Endocrine Abstracts

The risk of hypertension is 3-fold increased in women with Turner Syndrome (TS). Coarctation is a known cause of secondary hypertension but for others the aetiology of hypertension is unclear. Studies have demonstrated elevated plasma renin activity (PRA) in girls and young women with TS and hypothesized that the aetiology of hypertension is small vessel renovascular disease. To explore this possibility further blood pressure (BP) and PRA were measured routinely at the Adult TS Clinic at Christie Hospital.

42 TS patients were investigated using data from the baseline visit. Age, medication (oestrogen replacement and antihypertensives), and prevalence of cardiac and renal abnormalities were recorded. After 30 minutes of recumbency BP by manual sphygmomanometer in both arms and PRA were measured. BP data from TS patients were compared with age and sex matched data from Department of Health's Health Survey. Patients with known coarctation were excluded. Normal reference levels for PRA after lying down overnight are 1.1-2.7pmol/h/ml. Patients on ACE- or AT2-inhibitor medication were excluded.

The mean (SD) age of women attending the clinic was 29(7) years. 38/42 women were on oestrogen replacement (31 HRT, 7 OCP). 6/42 women were on antihypertensives. 24% and 33% of the patients had cardiac and renal abnormalities respectively. 3 women had coarctation. TS women were more likely to be hypertensive (>140/90) compared to the UK population (35%vs7%) (p<0.0001). Systolic BP was not significantly different from the normal population. Diastolic BP in TS patients was significantly higher than the normal population (median (range) z-score 0.89((-)0.52-(+)3.60))(p<0.001). Only 3/39 (8%) women had PRA above the normal range, mean PRA 1.21(0.77)pmol/h/ml.

Women with TS are more hypertensive than the normal population. The finding of a PRA within the normal range is contrary to previous studies. Our results may be due to the effect of age and/or the impact of oestrogen therapy on PRA. However they do not support the premise that there is an underlying renovascular aetiology for hypertension associated with TS.