Evidence for altered catecholamine metabolism in polycystic ovary syndrome.

It has been hypothesized by Yen et al. that there is decreased dopaminergic control of luteinizing hormone secretion in polycystic ovary syndrome. Levels of urinary homovanillic acid, dihydroxyphenyl acetic acid, and 3-methoxy-4-hydroxyphenylglycol were measured in seven women with polycystic ovary syndrome and in six matched control subjects to reflect, in part, central dopamine and norepinephrine metabolism. In addition, gonadotropin-releasing hormone stimulation tests were carried out in women with polycystic ovary syndrome and in control subjects. In patients with polycystic ovary syndrome, serum gonadotropin levels were determined before and after gonadotropin-releasing hormone stimulation, before and after treatment with 500 mg of L-dopa for 1 week, and again before and after treatment with 400 mg of L-dopa and 100 mg of carbidopa for 1 week the following month. Urinary homovanillic acid and dihydroxyphenyl acetic acid levels were significantly lower and the level of 3-methoxy-4-hydroxyphenylglycol was significantly higher in patients with polycystic ovary syndrome (p less than 0.05). There was a significant negative correlation between levels of homovanillic acid and serum luteinizing hormone (r = -0.57, p less than 0.05) and a positive correlation between the ratio of 3-methoxy-4-hydroxyphenylglycol/homovanillic acid and luteinizing hormone (r = 0.75, p less than 0.01). After gonadotropin-releasing hormone stimulation, delta max serum luteinizing hormone was elevated in patients with polycystic ovary syndrome but decreased to control levels after treatment with L-dopa. No changes occurred in baseline levels of serum luteinizing hormone or follicle-stimulating hormone. After treatment with L-dopa-carbidopa, baseline levels of luteinizing hormone and follicle-stimulating hormone were unchanged as were responses after gonadotropin-releasing hormone stimulation. These data suggest that there may be altered catecholamine metabolism in polycystic ovary syndrome. Viewed together with previous findings by Yen et al., our data support the hypothesis that there is decreased dopaminergic control of luteinizing hormone in polycystic ovary syndrome.