced hypertension is caused by the drug itself in a conventional dose or its interactions with other drugs, and when BP exceeds 140/90 mmHg, it should be considered as drug-induced hypertension (Table 17). The drugs involved mainly include: (1) hormone drugs; (2) central nervous drugs; (3) non-steroidal anti-inflammatory drugs; (4) Chinese herbal medicine; and (5) other drugs. Table 17. Drugs, mechanisms and treatment of drug-induced hypertension. Category Common drugs Mechanism Treatment and notes Hormones Estrogen Estradiol, ilestriol (1) Water-sodium retention Diuretic premarin, desogestreland ethinylestradiol (2) RAS activation(3) Insulin resistance ACEI (ARB) β-blocker Progestogen Medroxyprogesterone 17-acetate, nore-thindrone, medroxyprogesterone acetate Corticosteroid responses induced by High doses of drugs Androgen MethyltestosteroneNandroloniPhenylPropionas, stanozolol (1) Induce polycythemia(2) Affecting the regulation of potassium channels and androgen receptors, leading to retention of nitrogen, sodium, potassium and phosphorus and insulin resistance Oxytocin Antidiuretic effects will occur in large doses Pituitrin (1) Arterioles contraction(2) Increased water reabsorption Glucocorticoid Hydrocortisone, Prednisone, Dexamethasone Both cortisol and corticosterone have salt corticosteroid activity Pay attention to the change of serum potassiumDiuretic CCBACEI (ARB) Mineralocor-ticoid 9α-Fludrocortisone, Deoxycortone Acetate Increase sodium reabsorption and Promote potassium excretion DiureticPay attention to the change of serum potassium Thyroxine Sodium Euthyrox Increase the excitability of sympathetic nervous system Affecting sympathetic excitation Anesthetics Ketamine, desflurane, sevoflurane, naloxone hydrochloride, Increased sympathetic excitability α receptor blockers, clonidine, diltiazem, ritali, amphetamine, cocaine Promote the release of dopamine and NE from nerve endings and block their recovery, increase synaptic sites and prolong the action time α receptor blockers, verapamil, nitroglycerin Antiparkinsonian drug L-DOPA Stimulate dopamine receptors at the postsynaptic membrane to play the role of antiparkinsonian and elevate BP at the same time Diet pills Sibutramine Inhibit the re-uptake of 5-hydroxytryptamine and NE, increase the content of synaptic space and the excitability of sympathetic nerve Lose weight in other ways ACEI (ARB) β-blocker Adrenaline β2-agonist Salbutamol sulfate, bambuterol hydrochloride, terbutaline sulfate, clorprenaline Activate the adenylate cyclase and increase the synthesis of adenosine cyclophosphate in cells Should be used with caution for pheochromocytoma or hyperthyroidism Methylxanthines Aminophylline, doxofylline,dyphylline Increased the release of endogenous epinephrine and norepinephrine Nonsteroidal anti-inflammatory drugs Indomethacin, indomethacin,ibuprofen, phenylbutazone celebrex, arthrotec, antine (1) Water-sodium retention, (2) reduce the prostaglandins in circulation, (3) renal damage CCBACEI (ARB) Chinese herbal medicine Glycyrrhizin Glycyrrhizin, cholic acid, carbenoxolone (1) Inhibits the activity of 11beta-hydroxysteroid dehydro-genas, increase the production of cortisol-mediated mineral corticoid and elevate BP(2) Inhibit the