Blood Pressure and Hypertension in Childhood and Adolescence

Leumann, Ernst

doi:10.1007/978-3-642-67379-5_4

Cited by 16 publications

(10 citation statements)

References 291 publications

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“…Hypertension was noted to cause failure to thrive and vomiting in 29% of 45 infants reported in the literature 6 although the incidence of failure to thrive alone was not reported. In the same publication the incidence of growth retardation and weight loss in 600 older children was only 2.7%.…”

Section: Discussionmentioning

confidence: 96%

Hypertension: a cause of growth impairment

et al. 2002

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Section: Discussionmentioning

confidence: 96%

Hypertension: a cause of growth impairment

et al. 2002

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“…The overall incidence of hypertension in childhood is 1–3%1 2 and it is associated with a significant morbidity and mortality,3 4 as in adults 56 The increased blood pressure in children is often secondary to some underlying cause, in contrast with that in adults in whom it is usually primary (essential).…”

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confidence: 99%

Nitric oxide activity in childhood hypertension

Goonasekera

Shah

Rees

et al. 1997

Archives of Disease in Childhood

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Objectives-To investigate nitric oxide (NO) activity in childhood hypertension using nitrite and nitrate (NOx) concentrations in plasma as an index of nitric oxide generation. Design-Cross sectional study. Setting-Tertiary care paediatric centre and district general hospitals in the UK. Patients-Children attending the above centre for treatment of hypertension. The control subjects were normotensive healthy children attending district general hospitals for minor medical and surgical disorders. Interventions-None. Main outcome measures-Plasma (P) and urinary (U) NOx concentrations, blood pressure, and glomerular filtration rate. Results-Sixteen normal children (mean age 6.9 years), 13 children with renovascular hypertension (mean age 7.8 years), and 25 children with hypertension associated with renal parenchymal disease (mean age 10.7 years) were studied. Mean (SD) P NOx values of children with hypertension with renovascular disease (15.3 (11.4) µmol/l) and renal parenchymal disease (18.3 (11.4) µmol/l) were significantly above that of normal children (11.9 (5.9) µmol/l) after accounting for age and glomerular filtration rate influences. Higher concentrations of P NOx in normal children were associated with younger age, but not in the children with hypertension. Higher P NOx concentrations were also associated with a lower glomerular filtration rate in normal children and children with hypertension with renal parenchymal disease, but not in the children with hypertension with renovascular disease. U NOx excretion expressed as a ratio against urine creatinine (U creat ) excretion was not statistically diVerent among the study groups. Conclusions-P NOx is increased in children with hypertension even after statistical elimination of the glomerular filtration rate and age influences. This suggests a normal or increased NO synthase activity in childhood hypertension in contrast with adults with hypertension in whom it is described as reduced.

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“…Standard deviation scores of height were calculated as previously described (44). For blood pressure, the normal values of Leumann were used (45). Urinary steroids were determined by gas chromatography on a glass capillary column (37).…”

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Clinical and Biochemical Variability of Congenital Adrenal Hyperplasia Due to llβ-Hydroxylase Deficiency, A Study of 25 Patients*

Zachmann

Tassinari

Prader

1983

The Journal of Clinical Endocrinology & Metabolism

250

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Twenty five patients (10 males and 15 females) aged 0-23 yr with congenital adrenal hyperplasis due to 11 beta-hydroxylase deficiency were studied. They were divided into 13 classic (group A), and 12 mild (group B) patients. The patients of group A were diagnosed at a younger age and had more severe clinical symptoms (ambiguous genitalia in girls, pseudoprecocious puberty in boys). Two had neonatal salt wasting before treatment, and one gynecomastia. Seven had moderate to severe hypertension. Their mean 3 alpha,17,21-trihydroxy-5 beta-pregnan-20-one (THS) and 3 alpha, 21-dihydroxy-5 beta-pregnane-11,20-dione (THDOC) excretion was 14.2 +/- 4.1 and 7.2 +/- 4.2 mg/m2 . day, respectively. The patients of group B had mostly late onset of symptoms (hirsutism, amenorrhea in girls, pseudoprecocious puberty in boys, tall stature, and advanced bone age in both sexes). One boy had bilateral cryptorchidism. Four had moderate hypertension. In seven patients, THS (5.3 +/- 2.3 mg/m2 . day) and THDOC (3.9 +/- 0.5 mg/m2 . day) responded to ACTH. In five, only THS (4.3 +/- 1.1 mg/m2 . day) responded, but THDOC remained undetectable. It is concluded that the clinical and biochemical expression of 11 beta-hydroxylase deficiency is variable, that hypertension in not directly related to deoxycorticosterone, and that, regardless of the intensity of the defect, there are patients in whom the 11 beta-hydroxylation of 17 alpha-hydroxylated steroids only is impaired, and others in whom both the conversion of 17,20-dihydroxy-4-pregnene-3,20-dione and deoxycorticosterone are reduced.

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Blood Pressure and Hypertension in Childhood and Adolescence

Cited by 16 publications

References 291 publications

Hypertension: a cause of growth impairment

Hypertension: a cause of growth impairment

Nitric oxide activity in childhood hypertension

Clinical and Biochemical Variability of Congenital Adrenal Hyperplasia Due to llβ-Hydroxylase Deficiency, A Study of 25 Patients*

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