Injection is the most common method used by individuals administering AAS for non-medical purposes.The traditional routes of administration do not have differential effects on the efficacy of the drug. Studies indicate that the anabolic properties of AAS are relatively similar despite the differences in pharmacokinetic principles such as first-pass metabolism. However, the orally available forms of AAS may cause liver damage in high doses. Adverse effects
Known possible side effects of AAS include:
Dermatological/integumental: oily skin, acne vulgaris, acne conglobata, seborrhea, stretch marks (due to rapid muscle enlargement), hypertrichosis (excessive body hair growth), androgenic alopecia (pattern hair loss; scalp baldness), fluid retention/edema. Reproductive/endocrine: libido changes, reversible infertility, hypogonadotropic hypogonadism. Male-specific: spontaneous erections, nocturnal emissions, priapism, erectile dysfunction, gynecomastia (mostly only with aromatizable and hence estrogenic AAS), oligospermia/azoospermia, testicular atrophy, intratesticular leiomyosarcoma, prostate hypertrophy, prostate cancer. Female-specific: masculinization, irreversible voice deepening, hirsutism (excessive facial/body hair growth), menstrual disturbances (e.g., anovulation, oligomenorrhea, amenorrhea, dysmenorrhea), clitoral enlargement, breast atrophy, uterine atrophy, teratogenicity (in female fetuses). Child-specific: premature epiphyseal closure and associated short stature, precocious puberty in boys, delayed puberty and contrasexual precocity in girls. Psychiatric/neurological: mood swings, irritability, aggression, violent behavior, impulsivity/recklessness, hypomania/mania, euphoria, depression, anxiety, dysphoria, suicidality, delusions, psychosis, withdrawal, dependence, neurotoxicity, cognitive impairment. Musculoskeletal: muscle hypertrophy, muscle strains, tendon ruptures, rhabdomyolysis. Cardiovascular: dyslipidemia (e.g., increased LDL levels, decreased HDL levels, reduced apo-A1 levels), atherosclerosis, hypertension, left ventricular hypertrophy, cardiomyopathy, myocardial hypertrophy, polycythemia/erythrocytosis, arrhythmias, thrombosis (e.g., embolism, stroke), myocardial infarction, sudden death.
Epidemiology
Carrións disease, or Oroya fever, or Peruvian wart is a rare infectious disease found only in Peru, Ecuador, and Colombia. It is endemic in some areas of Peru, is caused by infection with the bacterium Bartonella bacilliformis, and transmitted by sandflies of genus Lutzomyia. Cat scratch disease occurs worldwide. Cats are the main reservoir of Bartonella henselae, and the bacterium is transmitted to cats by the cat flea Ctenocephalides felis. Infection in cats is very common with a prevalence estimated between 40 and 60%, younger cats being more commonly infective. Cats usually become immune to the infection, while dogs may be very symptomatic. Humans may also acquire it through flea or tick bites from infected dogs, cats, coyotes, and foxes.Trench fever, produced by Bartonella quintana infection,  is transmitted by the human body louse Pediculus humanus corporis. Humans are the only known reservoir. Thorough washing of clothing may help to interrupt the transmission of infection.A possible role for ticks in transmission of Bartonella species remains to be elucidated; in November 2011, Bartonella rochalimae, B. quintana, and B. elizabethae DNA was first reported in Rhipicephalus sanguineus and Dermacentor nitens ticks in Peru. History
Carrións disease
The disease was named after medical student Daniel Alcides Carrión from Cerro de Pasco, Peru. Carrión described the disease after being inoculated at his request with the pus of a skin lesion from patient Carmen Paredes in 1885 by Doctor Evaristo M. Chávez, a close friend and coworker in Dos de Mayo National Hospital.