synthesis of prostaglandin(3) Inhibit the synthesis and release of histamine DiureticsCCBACEI (ARB) Ephedrines Ephedrine nasal drops, ephedrine and chlorphenamine, diphenhydramine (1) Directly activate adrenaline α and β2 receptors(2) Indirectly promote the release of NE neurotransmitters(3) Significant central stimulating α receptor blockerβ receptor blocker Others Monoamine oxidase inhibitor Isoniazid, furazolidone, ketoconazole; Reserpine; TCA Antagonize monoamine oxidase and other enzymes, it is not beneficial to the inactivation of catecholamines both inside and outside the cell, therefore enhances vasoconstriction. α receptor blocker TZDs Rosiglitazone maleate, pioglitazone Water-sodium retention Use cautiously in patients with severe heart failure Recombinant human erythropoietin (1) Vasoconstriction and intracellular calcium homeostasis and increase sympathetic excitability(2) Stimulate the synthesis of endothelin in vascular endothelial cells(3) Polycythemia(4) Genetic mechanisms Preferred CCB or αreceptor blocker, Diuretics and ACEI are not sensitive for antihyper-tensive effects Ciclosporin and immuno-suppressant Cyclosporin Tacrolimus (1) Activation of sympathetic nervous system(2) Diuretic response is unresponsive when dilatation of blood volume happen(3) NO-mediated vasodilation is impaired and endothelin release increased(4) Afferent nerve of renal sympathetic nerve is activated after neurocalcin was blocked CCB (may increase in serum cyclosporin concentration) Combination of multiple antihypertensive drugs (Clonidine) ACEI: angiotensin converting enzyme inhibitor; ARB: angiotensin receptor blockers; CCB: calcium channel blockers. 9.7 Monogenic inherited hypertension The mutations of monogenic inherited hypertension are mostly associated with gene mutations on renal unit ion transporters or RAS components causing dysfunction. It can be divided into the following categories: (1) Gene mutations directly affect the function of related proteins in renal tubu-lar ion channel transport system: Liddle syndrome, Gordon syndrome, apparent mineralocortixoid excess, pregnancy-I resistancenduced hypertension caused by corticosteroid receptor mutations (2) abnormal steroid synthesis in the adrenal gland caused by Gene mutations: familial hyperaldosteronism (I, II, III), congenital adrenal hyperplasia (11β-hydroxylase deficiency, 7 α-hydroxylase/17, 20-lyase deficiency, 17OHD), familial glucocorticoid resistance (3) Various neuroendocrine tumors, such as pheochromocytoma, hypertension with brachydactylia, multipleendocrineneoplasm (MEN) and Von Hippel-Lindau (VHL). 10 Research prospection In 2015, researchers from Chinese Center for Disease Control and Prevention published an article focusing on the burden of disease in China, showing that from 1990 to 2013 the age-standardized death rate of stroke decreased by 21% and that rate of hemorrhagic stroke decreased by 38% respectively.