Treatment of true precocious puberty

Because people's living standards are much higher now than before, and most of them are only children, so they try their best to satisfy their children no matter what they want. However, this is not good for their children at all, because some of the fried foods they eat may cause precocious puberty. So what is the best way to treat this situation?

1. Medroxyprogesterone acetate: directly inhibits the hypothalamic GnRH pulse generator and pituitary gonadotropin, reducing the synthesis and secretion of sex hormones, thus treating precocious puberty. Medroxyprogesterone acetate also has glucocorticoid-like effects, inhibiting the normal secretion of ACTH and cortisol, increasing food intake and weight, causing hypertension and Cushing's syndrome facies. The dosage is 5~10 mg, orally twice a day.

2. Cyproterone acetate: It has anti-androgenic and gonadotropin-inhibiting effects, and also inhibits the secretion of ACTH and cortisol. The daily dose is 70-100 mg/m2 body surface area, taken orally in 2 divided doses. Adverse reactions include fatigue, depression, thrombosis and anemia.

3. GnRH agonist: GnRH agonist is an artificially synthesized analogue of natural GnRH decapeptide, and its biological efficacy is 20 to 150 times stronger than that of natural GnRH decapeptide. It binds to the GnRH receptors of the anterior pituitary gonadotropins, causing receptor down-regulation and dissociation of the intracellular signaling system. Therefore, after a short-term excitatory effect, it turns into a long-lasting inhibitory effect, inhibiting the pulsatile secretion of LH and FSH, sex hormone synthesis and secretion, and follicle maturation or spermatogenesis. The inhibitory effect disappears after discontinuation of the drug. It is the first choice drug for the treatment of idiopathic true precocious puberty.

Commonly used preparations include leuprorelin and tryptorelin. The structure of leuprorelin is D-Leu-Pro ethylamide, and its physiological strength is 20 times that of natural Gn-RH decapeptide. The dose of its sustained-release agent is 140~300/μg/kg, and it is injected intramuscularly once a month. The structure of triptorelin is D-Trp-GnRH, and its potency is 35 times that of the natural type. The sustained-release dosage is 60 μg/kg, and it is injected intramuscularly once a month.

1. CNS tumors: Hamartomas in the hypothalamus contain ectopic secretory neurons that can ectopically secrete GnRH in a pulsatile manner, causing precocious puberty. There may also be symptoms such as giggles, grand mal or petit mal seizures, mental retardation and abnormal behavior. Gliomas, astrocytomas, and ependymomas in the hypothalamic region can also cause precocious puberty, possibly due to interference with the normal inhibitory effect on the GnRH pulse generator. These tumors often cause headaches, nausea, vomiting, vision loss, visual field defects, diabetes insipidus, and hydrocephalus. CNS tumors are easily found on MRI scans. 2. Other CNS lesions: Other CNS lesions or abnormalities that can cause precocious puberty include encephalitis, brain abscess, sarcoidosis or tuberculous granuloma in the hypothalamic area, brain trauma, hydrocephalus, arachnoid cysts, and septum pellucidum-optic nerve hypoplasia syndrome. The cause of precocious puberty may be that the lesion blocks the channel of CNS that inhibits the secretion of GnRH pulses. These lesions are often accompanied by symptoms of CNS compression and increased intracranial pressure, and patients will experience varying degrees of growth stagnation. MRI scans can help detect lesions.

After reading this article, I believe everyone has an understanding of the treatment of true precocious puberty. Basically, during the treatment process, we must also pay attention to dietary restraint. We cannot feed them animal offal or necks, because the thyroid gland in the offal contains certain hormone substances.