What is the clinical manifestation associated with the low levels of FSH and LH in peripheral precocious puberty?

In peripheral precocious puberty, the low levels of FSH (follicle-stimulating hormone) and LH (luteinizing hormone) indicate that the precocious development of secondary sexual characteristics is not due to central activation of the hypothalamic-pituitary-gonadal (HPG) axis. Instead, it is caused by the excess production of sex hormones—estrogen or testosterone—from sources outside of the normal regulatory feedback loop, such as tumors or adrenal dysregulation.

These excess sex hormones can lead to signs such as breast development in girls or testicular enlargement in boys, even though there is a deficiency in the stimulation normally provided by FSH and LH. Therefore, in this context, the clinical manifestation directly linked to the low levels of these gonadotropins is the excessive accumulation of sex hormones, which prompts the early appearance of secondary sexual characteristics.

The other options do not accurately reflect the physiological changes in peripheral precocious puberty. Immature gonads, increased growth velocity, and delayed bone age typically relate to conditions influenced by high levels of FSH and LH, as seen in central precocious puberty or other forms of endocrine disorders. In peripheral precocious puberty, however, the situation is characterized by inappropriate hormonal excess despite