PCOS in teenagers

 Adolescent PCO: While acknowledging all these knowledge gaps,this review will critically explore the opinions expressed by different international organizations and experts in this field so as to define which teenagers should be leveled as PCOS keeping in mind that the definition of this syndrome will evolve over time to incorporate new research findings . The author also likes to highlight that the association of this syndrome with so called ultrasonographic features of polycystic ovaries i.e. PCOM (polycystic ovarian morphology) is fading out 8, 9

Transient but exaggerated 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 t this age group,,

Supra physiological production of androgens or exaggerated response of androgen sensitive tissues in this age group. 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 group

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

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.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 hyperinsulinaemia... 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. 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 conscientiously at a subsequent date. As stated earlier in some girls with such exaggerated physiological changes will not reverse as she grows up .

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 adolescents who are destined to develop from mini PCOS to full-fledged PCOS