1278
adrenal enzyme defects and exaggerated adrenarche. J Clin Endocrinol Metab 1986; 62: 840-48. 4. Mawszowicz I, Melanitou E, Kirckhoffer MD, Mauvais-Jarvis P. Dihydrotestosterone stimulates 5&agr;-reductase activity in pubic skin fibroblasts. J Clin Endocrinol Metab 1983; 56: 320-25. 5. Hay JB, Hodgins MD. Distribution of androgen metabolizing enzymes in isolated tissues of human forehead and axillary skin. J Endocrinol 1978; 79: 29. 6. Barnes RB, Rosenfield RL, Burstein S, Ehrmann DA. Pituitary-ovarian responses to nafarelin testing in the polycystic ovary syndrome. N Engl J Med 1989; 320: 559-65.
**These letters have been shown
to
P, Ablan F, Lobo RA. 5&agr;-reductase activity in the genital skin of hirsute women. J Clin Endocrinol Metab 1985; 60: 349-55. 4. McKenna TJ. Pathogenesis and treatment of polycystic ovary syndrome. N Engl J 3. Serafini
Med 1988; 318: 558-62. 5.
Chang RJ, Mandel FP, Wolfsen AR, Judd HL. Circulating levels of plasma adrenocorticotrophin in polycystic ovary disease. J Clin Endocrinol Metab 1982; 54: 1265-67.
Improving communication syndrome
Dr Stewart and Professor
Edwards, whose reply follows.-ED. L.
SIR,-Dr Chayen, Dr van Seters, and their colleagues raise an important methodological principle. Studies of this sort should have a clearly defined control population for comparison and not just "established" reference ranges. This is especially important with polycystic ovary syndrome (PCOS) since 10-20% of "normal" women may have the condition.1 This may explain why our control population had androsterone/aetiocholanolone ratios lower than reference ranges. Our controls were matched for height and weight, and changes in body mass index and hence lean body for our results. It is better to compare like with like than to use a correction factor such as urinary creatinine. In reply to Professor Rosenfield we would say that we demonstrated an increase in cortisol-5;x-reductase activity in patients with PCOS, and clinical studies suggest that this enzyme also metabolises testosterone to dihydrotestosterone in androgendependent tissues.2 5
adrenal enzyme defects and exaggerated adrenarche. J Clin Endocrinol Metab 1986; 62: 840-48. 4. Mawszowicz I, Melanitou E, Kirckhoffer MD, Mauvais-Jarvis P. Dihydrotestosterone stimulates 5&agr;-reductase activity in pubic skin fibroblasts. J Clin Endocrinol Metab 1983; 56: 320-25. 5. Hay JB, Hodgins MD. Distribution of androgen metabolizing enzymes in isolated tissues of human forehead and axillary skin. J Endocrinol 1978; 79: 29. 6. Barnes RB, Rosenfield RL, Burstein S, Ehrmann DA. Pituitary-ovarian responses to nafarelin testing in the polycystic ovary syndrome. N Engl J Med 1989; 320: 559-65.
**These letters have been shown
to
P, Ablan F, Lobo RA. 5&agr;-reductase activity in the genital skin of hirsute women. J Clin Endocrinol Metab 1985; 60: 349-55. 4. McKenna TJ. Pathogenesis and treatment of polycystic ovary syndrome. N Engl J 3. Serafini
Med 1988; 318: 558-62. 5.
Chang RJ, Mandel FP, Wolfsen AR, Judd HL. Circulating levels of plasma adrenocorticotrophin in polycystic ovary disease. J Clin Endocrinol Metab 1982; 54: 1265-67.
Improving communication syndrome
Dr Stewart and Professor
Edwards, whose reply follows.-ED. L.
SIR,-Dr Chayen, Dr van Seters, and their colleagues raise an important methodological principle. Studies of this sort should have a clearly defined control population for comparison and not just "established" reference ranges. This is especially important with polycystic ovary syndrome (PCOS) since 10-20% of "normal" women may have the condition.1 This may explain why our control population had androsterone/aetiocholanolone ratios lower than reference ranges. Our controls were matched for height and weight, and changes in body mass index and hence lean body for our results. It is better to compare like with like than to use a correction factor such as urinary creatinine. In reply to Professor Rosenfield we would say that we demonstrated an increase in cortisol-5;x-reductase activity in patients with PCOS, and clinical studies suggest that this enzyme also metabolises testosterone to dihydrotestosterone in androgendependent tissues.2 5
