Clinical Endocrinology (1998) 49, 221–228 221  1998 Blackwell Science Ltd Peripheral catecholamine alterations in adolescents with polycystic ovary syndrome Cecilia Garcia-Rudaz, Ines Armando, Gloria Levin, Marı ´a Eugenia Escobar and Marta Barontini Centro de Investigaciones Endocrinologicas (CONICET), Hospital de Nin ˜ os ‘R. Gutierrez’, Buenos Aires, Argentina (Received 26 August 1997; returned for revision 21 October 1997; finally revised 27 January 1998; accepted 28 February 1998) Summary 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 mg GnRH. Plasma con- centrations of dihydroxyphenylalanine (Dopa), nor- adrenaline (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 nor- metanephrine (NMN)) were determined by HPLC with electrochemical detection. RESULTS Basal plasma LH, testosterone, andros- tenedione, 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 mmol/d) than in controls (0·73 0·09 mmol/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 mmol/d, P < 0·05). CONCLUSIONS Our results show the same endocri- nological features in adolescent PCO patients as those reported in adults. The results also demonstrate a peripheral catecholaminergic alteration which sug- gests 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. Polycystic ovary syndrome (PCO) is one of the most common endocrine disorders affecting women. (Franks, 1989; Vaitukai- tis, 1983). The syndrome is characterized by menstrual cycle irregularities or amenorrhoea, chronic anovulation, clinical and laboratory findings of hyperandrogenism and inappropriate gonadotrophin secretion (Rebar et al., 1976). It has been suggested that these alterations are already present around the time of menarche (Yen, 1991). Although anovulatory and irregular menstrual cycles with modestly increased androgen levels are frequently observed in normal adolescent girls (Apter, 1980; Siegberg et al., 1986) the development of regular and ovulatory cycles occurs within a few years after menarche (Southam & Richart, 1966; Apter & Vihko, 1990). In spite of extensive investigation, the aetiology of PCO remains poorly understood. Altered central catecholamine metabolism leading to inappropriate gonadotrophin secretion has been suggested as a possible cause of PCO, even though contradictory data have been reported (Lobo et al., 1983). Decreased urinary homovanillic acid (HVA) and increased urinary and plasma 3-methoxy-4-hydroxyphenylglycol (MHPG) have been reported in some adult PCO patients (Paradisi et al., 1989; Yoshino et al., 1992; Shoupe & Lobo, 1984). These findings were interpreted as supporting the suggestion of both decreased dopaminergic control of LH secretion and increased noradrenergic activity in hypothalamic GnRH neurons in PCO Correspondence: Dr. Marta Barontini, Centro de Investigaciones Endocrinologicas, Hospital de Nin ˜os ‘R. Gutierrez’, Gallo 1330, 1425 Buenos Aires, Argentina. Fax: þ54 1 963 5930.