Monday, 20 January 2020

A B C of Precocious Puberty


What does “isolated Premature Thelarche” means?
,To all of us it(PT)  appears to mostly a benign, self-limiting condition which is characterized by breast development with no other signs of sexual maturation. As understandable, there will be no pubic or axillary hair development, girls behavior at home and at school is normal, growth is normal and the skeletal age is appropriate. But the  breast development has atypical appearance with relatively immature nipple development and is never more than Tanner Breast Stage III. Breast development is usually asymmetrical.

The condition tends to resolve after about 1–2 years and then the onset of normal puberty(adrenarche, Menarche, increments f Ht & other growth spurt  )occurs at the appropriate age and in the normal way. Very occasionally, vaginal bleeding can occur. There have been some reports of women who have had premature thelarche as a child developing large follicular cysts during their menstrual cycles and, thereby, having reduced fertility. However, this has not been substantiated and what limited follow-up has been achieved in further series suggests that there are no long-term sequelae.

Etiology ? Isolated premature thelarche is a relatively common condition and mothers come to doctors more will be recorded prevalence!!  It is characterised by FSH dominance and overnight gonadotrophin secretion, which is characterised by single FSH pulses.
There may well be two types of premature thelarche. The classical type commences during the first year of life and tends to resolve by the age of 2.
There is a second form of premature thelarche, of which the age of onset is over 2 years of age and this tends to be more persistent and with a higher incidence of uterine bleeding. In this ‘non-classical’ form of premature thelarche, it may well be associated with progression to gonadotrophin-dependent precocious puberty. Isolated premature thelarche is a condition which is easy to diagnose clinically and requires no treatment.
Precocious Puberty (Complete, Partial)
Girls suspected of having central precocious puberty, are otherwise healthy children whose pubertal maturation begins at the early end of the normal distribution curve.

 CNS imaging studies of these otherwise healthy 6-year-old to 8-year-old girls usually reveal no structural abnormalities. A study of 200 girls in France identified abnormal brain imaging findings in 2% of girls whose onset of puberty was between age 6-8 years and in 20% of girls whose onset of puberty was before age 6 years.
[1] A smaller study from the United Kingdom reported abnormal findings in 15% of 67 girls.[2] Abnormal CT scan or MRI findings are more frequent among boys with central precocious puberty than among girls with central precocious puberty.
The onset of puberty is caused by the secretion of high-amplitude pulses of gonadotropin-releasing hormone (GnRH) by the hypothalamus. The hypothesize HPG axis, which is highly sensitive to feedback inhibition by small amounts of sex steroids, and (2) central neural pathways that suppress the release of GnRH pulses.
Admittedly, I am more theoretician: Very very associate or should I say  etiology of PT:- CNS abnormalities associated with precocious puberty include the following:
·         Tumors (eg, astrocytomas, gliomas, germ cell tumors secreting human chorionic gonadotropin [HCG])
·         Hypothalamic hamartomas
·         Acquired CNS injury caused by inflammation, surgery, trauma, radiation therapy, or abscess
·         Congenital anomalies (eg, hydrocephalus, arachnoid cysts, suprasellar cysts)
High-amplitude pulses of GnRH cause pulsatile increases in the pituitary gonadotropin-luteinizing hormone (LH) and follicle-stimulating hormone (FSH). Increased LH levels stimulate production of sex steroids by testicular Leydig cells or ovarian granulosa cells. Pubertal levels of androgens or estrogens cause the physical changes of puberty, including d mechanisms that suppress onset of puberty include (1) the gonadotropin-releasing hormone (GnRH) by the hypothalamus. The hypothesize HPG axis, which is highly sensitive to feedback inhibition by small amounts of sex steroids, and (2) central neural pathways that suppress the release of GnRH pulses. On ultrasound the ovaries are small, but often contain large follicular cysts, which increase and decrease in synchrony with the breast development.
CNS abnormalities associated with precocious puberty include the following:
·         Tumors (eg, astrocytomas, gliomas, germ cell tumors secreting human chorionic gonadotropin [HCG])
·         Hypothalamic hamartomas
·         Acquired CNS injury caused by inflammation, surgery, trauma, radiation therapy, or abscess
·         Congenital anomalies (eg, hydrocephalus, arachnoid cysts, suprasellar cysts)
High-amplitude pulses of GnRH cause pulsatile increases in the pituitary gonadotropin-luteinizing hormone (LH) and follicle-stimulating hormone (FSH). Increased LH levels stimulate production of sex steroids by testicular Leydig cells or ovarian granulosa cells. Pubertal levels of androgens or estrogens cause the physical changes of puberty, including d mechanisms that suppress onset of puberty include (1) the



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