Peripheral catecholamine alterations in adolescents with polycystic ovary syndrome

Document Type

Journal Article

Publication Date

8-24-1998

Journal

Clinical Endocrinology

Volume

49

Issue

2

DOI

10.1046/j.1365-2265.1998.00511.x

Abstract

OBJECTIVE: Polycystic ovary syndrome (PCO) is one of the most common endocrine disorders affecting women. Several lines of evidence have suggested the involvement of the sympathetic nervous system (SNS) in this condition. The present work was designed to assess neurochemically SNS activity in patients during the early stages of PCO. DESIGN AND PATIENTS: Fourteen patients with PCO (aged 14 to 21 years) were studied on a random day and 9 normal regularly cycling adolescents (aged 14 to 20 years) were studied during the early follicular phase (days 2 to 5). MEASUREMENTS: Hormonal profile was determined in basal conditions. LH and FSH were also measured after iv administration of 100 μg GnRH. Plasma concentrations of dihydroxyphenylalanine (Dopa), noradrenaline (NA), adrenaline (A), total dopamine (DA) and dihydroxyphenylglycol (DHPG) were determined in basal conditions and in response to GnRH by HPLC with electrochemical detection or a radioenzymatic method. Basal urinary Dopa, catecholamines and catechol metabolites (DHPG, vanillylmandelic acid (VMA), 3-methoxy-4- hydroxyphenylglycol (MHPG), homovanillic acid (HVA), metanephrine (MN) and normetanephrine (NMN)) were determined by HPLC with electrochemical detection. RESULTS: Basal plasma LH, testosterone, androstenedione, oestrone and LH/FSH ratio were higher (P<0.01) and serum sex hormone-binding globulin (SHBG) were lower (P<0.01) in PCO patients than in control subjects. Basal and GnRH-stimulated plasma free Dopa, A, NA and total DA were similar in patients and controls. Plasma DHPG was lower (P<0.01) in PCO patients (4.20 ± 0.30 nmol/l) than in controls (8.0 ± 1.0 nmol/l) throughout the study. Urinary A, NA, DA, Dopa, MN, MHPG, HVA, and VMA were similar in patients and controls. Urinary DHPG was lower (P<0.01) in PCO patients (0.50 ± 0.02 μmol/d) than in controls (0.73 ± 0.09 μmol/d). On the other hand PCO patients had a higher urinary excretion of NMN than controls (PCO: 1.20 ± 0.10; C: 0.78 ± 0.10 μmol/d, P < 0.05). CONCLUSIONS: Our results show the same endocrinological features in adolescent PCO patients as those reported in adults. The results also demonstrate a peripheral catecholaminergic alteration which suggests an alteration in noradrenaline deamination and/or uptake in adolescent patients. This study however does not permit us to conclude that PCO is primarily caused by this sympathetic alteration.

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