Searchable abstracts of presentations at key conferences in endocrinology
Endocrine Abstracts (2008) 17 P20

BSPED2008 Poster Presentations (1) (56 abstracts)

Clinical and biochemical features of exaggerated adrenarche in a Scottish cohort: what investigations are justified?

WF Paterson 1 , SF Ahmed 1 , L Bath 2 , MDC Donaldson 1 , SA Greene 3 , I Hunter 4 , CJH Kelnar 2 , A Mayo 5 , JS Schulga 6 , PJ Smail 5 & AM Wallace 7


1Royal Hospital for Sick Children, Glasgow, Scotland, UK; 2Royal Hospital for Sick Children, Edinburgh, Scotland, UK; 3Ninewells Hospital and Medical School, Dundee, Scotland, UK; 4Wishaw General Hospital, Lanarkshire, Scotland, UK; 5Royal Aberdeen Children’s Hospital, Aberdeen, Scotland, UK; 6Stirling Royal Infirmary, Stirling, Scotland, UK; 7Glasgow Royal Infirmary, Glasgow, Scotland, UK.

Exaggerated adrenarche (EA) has been linked with low birth weight (LBW) and future development of hyperinsulinaemia and ovarian hyperandrogenism. The Scottish Paediatric Endocrine Group conducted a 3-year prospective study (2004–07) to examine the auxology, insulin status and steroid biochemistry of patients with a clinical diagnosis of EA. Fifty-one patients (43F:8M) were recruited. A 10 ml blood sample (fasted) was taken for biochemical analysis. Pubertal status was assessed and girls underwent pelvic ultrasound examination. The clinical diagnosis of EA was supported in all but one girl who was found to have non-classical congenital adrenal hyperplasia (NC-CAH). Mean (S.D.) age (year) at presentation in the 50 EA patients was 7.7 (0.99) for girls versus 8.8 (0.67) for boys. BW was close to the population mean (F −0.05 S.D.; M −0.53 S.D.). Both sexes were above average in height (HtSDS 1.13 F; 1.69 M), tall relative to their parents and overweight (WtSDS 1.69 F; 1.88 M). Uterine and ovarian development was pre-pubertal with no evidence of multicystic or polycystic ovaries. Biochemistry data are shown below (presented as median (range)).

GirlsNRef. rangeBoysNRef. range
Insulin (mU/l)9.0 (1.9–62)38<13.015.0 (6.2–25)8<13.0
SHBG (nmol/l)48.0 (11–124)3944–14269.0 (34–124)745–147
A’dione (nmol/l) 3.1 (1.4–7.3)36 (5 ur)<2.03.8 (2.8–4.3)7 (1 ur)<2.0
DHAS (μmol/l)2.1 (0.8–4.4)39 (2 ur)<2.004.1 (2.2–8.7)8<2.00
Testosterone (nmol/l)0.75 (0.4–1.7)28 (6 ur)<0.81.0 (0.4–2.4)5 (1 ur)<0.7
17-OHP (nmol/l)2.0 (1–8)40<132.0 (1–3)8<13
ur, unrecordable. DHAS and androstenedione were only modestly elevated, 17-OHP normal. Insulin was in the upper range of normal in girls and slightly raised in boys, with concomitant low normal SHBG in both. The girl with NC-CAH was similar to the EA girls in age (8.3 years) and height (HtSDS 1.27). Her biochemistry showed DHAS 1.8 μmol/l, A’dione 5.9, testosterone 0.6 and 17-OHP 13 nmol/l. We have found no evidence of LBW in our cohort, mild elevation of adrenal androgens and insulin/SHBG levels that reflect the weight status of the subjects. A single blood sample for DHAS, A’dione, 17-OHP and SHBG should distinguish EA from NC-CAH and androgen-secreting tumours.

Volume 17

36th meeting of the British Society for Paediatric Endocrinology and Diabetes

British Society for Paediatric Endocrinology and Diabetes 

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