Familial male-limited precocious puberty
| Familial male-limited precocious puberty | |
|---|---|
| Other names | Familial sexual precocity |
 | |
| Male-limited precocious puberty has an autosomal dominant pattern of inheritance. However, only males are affected; females with the mutant gene are not affected. | |
Familial male-limited precocious puberty, often abbreviated as FMPP, also known as familial sexual precocity or gonadotropin-independent testotoxicosis,[1] is a form of gonadotropin-independent precocious puberty in which boys experience early onset and progression of puberty.[2] Signs of puberty can develop as early as an age of 1 year.[citation needed]
The spinal length in boys may be short due to a rapid advance in epiphyseal maturation. It is an
steroidogenesis, such as cyproterone acetate, ketoconazole, spironolactone, and testolactone.[3] Alternatively, the combination of the androgen receptor antagonist bicalutamide and the aromatase inhibitor anastrozole may be used.[4]
Robert King Stone, personal physician to American president Abraham Lincoln, described the first case of FMPP in 1852.[5]
See also
- Follicle-stimulating hormone insensitivity
- Gonadotropin-releasing hormone insensitivity
- Hypergonadism, hyperandrogenism, and precocious puberty
- Inborn errors of steroid metabolism
- Leydig cell hypoplasia (or LH insensitivity)
References
External links
- Testotoxicosis at NIH's Office of Rare Diseases
 | This genetic disorder article is a stub. You can help Wikipedia by expanding it. |