[313] Stroke, especially hemorrhagic stroke, is a major complication of hypertension, therefore the results reflects the hypertension prevention and treatment has achieved some effect in terms of cardiac outcomes. Presently, the important ongoing hypertension researches in China include Study of Antihypertensive Treatment in Patients with High-normal Blood Pressure and Risk Factors (CHINOM), Optimal Blood Pressure and Cholesterol Targets for Preventing Recurrent Stroke in Hypertensives (SHOT), Strategy of Blood Pressure Intervention in the Elderly Hypertensive Patients (STEP), Systolic hypertension in the elderly: Chinese Trial-2 (Syst-China-2), Intervention Study of Blood Pressure in People with High Normal or Borderline Hypertension and Type 2 Diabetes (IPAD), China Stroke Primary Prevention Trial-2 (CSPPT-2) and so on. The report of Comparative Effect Study of L-amlodipine Maleate and Amlodipine Besylate in the Hypertensive Patients (LEADER Study), supported by the National Science and Technology Major Project for Drug Discovery, is being summarized, and important results will be released for clinical reference. The CHIEF study will also continue to summarize data on cardiovascular events. Supplement 1. Blood pressure references for children and adolescents aged 3 to 17 years old in China by sex and height. Supplement Table 1-1. Blood pressure references for children and adolescents aged 3 to 17 years old in China, male Age, year Height percentile Height range, cm SBP, mmHg DBP, mmHg 50th 90th 95th 99th 50th 90th 95th 99th 3 P5 < 96 88 99 102 108 54 62 65 72 P10 96–97 88 100 103 109 54 63 65 72 P25 98–100 89 101 104 110 54 63 66 72 P50 101–103 90 102 105 112 54 63 66 73 P75 104–106 91 103 107 113 55 63 66 73 P90 107–108 92 104 107 114 55 63 66 73 P95 ≥ 109 93 105 108 115 55 63 66 73 4 P5 < 102 89 101 104 111 55 64 67 74 P10 102–104 90 102 105 111 55 64 67 74 P25 105–107 91 103 106 113 55 64 67 74 P50 108–110 92 104 108 114 56 64 67 74 P75 111–113 93 106 109 115 56 64 67 74 P90 114–116 94 107 110 117 56 65 68 75 P95 ≥ 117 95 107 111 117 56 65 68 75 5 P5 < 109 92 104 107 114 56 65 68 75 P10 109–110 92 104 107 114 56 65 68 75 P25 111–113 93 105 109 115 56 65 68 75 P50 114–117 94 106 110 117 57 65 69 76 P75 118–120 95 108 111 118 57 66 69 76 P90 121–123 96 109 112 119 58 67 70 77 P95 ≥ 124 97 110 113 120 58 67 70 77 6 P5 < 114 93 105 109 115 57 66 69 76 P10 114–116 94 106 110 116 57 66 69 76 P25 117–119 95 107 111 117 58 66 69 77 P50 120–123 96 108 112 119 58 67 70 78 P75 124–126 97 110 113 120 59 68 71 78 P90 127–129 98 111 115 121 59 69 72 79 P95 ≥ 130 99 112 116 123 60 69 73 80 7 P5 < 118 94 106 110 117 58 67 70 77 P10 118–120 95 107 111 118 58 67 70 78 P25 121–123 96 108 112 119 59 68 71 78 P50 124–127 97 110 113 120 59 68 72 79 P75 128–131 98 112 115 122 60 70 73 81 P90 132–135 100 113 117 124 61 71 74 82 P95 ≥ 136 100 114 117 125 62 71 74 82 8 P5 < 121 95 108 111 118 59 68 71 78 P10 121–123 95 108 112 119 59 68 71 79 P25 124–127 97 110 113 120 60 69 72 80 P50 128–132 98 111 115 122 61 70 73 81 P75 133–136 99 113 117 124 62 71 74 82 P90 137–139 101 114 118 125 62 72 75 83 P95 ≥ 140 102 115 119 127 63 73 76 84 9 P5 < 125 96 109 112 119 60 69 72 80 P10 125–128 96 109 113 120 60 69 73 80 P25 129–132 98 111 115 122 61 71 74 82 P50 133–137 99 113 117 124 62 72 75 83 P75 138–142 101 115 119 126 63 73 76 84 P90 143–145 102 116 120 128 64 73 77 85 P95 ≥ 146 103 117 121 129 64 74 77 85 10 P5 < 130 97 110 114 121 61 70 74 81 P10 130–132 98 111 115 122 62 71 74 82 P25 133–137 99 113 116 124 62 72 75 83 P50 138–142 101 115 