Endocrine causes of pediatric hypertension are relatively rare but important because of their distinct treatment options. Adrenal diseases accompanied by an excess of mineralocorticoids, glucocorticoids, and catecholamines are major causes of endocrine hypertension. Typical causes of mineralocorticoid-related hypertension include primary aldosteronism, congenital adrenal hyperplasia (11β- and 17α-hydroxylase deficiencies), and apparent mineralocorticoid excess. Cushing syndrome and pheochromocytoma/paraganglioma are the primary causes of glucocorticoid- and catecholamine-related hypertension, respectively. This review provides an overview of the diagnostic evaluations, including hormonal assays and imaging studies, used to identify the underlying causes of pediatric endocrine hypertension, focusing on adrenal disorders. It presents details regarding the major adrenal disorders and recommended therapeutic approaches, emphasizing the importance of early detection and disease-specific management to prevent cardiovascular and metabolic complications in affected children.
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: This study aimed to characteristic the systolic blood pressure (SBP), diastolic pressure, pulse pressure, glucose, creatine, and lipid profile. This study also aimed to investigate the prevalence of hypertension and the relationship between hypertension and the lipid profile in Uzbekistan.
The subjects consisted of 58 Uzbekistan subjects recruited from Ewha Medical Care patients. Blood samples were collected from the patients for the lipid profile and random glucose and creatinine levels. Paired t tests were used for the group means and a chi-square or Fisher’s exact test for categorical variables. A multiple logistic regression analysis was performed.
Among the 58 patients constituting the baseline population, hypertension developed in 42 patients. Among them, the triglyceride (TG) level was significantly higher in the hypertension group than normal group (173.19 vs. 127.06 mg/dL, P=0.014). The SBP had a positive correlation with the TG (r=0.979, P<0.01) and creatinine (r=0.002, P<0.05) levels and also, the pulse pressure had a positive correlation with the cholesterol level (r=0.539, P<0.05). A multivariate analysis (adjusted for age and sex) indicated that there was a positive correlation between the SBP and TG level (r=0.941, P<0.05).
There was a positive correlation between the SBP and TG level in the Uzbekistan population according to this study.
Elevated pulmonary pressure and right ventricular (RV) dysfunction are the hallmarks of pulmonary vascular disease in animal models and human patients with pulmonary arterial hypertension (PAH). Monocrotaline models of PAH are widely used to study the pathophysiology of PAH. The purpose of this study was to evaluate the severity of PAH rat model by tissue Doppler imaging (TDI).
PAH was induced in Sprague-Dawley rats by monocrotaline (M) group. The peak systolic (s'), early diastolic (e'), and late diastolic myocardial velocities (a') were measured using TDI at basal segments. Tricuspid annular plane systolic excursion (TAPSE) was measured in the 4-chamber view. Velocity of a tricuspid regurgitation (TR) jet was measured to estimate the pulmonary artery pressure to assess the severity of PAH.
Decrease in the RV shortening fraction and ejection fraction were observed in the M group compared with the control (C) group. RV e' velocity and s' velocity were significantly lower in the M group compared with the C group. The TAPSE was significantly lower in the M group compared with the C group (1.26±0.22 mm vs. 2.83±0.34 mm). The TR velocity was significantly higher in the M group compared with the C group (4.48±0.34 m/sec vs. 1.23±0.02 m/sec).
TAPSE is an easily obtainable, widely recognized and clinically useful echocardiographic parameter of global RV function in the PAH rat model. We recommend that TDI would be a helpful diagnostic tool to evaluate the RV function in PAH rat model.
Simvastatin has been reported to attenuate the development of pulmonary hypertension through increased apoptosis as well as reduced proliferation of smooth muscle cells in obstructive vascular lesions. Microarray experiment can accomplish many genetic tests in parallel. The purpose of this study is to evaluate altered expressions of gene in rat hearts with monocrotaline (MCT)-induced pulmonary arterial hypertension after simvastatin treatment.
Six-week-old male rats were grouped as follows: control group (C group, saline injection), M group (MCT 60 mg/kg), and S group (MCT 60 mg/kg plus 10 mg/kg/day simvastatin by gavage during 28 days). Body weight, right ventricular pressure and right ventricular/left ventricle+septum ratio in each group were measured. The rats were sacrificed after 28 days. Total RNA was extracted from the rat heart tissue and microarray analysis was performed.
