title: The influence of renal and cardiovascular abnormalities on blood pressure in Turner syndrome.
abstract: BACKGROUND
  Patients with Turner syndrome (TS) are at an increased risk of morbidity and mortality from cardiovascular disease. This study was undertaken to establish the prevalence of hypertension in patients with TS and to establish to what extent cardiovascular or renal abnormalities contribute to the measured blood pressure.
  
  
  METHODS
  62 patients with TS, age 5.4-22.4 years, had 24 h-ABPM (ambulatory blood pressure monitoring), echocardiography, renal imaging and measurement of recumbent plasma renin activity (PRA). Blood pressure was compared with population standards.
  
  
  RESULTS
  21% of the TS study population had mean systolic and 17% mean diastolic 24 h-ABPM measurements above the 95th percentile for age and sex (i.e. mild hypertension). Borderline blood pressure (i.e. 90th to 95th percentile) was found in another 17% of the patients. 57% of the patients had a blunted (i.e. less than 10%) fall in the night-time blood pressure. 24% of the patients had a detectable cardiac abnormality, 42% a detectable renal abnormality and 52% were found to have raised plasma renin activity. The presence of a cardiac or renal abnormality had no significant effect on blood pressure. Blood pressure of patients on growth and/or pubertal therapy was not different from those patients on no such treatment.
  
  
  CONCLUSIONS
  Over 30% of patients with Turner syndrome were found to be mildly hypertensive and over 50% had an abnormal diurnal blood pressure profile. In this study we were unable to demonstrate that the presence of renal or cardiac abnormalities had an effect on recorded blood pressure. The use of growth hormone and oestrogen to manage growth failure and pubertal delay did not seem to affect blood pressure. This study suggests that there is a high prevalence of raised blood pressure in Turner syndrome patients. The 24 h-ambulatory blood pressure monitoring profile suggests that this may be secondary in origin, but we were unable to demonstrate an underlying mechanism with the renal and cardiac investigations performed.
authors.affiliation: The London Centre for Paediatric Endocrinology, University College London, UK. n.nathwani@ucl.ac.uk
authors.forename: N C
authors.initials: NC
authors.lastname: Nathwani
authors.forename: R
authors.initials: R
authors.lastname: Unwin
authors.forename: C G
authors.initials: CG
authors.lastname: Brook
authors.forename: P C
authors.initials: PC
authors.lastname: Hindmarsh
mesh_terms: D000293:Adolescent; D000328:Adult; D045930:Anabolic Agents / Q000627:therapeutic use; D000704:Analysis of Variance; D018660:Blood Pressure Monitoring, Ambulatory; D002648:Child; D002675:Child, Preschool; D003430:Cross-Sectional Studies; D004359:Drug Therapy, Combination; D004997:Ethinyl Estradiol / Q000627:therapeutic use; D005260:Female; D013006:Growth Hormone / Q000627:therapeutic use; D006330:Heart Defects, Congenital / Q000150:complications* / Q000503:physiopathology; D006801:Humans; D006973:Hypertension / Q000209:etiology* / Q000503:physiopathology; D007668:Kidney / Q000002:abnormalities / Q000503:physiopathology; D010074:Oxandrolone / Q000627:therapeutic use; D015995:Prevalence; D011374:Progesterone / Q000627:therapeutic use; D012083:Renin / Q000097:blood; D014424:Turner Syndrome / Q000150:complications* / Q000503:physiopathology
chemical_list: D045930:Anabolic Agents; D004997:Ethinyl Estradiol; D011374:Progesterone; D010074:Oxandrolone; D013006:Growth Hormone; D012083:Renin