119 126 63 73 77 85 P75 143–147 102 117 120 128 64 74 77 85 P90 148–151 104 118 122 130 64 74 77 86 P95 ≥ 152 105 119 123 131 64 74 77 86 11 P5 < 134 98 111 115 122 62 72 75 83 P10 134–137 99 112 116 124 63 72 76 84 P25 138–142 100 114 118 126 64 73 77 85 P50 143–148 102 116 120 128 64 74 78 86 P75 149–153 104 119 123 130 64 74 78 86 P90 154–157 106 120 124 132 64 74 78 86 P95 ≥ 158 106 121 125 133 64 74 78 86 12 P5 < 140 100 113 117 125 64 73 77 85 P10 140–144 101 115 119 126 64 74 78 86 P25 145–149 102 117 121 128 65 75 78 86 P50 150–155 104 119 123 131 65 75 78 86 P75 156–160 106 121 125 133 65 75 78 86 P90 161–164 108 123 127 135 65 75 78 87 P95 ≥ 165 108 124 128 136 65 75 78 87 13 P5 < 147 102 116 120 128 65 75 78 86 P10 147–151 103 117 121 129 65 75 78 87 P25 152–156 104 119 123 131 65 75 79 87 P50 157–162 106 121 125 133 65 75 79 87 P75 163–167 108 123 128 136 65 75 79 87 P90 168–171 110 125 130 138 66 76 79 87 P95 ≥ 172 110 126 130 139 66 76 79 88 14 P5 < 154 103 118 122 130 65 75 79 87 P10 154–157 104 119 124 132 65 75 79 87 P25 158–162 106 121 125 133 65 75 79 87 P50 163–167 108 123 128 136 65 75 79 87 P75 168–172 109 125 130 138 66 76 79 88 P90 173–176 111 127 131 140 66 76 80 88 P95 ≥ 177 112 128 133 141 67 77 80 89 15 P5 < 158 105 120 124 132 65 76 79 87 P10 158–161 106 121 125 133 65 76 79 87 P25 162–166 107 122 127 135 66 76 79 88 P50 167–170 109 124 128 137 66 76 80 88 P75 171–174 110 126 131 139 66 77 80 89 P90 175–178 112 128 132 141 67 77 81 89 P95 ≥ 179 113 129 133 142 67 77 81 90 16 P5 < 161 105 121 125 133 66 76 79 88 P10 161–164 106 121 126 134 66 76 79 88 P25 165–168 107 123 127 136 66 76 80 88 P50 169–172 109 125 129 138 66 76 80 88 P75 173–176 111 126 131 140 67 77 80 89 P90 177–179 112 128 133 141 67 77 81 90 P95 ≥ 180 113 129 134 142 67 78 81 90 17 P5 < 163 106 121 126 134 66 76 80 88 P10 163–165 107 122 126 135 66 76 80 88 P25 166–169 108 124 128 136 66 76 80 88 P50 170–173 109 125 130 138 67 77 80 89 P75 174–177 111 127 131 140 67 77 81 89 P90 178–180 112 129 133 142 67 78 81 90 P95 ≥ 181 113 129 134 143 68 78 82 90 Supplement Table 1-2. Blood pressure references for children and adolescents aged 3 to 17 years old in China, female Age, year Height percentile Height range, cm SBP, mmHg DBP, mmHg 50th 90th 95th 99th 50th 90th 95th 99th 3 P5 < 95 87 99 102 108 55 63 67 74 P10 95–96 88 99 103 109 55 63 67 74 P25 97–99 88 100 103 110 55 64 67 74 P50 100–102 89 101 104 111 55 64 67 74 P75 103–105 90 102 105 112 55 64 67 74 P90 106–107 91 103 106 113 55 64 67 75 P95 ≥ 108 91 103 107 113 56 64 67 75 4 P5 < 101 89 101 105 111 56 64 67 75 P10 101–103 89 101 105 111 56 64 67 75 P25 104–106 90 102 106 112 56 64 67 75 P50 107–109 91 103 107 113 56 64 67 75 P75 110–112 92 104 107 114 56 65 68 75 P90 113–114 93 105 109 115 56 65 68 76 P95 ≥ 115 93 105 109 115 56 65 68 76 5 P5 < 108 91 103 106 113 56 65 68 76 P10 108–109 91 103 107 113 56 65 68 76 P25 110–112 92 104 107 114 56 65 68 76 P50 113–116 93 105 109 115 57 65 68 76 P75 117–119 93 106 109 116 57 66 69 77 P90 120–122 94 107 111 117 58 66 70 77 P95 ≥ 123 95 108 111 118 58 67 70 78 6 P5 < 113 92 104 108 115 57 65 69 76 P10 113–114 92 105 108 115 57 66 69 77 P25 115–118 93 106 109 116 57 66 69 77 P50 119–121 94 107 110 117 58 67 70 