Administration of simvastatin significantly inhibited the progression of right ventricular hypertrophy at day 28 in the S group than in the M group. Compared with the C group, MCT was associated with a significant difference in expression of genes related to biosynthesis and with the regulation of heart contraction rate. Simvastatin treatment resulted in a significantly changed expression of genes about the regulation of progression through cell cycle and system development compared to the M group. The expressions of nitric oxide synthase and brain natriuretic peptide were significantly decreased after simvastatin treatment.
Administration of simvastatin exerted inhibitory effects on right ventricular hypertrophy during the development of MCT-induced pulmonary arterial hypertension in rats. Simvastatin changes the expression of genes associated with various functions.
This study was conducted to determine the prevalence of hypertension in adolescents and to find the relationship between an increase of body mass index and waist circumference (WC) and blood pressure (BP).
Four hundred twenty-nine adolescents between the ages of 15 and 18 at high school in Seoul were enrolled and their anthropometric data and body composition were measured. BP was measured by oscillometric devices at least twice. Hypertension was defined according to the normative BP reference for Korean children and adolescents.
The prevalence of prehypertension and hypertension was 14.0%, 9.2% in boys and 9.0%, 10.2% in girls. The prevalence of prehypertension and hypertension was 9.0%, 6.0% in the normal body mass index group, 14.6 %, 16.7% in the overweight group, 21.7%, 29.8% in the obese group. The prevalence of systolic hypertension was 3.6% in the normal group, 12.5% in the overweight group and 29.8% in the obese group. However, the prevalence of diastolic hypertension had significant differences between the groups, which were 3.3% in the normal group, 6.3% in the overweight group and 4.3% in the obese group. According to WC, the prevalence of hypertension was 6.2% in the below 75th percentile WC group, 22.2% in the75th to 90th percentile WC group and 25.6% in ≥90th percentile WC group. The risk of hypertension was 5.55 times higher in the obese group and 2.04 times higher in the overweight group, 3.93 times higher in ≥90th percentile of WC group.
The risk of hypertension is markedly increased with obesity in high school students.
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A 35-year-old man presented with progressive dyspnea and hemoptysis. His blood pressure was 230/140 mmHg and serum creatinine level was 20.13 mg/dL. Chest radiography and computed tomography revealed pulmonary hemorrhage. His renal function was low, thus emergent renal replacement therapy was required. Malignant hypertension and acute kidney injury were diagnosed, and antihypertensive therapy and hemodialysis started immediately. Renal biopsy was performed to examine the underlying disease. Typical pathological changes of malignant hypertension, fibrinoid necrosis of the afferent arterioles, and proliferative endoarteritis at the interlobular arteries were observed. His renal function improved gradually and pulmonary hemorrhage completely disappeared with administration of antihypertensive agents. Here, we report this rare case of malignant hypertension with pulmonary alveolar hemorrhage and speculate that the hemorrhage may be related to vascular injuries at the alveolar capillary level caused by malignant hypertension.
Spontaneously hypertensive rats (SHR) are frequently used as rat models of essential hypertension. The mechanism for the development of hypertension is complicated and it is unknown. The renin-angiotensin system (RAS) plays a key role in the control of blood pressure. Microarrays are a powerful tool for studying genetics. The purpose of this study was to investigate changes of gene expression in the heart tissues of SHR after losartan treatment to provide basic data that is useful in the early diagnosis of hypertension and gene treatment.
Rats were divided into three groups: the control (C) group; the hypertension (H) group (SHR), and the losartan (L) group; treated with losartan (10 mg/kg/day) in SHR. Rats were sacrificed at week 5 and microarray analysis was performed.
102 gene expressions including the genes associated with cell proliferation such as
According to microarray analysis, there was significant gene expression change in SHR compared with normal rats as well as significant gene expression changes after losartan treatment in SHR.
The Measurement of blood pressure by a doctor may trigger a pressor response, so there are marked differences between office and ambulatory or self-measured blood pressure and the subjects may misdiagnosed as hypertensives and receive unneccesary medication. The study is designed to evaluate the charicteristic of white coat hypertension, the degree of white coat effect and the relationship between the white coat hypertension and persistent hypertension.
