Through activation of the ARs (as well as the mARs), testosterone has many effects, including the following:
Promotes growth, function, and maintenance of the prostate gland, seminal vesicles, and penis during puberty and thereafter
Promotes growth and maintenance of muscles, particularly of the upper body
Causes subcutaneous fat to be deposited in a masculine pattern and decreases overall body fat
Suppresses breast development induced by estrogens, but can also still produce gynecomastia via excessive conversion into estradiol if levels are too high
Maintains skin health, integrity, appearance, and hydration and slows the rate of aging of the skin, but can also cause oily skin, acne, and seborrhea
Promotes the growth of facial and body hair, but can also cause scalp hair loss and hirsutism
Contributes to bone growth and causes broadening of the shoulders at puberty
Modulates liver protein synthesis, such as the production of sex hormone-binding globulin and many other proteins
Increases production of erythropoietin in the kidneys and thereby stimulates red blood cell production in bone marrow and elevates hematocrit
Exerts negative feedback on the hypothalamic–pituitary–gonadal axis by suppressing the secretion of the gonadotropins follicle-stimulating hormone (FSH) and luteinizing hormone (LH) from the pituitary gland, thereby inhibiting gonadal sex hormone production as well as spermatogenesis and fertility
Regulates the vasomotor system and body temperature via the hypothalamus, thereby preventing hot flashes
Modulates brain function, with effects on mood, emotionality, aggression, and sexuality, as well as cognition and memory
Increases sex drive and erectile capacity and causes spontaneous erections and nocturnal emissions
Increases the risk of benign prostatic hyperplasia and prostate cancer and accelerates the progression of prostate cancer
Decreases breast proliferation and the risk of breast cancer

Pharmacokinetics
Testosterone can be taken by a variety of different routes of administration.
Conservative treatment can also be uterus sparing but may not be as successful and has a higher risk of complications. Techniques include:

Leaving the placenta in the uterus and curettage of uterus. Methotrexate has been used in this case. Intrauterine balloon catheterisation to compress blood vessels
Embolisation of pelvic vessels
Internal iliac artery ligation
Bilateral uterine artery ligationIn cases where there is invasion of placental tissue and blood vessels into the bladder, it is treated in similar manner to abdominal pregnancy and manual placental removal is avoided. However, this may eventually need hysterectomy and/or partial cystectomy.If the patient decides to proceed with a vaginal delivery, blood products for transfusion and an anesthesiologist are kept ready at delivery. Epidemiology
The reported incidence of placenta accreta has increased from approximately 0.8 per 1000 deliveries in the 1980s to 3 per 1000 deliveries in the past decade. Incidence has been increasing with increased rates of caesarean deliveries, with rates of 1 in 4,027 pregnancies in the 1970s, 1 in 2,510 in the 1980s, and 1 in 533 for 1982–2002. In 2002, ACOG estimated that incidence has increased 10-fold over the past 50 years. The risk of placenta accreta in future deliveries after caesarian section is 0.4-0.8%. For patients with placenta previa, risk increases with number of previous caesarean sections, with rates of 3%, 11%, 40%, 61%, and 67% for the first, second, third, fourth, and fifth or greater number of caesarean sections. References
External links
National Accreta Foundation