78 P75 122–125 95 108 112 118 58 67 71 79 P90 126–128 96 109 113 119 59 68 71 79 P95 ≥ 129 97 110 114 121 59 69 72 80 7 P5 < 116 93 105 109 115 57 66 69 77 P10 116–118 93 106 109 116 57 66 69 77 P25 119–122 94 107 110 117 58 67 70 78 P50 123–126 95 108 112 119 59 68 71 79 P75 127–130 96 109 113 120 59 69 72 80 P90 131–133 97 111 114 122 60 69 73 81 P95 ≥ 134 98 112 115 122 61 70 73 82 8 P5 < 120 94 106 110 116 58 67 70 78 P10 120–122 94 107 111 117 58 67 71 79 P25 123–126 95 108 112 119 59 68 71 79 P50 127–131 96 109 113 120 60 69 72 80 P75 132–135 98 111 115 122 61 70 73 82 P90 136–138 99 112 116 123 61 71 74 83 P95 ≥ 139 100 113 117 124 62 71 75 83 9 P5 < 124 95 108 111 118 59 68 71 79 P10 124–127 95 108 112 119 59 68 72 80 P25 128–132 97 110 113 120 60 69 73 81 P50 133–136 98 111 115 122 61 71 74 82 P75 137–141 100 113 117 124 62 72 75 84 P90 142–145 101 114 118 125 63 72 76 84 P95 ≥ 146 102 115 119 126 63 73 76 85 10 P5 < 130 96 109 113 120 60 69 73 81 P10 130–133 97 110 114 121 61 70 73 82 P25 134–138 99 112 116 123 62 71 75 83 P50 139–143 100 113 117 124 63 72 76 84 P75 144–147 101 115 119 126 63 73 76 85 P90 148–151 103 116 120 128 63 73 77 85 P95 ≥ 152 103 117 121 129 64 73 77 86 11 P5 < 136 98 112 115 122 62 71 75 83 P10 136–139 99 113 116 123 62 72 75 84 P25 140–144 101 114 118 125 63 73 76 85 P50 145–149 102 116 120 127 64 73 77 86 P75 150–154 103 117 121 128 64 74 77 86 P90 155–157 104 118 122 129 64 74 77 86 P95 ≥ 158 104 118 122 130 64 74 77 86 12 P5 < 142 100 113 117 124 63 73 76 85 P10 142–145 101 114 118 125 63 73 77 85 P25 146–150 102 116 120 127 64 74 77 86 P50 151–154 103 117 121 129 64 74 78 86 P75 155–158 104 118 122 130 64 74 78 87 P90 159–162 105 119 123 130 64 74 78 87 P95 ≥ 163 105 119 123 131 64 74 78 87 13 P5 < 147 101 115 119 126 64 74 77 86 P10 147–149 102 116 120 127 64 74 78 87 P25 150–153 103 117 121 128 64 74 78 87 P50 154–157 104 118 122 129 65 74 78 87 P75 158–161 105 119 123 130 65 74 78 87 P90 162–164 105 119 123 131 65 74 78 87 P95 ≥ 165 105 119 123 131 65 75 78 87 14 P5 < 149 102 116 120 127 65 74 78 87 P10 149–152 103 117 121 128 65 75 78 87 P25 153–155 104 118 122 129 65 75 78 87 P50 156–159 104 118 122 130 65 75 78 87 P75 160–163 105 119 123 130 65 75 78 87 P90 164–166 105 119 123 131 65 75 79 87 P95 ≥ 167 106 120 124 131 65 75 79 88 15 P5 < 151 103 116 120 128 65 75 79 87 P10 151–152 103 117 121 128 65 75 79 88 P25 153–156 104 118 122 129 65 75 79 88 P50 157–160 105 119 123 130 65 75 79 88 P75 161–163 105 119 123 131 65 75 79 88 P90 164–166 105 120 124 131 65 75 79 88 P95 ≥ 167 106 120 124 131 65 75 79 88 16 P5 < 151 103 117 121 128 65 75 79 88 P10 151–153 103 117 121 129 65 75 79 88 P25 154–157 104 118 122 130 65 75 79 88 P50 158–160 105 119 123 130 65 75 79 88 P75 161–164 105 119 123 131 66 76 79 88 P90 165–167 106 120 124 131 66 76 79 88 P95 ≥ 168 106 120 124 132 66 76 79 88 17 P5 < 152 103 117 121 129 66 76 79 88 P10 152–154 104 118 122 129 66 76 79 89 P25 155–157 104 118 122 130 66 76 80 89 P50 158–161 105 119 123 130 66 76 80 89 P75 162–164 105 119 124 131 66 76 80 89 P90 165–167 106 120 124 132 66 76 80 89 P95 ≥ 168 106 120 124 132 66 76 80 89
- Record: found
- Abstract: found
- Article: not found
Regulation of uric acid metabolism and excretion.