Thirteen patients with office hypertension receiving no medication, were recruited from 434 patients experienced in ambulatory blood pressure. Past history, physical examination, office blood pressure, 12-channel standard electrocardiography, chest X-ray, plasma lipid battery, echocardiography and 24-hr ambulatory blood pressure monitoring with BP3 MEDIANA were performed.
1) White coat hypertensive patients were 13 of 434 patients(2.99%) who were performed 24-hr ambulatory blood pressure monitoring. The mean age was 45±12 years with 6 men and 7 women and rage of age was 26-65 years.
2) The lipid battery, chest X-ray and 12-channel standard electrocardiographty showed no significant finding.
3) The LV mass index was 90.7±11.0g/m3 but one of 8 who performed echocardiography showed concentric hypertrophty.
4) The LV ejection traction was 60.8±8.7% which normal range.
5) The mitral flow velocity parameters were E velocity 0.71±0.14m/sec, A velocity 0.54±0.24m/sec, E/A ratio 1.6±0.8, mitral valve deceleration time 214±27.6msec and isovolumic relaxation time 104±11.4msec but one of 8 showed LV relaxation abnormality.
6) The mean office systolic blood pressure was 159±13.8mmHg, mean office diastolic blood pressure 101±9.0mmHg, 24-hr mean ambulatory systolic blood pressure 128±4.9mmHg and 24-hr diastolic bliid pressure 82±8.6mmHg.
7) The night day ratio of systolic blood pressure was 0.93±0.06 and the night day ratio of diastolic blood pressure was 0.92±0.06 suggestive of blunted diurnal variation. The Dipper were 5 of 13 patients(38.5%) and the non-Dipper were 8 of 13 patients(61.5%).
8) Two of 13 white coat hypertensives were diagnosed as persistent hypertensives in follow-up periods and antihypertensive drug had been initiated.
White coat hypertension can be diagnosed by 24-hr ambulatory blood pressure monitoring. The influence of white coat effect to cardiovascular system was not established. Sixty-two percent of white coat hypertensives showed blunted diurnal variation in 24-hr ambulatory blood pressure monitoring and two of 13 were diagnosed as persistent hypertensives in our F/U study, so white coat effect cannot be merely innocent and need strict evaluation and regular follow-up.
Aortic dissection is caused by a circumferential or transverse tear of the intima by a discrepancy between the strength of the aortic wall and the intraluminal pressure.
Arterial hypertension seems clearly to be a factor in the genesis of aortic dissection.
An elevated blood pressure or evidence of its existence can be found in 70-80 percent of patients. Other factors predisposing to aortic dissection are congenital disorder of connective tissue, vasculitis, etc. But trauma or physical strain is unusual cause of classic dissection.
Diagnosis is confirmed by computed tomography, aortography or echocardiography.
A 62-year-old man without a history of hypertension, emphysema or congestive heart failure visited our hospital because of hoarseness which developed suddenly during the physical strain. A contrast material-enhanced computed tomographic (CT) scan was performed at an other hospital due to hoarseness, mild fever and general weakness. Then he visited to our ENT department and performed laryngeal CT due to hoarseness. The CT shows somewhat mass-like soft tissue, so he was transferred to our internal medical department.
The chest CT scan and simple chest PA was done and we found a dissecting aneurysm.
This case developed by Physical strain and diagnosed by hoarseness is unusual and rare.
Pulmonary tumor thrombotic microangiopathy (PTTM) is an uncommon and fatal malignancy-related pulmonary complication characterized by fibrocellular intimal proliferation of small pulmonary arteries and arterioles. It causes marked pulmonary hypertension, right-side heart failure, and sudden death. Diagnosis of PTTM is extremely difficult while the patient is alive. Here, we report a 44-year-old woman who presented with complaining of progressing dyspnea and pulmonary hypertension but with no history of cancer. She was diagnosed with PTTM caused by advanced gastric cancer
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To compare the clnical data of general and regional anesthesia for cesarean section in patients with systemic hypertension.
