Whatisnascent PCO in adolecents 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.

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.

The issue of regression or progression of   mini-PCOS / nascent PCOS/ hyperpubertal symptoms.

Whether the pathogenesis is initiated by hyperandrogeniaemia or hyperinsulinaemia is still controversial but the clinical expressions of such changes were earlier used to be designated as nascent PCOS, hyperpubertal state or physiological mini-PCOS^13,14.  According to present author such a term or clinical note in the case sheet is appropriate as such a note will remind the treating physician to follow her up more scrupulously at a subsequent date. As stated earlier in some girls with such exaggerated physiological changes will not reverse with passage of time. (CR Rudely no 13,Nobles F, Dewailly D. Puberty and polycystic ovary syndrome: The insulin/insulin like growth factor1 hypothesis. Fertil Steril 1992; 58:655-66. which author feels is quite appropriate  12 (Venturoli S, Poreu E, Fabbri R, Magrini O, Paradrisi R, Pallotti G, Gammi I, Flamigni C. Postmenarcheal evolution of endocrine pattern and ovarian aspects in  adolescents with menstrual irregularities. Fertil Steril 1987; 48:78-85).  Fortunately in most girls clinical and hormonal parameters induced by   such temporary hyperandrogenemia and or hyperinsulinaemia will normalize with passage of time but   it is difficult to distinguish biologically and ultrasonically those adolescent at the age group 12-17 years where such normal evolutionary changes will persist and aggravate giving rise to full- fledged PCOS. The author feels the task of researchers now bestow to find out some biological markers to identify such at- risk cases who are destined to develop from mini PCOS to full-fledged PCOS ¹⁴

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

The phenotypic expression of this syndrome is heterogeneous but in most cases this syndrome commences with ordinary normal pubertal symptom like oligomenorrhea, obesity, persistent acne, hyperseborrhoea and occasionally with hirsutism. Rarely there may be only one finding like central adiposity, acanthosis nigricans, alopecia or even secondary amenorrhoea ¹⁵. The symptoms quoted above are often common accompaniment of normal adolescence and such trivial symptoms are becoming more common as nutritional status of our adolescents is improving in our country too¹⁶.Karla P,   Bansal B, Nag P, Singh JK, Gupta RK, Kumar S et al . Abdominal fat distribution and insulin resistance in Indian women with polycystic ovary syndrome. Steril 2009; 91:1437-40

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