Purines perform many important functions in the cell, being the formation of the monomeric precursors of nucleic acids DNA and RNA the most relevant one. Purines which also contribute to modulate energy metabolism and signal transduction, are structural components of some coenzymes and have been shown to play important roles in the physiology of platelets, muscles and neurotransmission. All cells require a balanced quantity of purines for growth, proliferation and survival. Under physiological conditions the enzymes involved in the purine metabolism maintain in the cell a balanced ratio between their synthesis and degradation. In humans the final compound of purines catabolism is uric acid. All other mammals possess the enzyme uricase that converts uric acid to allantoin that is easily eliminated through urine. Overproduction of uric acid, generated from the metabolism of purines, has been proven to play emerging roles in human disease. In fact the increase of serum uric acid is inversely associated with disease severity and especially with cardiovascular disease states. This review describes the enzymatic pathways involved in the degradation of purines, getting into their structure and biochemistry until the uric acid formation.
- Record: found
- Abstract: found
- Article: found
Prevalence of Hyperuricemia and Gout in Mainland China from 2000 to 2014: A Systematic Review and Meta-Analysis
Rui Liu, Cheng-Cheng Han, Di Wu … (2015)
We systematically identified the prevalence of hyperuricemia and gout in mainland China and provided informative data that can be used to create appropriate local public health policies. Relevant articles from 2000 to 2014 were identified by searching 5 electronic databases: PubMed, Google Scholar, Chinese Wanfang, CNKI, and Chongqing VIP. All of the calculations were performed using the Stata 11.0 and SPSS 20.0 software. The eligible articles (n = 36; 3 in English and 33 in Chinese) included 44 studies (38 regarding hyperuricemia and 6 regarding gout). The pooled prevalence of hyperuricemia and gout was 13.3% (95% CI: 11.9%, 14.6%) and 1.1% (95% CI: 0.7%, 1.5%), respectively. Although publication bias was observed, the results did not change after a trim and fill test, indicating that that impact of this bias was likely insignificant. The prevalence of hyperuricemia and gout was high in mainland China. The subgroup analysis suggested that the geographical region, whether the residents dwell in urban or rural and coastal or inland areas, the economic level, and sex may be associated with prevalence.
Author and article information
Journal
Journal ID (nlm-ta): Risk Manag Healthc Policy
Journal ID (iso-abbrev): Risk Manag Healthc Policy
Journal ID (publisher-id): rmhp
Journal ID (pmc): rmhp
Title:
Risk Management and Healthcare Policy
Publisher:
Dove
ISSN
(Electronic):
1179-1594
Publication date
(Electronic):
16
February
2021
Publication date Collection: 2021
Volume: 14
Pages: 655-663
Affiliations
[1
]Department of Clinical Laboratory, Maternal and Children Health Care Hospital (Huzhong Hospital) of Huadu , Guangzhou, Guangdong, 510800, People’s Republic of China
[2
]Department of Clinical Laboratory, Chancheng Centre Hospital , Foshan, Guangdong, 528000, People’s Republic of China
[3
]Department of Clinical Laboratory, Taishan People’s Hospital , Jiangmen, Guangdong, 529200, People’s Republic of China
[4
]Department of Clinical Laboratory, Boai Hospital of Zhongshan , Zhongshan, Guangdong, 528402, People’s Republic of China
[5
]Department of Clinical Laboratory, Humen Hospital , Dongguan, Guangdong, 523899, People’s Republic of China
[6
]Department of Clinical Laboratory, Shenzhen Maternity & Child Healthcare Hospital , Shenzhen, Guangdong, 518028, People’s Republic of China
[7
]Department of Clinical Laboratory, Huiyang Sanhe Hospital , Huizhou, Guangdong, 516211, People’s Republic of China
Author notes
Author information
Shaoling Wang
http://orcid.org/0000-0002-2469-4647
Article
Publisher ID: 293913DOI: 10.2147/RMHP.S293913
PMC ID: 7896760
PubMed ID: 33623455
SO-VID: 0b368a8e-d32d-4a89-a28a-343dba2397ef
Copyright © © 2021 Liu et al.
License:
This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License ( http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms ( https://www.dovepress.com/terms.php).
History
Date
received
: 02
December
2020
Date
accepted
: 01
February
2021
Page count
Figures: 4,
Tables: 10,
References: 51,
Pages: 9
Funding
Funded by: funding;
There is no funding to report.
Categories
Subject:
Original Research
ScienceOpen disciplines: Social policy & Welfare