What are the reasons for medical attention? What are, then the common symptoms of adolescent PCOS?

Transient but exaggagerated functional hyperandrogenism of adolescence.  The issue of ‘physiological hyperandrogenism’ and/ or ‘physiological hyperinsulinaemia’ of puberty in the causation of so called mini-PCOS or nascent PCOS.

Scientists now believe that most, but not all healthy adolescents reveal demonstrable hyperandrogeniaemia and or features of hyperandrogenism which is quite physiological and transitory in nature at this age group, ^{6, 10},   Cortet-Rudelli C, Dewailly D. Hyperandrogenism in adolescent girls. In Sultan C(ed) Paediatric and Adolescent Gynaecology, Evidence-Based Clinical Practice. Endocrine Dev. Basel, Karger, 2004, vol 7, pp148-62.

 Supraphysiological production of androgens or exaggerated response of androgen sensitive tissues is now proposed as the core defect of PCOS and augmented androgen levels is primarily produced in ovaries due to altered  sensitivity of ovaries to amplified LH secretion as observed in this age group5( Roe, AH, Dokras A-The Diagnosis of polycystic Ovary Syndrome in Adolescents.5^. The dynamics of acquisition of maturity of hypothalamo-pituitary axis and quantum of response of ovaries to amplified LH pulse frequency show an incongruity in different girls leading to overproduction of androgens in some girls. This action of LH may be potentiated by associated hyperinsulinaemia and diminution of insulin like growth factor binding protein -1(IGFBP-1) in few cases ^10,11 Ibanez L, Potau N, Carrascosa A: Possible genesis of polycystic ovary syndrome in periadolescent girl. Curr. Opin Endocrinol Diab. 1998, 5:19-25.

 Azziz R, Carmina E, Dewailly D, Diamanti-Kandarakis E, Escobar-Morreale HF, Futterweit W, Janssen OE, Legro RS, Norman RJ, Taylor AE, et al. Position statement: criteria for defining polycystic ovary syndrome as a predominantly hyperandrogenic syndrome: an Androgen Excess Society guideline. J Clin Endocrinol Metab 2006; 91:4237-4245.) Azziz R, Carmina E, Diamanti-Kandarakis E, Escobar-Morreale HF, Futterweit W, Janssen OE, Legro RS, Norman RJ, Taylor AE, Witchel SF-Criteria for defining Polycystic ovary Syndrome as a predominantly Hyperandrogenic Syndrome: An Androgen Excess Society Guideline” J Clinical Endocrinol Metab 2006;91:4237-4245.)

Researchers have also noticed that are is a subset of otherwise normal adolescents who  demonstrate physiological hyperinsulinaemia  initially unaccompanied by hyperandrogeniaemia  and such changes are believed to be due to altered growth hormone/ IGF1 axis, whose hyperactivity induces a selective insulin resistance Hannon TS, Jannosky J, Arslanian SA. Longitudinal study of physiologic insulin resistance and metabolic changes of puberty. Paediatr res .2006; 60:759-63-ref CR Dokras 10     Primary supraphysiological hyperinsulinaemia in turn is responsible for the increase in insulin plasma level and decrease in SHBG and IGFBP-1 hepatic production. Afterwards hyperinsulinaemia lead to hyperandrogeniaemia. It is also believed that ethnic differences play a major role in the clinical expression of features of hyperinsulinaemia¹².