We conducted a retrospective survey with the medical records of the patients with hypertensive disorders in pregnancy, who under went cesarean section from January 1998 to December 2012. We collected data including patients' demographics, anesthesia and maternal and neonatal outcome. According to anesthetic method, the subjects were divided into general anesthesia and regional anesthesia group and the clinical outcome were compared. We reclassified the patients according to the use of magnesium sul fate (MgSO4) and compared the clinical outcomes.
Of the 1,050 hypertensive parturients, 848 (80.8%) patients went through cesarean section. Three hundred and sixty three patients (42.8%) underwent epidural anesthesia, general and spinal anesthesia were used in 268 (31.6%), and 217 (25.6%) patients, respectively. There was no significant difference in maternal and neonatal outcome according to anesthetic method. In the patients administered MgSO4, 1 minute Apgar score was lower and maternal gestational age and birth weight were less than the patients not receiving MgSO4.
Anesthetic methods did not have effect on outcome of cesarean section of the patients with hypertensive disorder of pregnancy.
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There are 3 subtypes of natriuretic peptide (NP) receptors: type A natriuretic peptide receptor (NPRA), NPRB, and NPRC. The NPRA gene polymorphism, consisting of substition of methionine (ATG) to isoleucine (ATC) at nucleotide 1023 (M341I) of exon 3 was revealed to be associated with increased risk for essential hypertension (EH) in Japanese people. The purpose of this study is to investigate association between EH and the M341I polymorphism in the NPRA gene in Korea.
Eighty patients in whom type B natriuretic peptide (BNP) was measured were enrolled in this study. 66 patients had EH and 14 patients did not. The polymorphism of M341I was evaluated by multiplex genotyping polymerase chain reaction and by sequencing analysis.
The overall distribution of alleles was not significantly different between the control and EH groups. However, the C/C homozygous genotype was found only in the EH group. In the EH group, patient carrying the C/C homozygous genotype had the trend of having higher systolic and diastolic BP levels regardless of the previous treatment, even though other laboratory markers including BNP levels had no significant differences according to the genotypes.
This would be meaningful for the first identification of the M341I polymorphism in the NPRA gene and for the first suggestion of association of the EH with it in Korea.
Although angiotensin converting enzyme inhibitors have provided plausible effect for the management of hypertension and congestive heart failure, it does have drawbacks such as dry cough in as much as 15 to 30% of patients and incomplete blocking of angiotensin II production. Losartan(Cozaar®) is the first angiotensin II receptor antagonist that has become clinically available as an antihypertensive agent. Because the agent effectively blocks the final common pathway of renin-angiotensin system, it is recognized as an ideal drug for the treatment of hypertension.
We tested the antihypertensive effect and clinical safety of Losartan(Cozaar®) 50mg/day in 22 patients(male : 12, female : 10, age : 51±11, range : 33-70) with stage I and II hypertension from July 1998 to October 1999. The patients were enrolled in the study after two weeks of washout period if the patient was using other antihypertensive drugs. Blood pressure and side effects were monitored at zero, second, sixth, and twelfth week. Baseline chemistry was done before drug administration and follow-up chemistry was done at twelfth week.
Losartan(Cozaar®) showed good patient compliance and good antihypertensive effect without significant changes of laboratory results or clinical complications. At twelfth week, mean systolic blood pressure dropped l9mmHg, and mean diastolic blood pressure dropped 11mmHg. The heart rate showed no significant change during the study period. Blood pressure was controlled below 140/90mmHg in 12(54.5%) patients with Losartan 50mg/day. Five patients complained of minor side effects(dizziness, facial numbness, epigastric discomfort, etc) but no patients discontinued medication due to side effects.
Losartan(Cozaar®) is a safe and effective antihypertensive agent for the treatment of stage I and II hypertensive patients as a single once-a-day treatment.
Most pulmonary thromboemboli arise from the deep vein thrombosis, which have complete clinical and at least near complete roentgenographic and angiographic resolution within four to six week of the acute event.
But chronic pulmonary hypertension and cor pulmonale from unresolved pulmonary embolism complicate acute embolic episode with a frequency of less than 1 percent. Rarely pulmonary thromboemboli can result from right atrial thrombi.
We experienced a case of chronic thromoboembolic pulmonary hypertension, which wrose from right atrial thrombi in the patient with rheumatic valvaular heart disease and thoracic aorta atherosclerotics stenosis.