Hepatic: elevated liver function tests (AST, ALT, bilirubin, LDH, ALP), hepatotoxicity, jaundice, hepatic steatosis, hepatocellular adenoma, hepatocellular carcinoma, cholestasis, peliosis hepatis; all mostly or exclusively with 17α-alkylated AAS. Renal: renal hypertrophy, nephropathy, acute renal failure (secondary to rhabdomyolysis), focal segmental glomerulosclerosis, renal cell carcinoma. Others: glucose intolerance, insulin resistance, immune dysfunction. Physiological
Depending on the length of drug use, there is a chance that the immune system can be damaged. Most of these side-effects are dose-dependent, the most common being elevated blood pressure, especially in those with pre-existing hypertension. In addition to morphological changes of the heart which may have a permanent adverse effect on cardiovascular efficiency. AAS have been shown to alter fasting blood sugar and glucose tolerance tests. AAS such as testosterone also increase the risk of cardiovascular disease or coronary artery disease. Acne is fairly common among AAS users, mostly due to stimulation of the sebaceous glands by increased testosterone levels. Conversion of testosterone to DHT can accelerate the rate of premature baldness for males genetically predisposed, but testosterone itself can produce baldness in females.A number of severe side effects can occur if adolescents use AAS. For example, AAS may prematurely stop the lengthening of bones (premature epiphyseal fusion through increased levels of estrogen metabolites), resulting in stunted growth. Other effects include, but are not limited to, accelerated bone maturation, increased frequency and duration of erections, and premature sexual development. AAS use in adolescence is also correlated with poorer attitudes related to health.
Together these features produce a valvelike effect that occludes the ureteric opening during storage and voiding of urine. In people with VUR, failure of this mechanism occurs, with resultant backward (retrograde) flow of urine. Primary VUR
Insufficient submucosal length of the ureter relative to its diameter causes inadequacy of the valvular mechanism. This is precipitated by a congenital defect or lack of longitudinal muscle of the portion of the ureter within the bladder resulting in an ureterovesicular junction (UVJ) abnormality. Secondary VUR
In this category the ureters valvular mechanism is initially intact and healthy but becomes overwhelmed by increased bladder pressures associated with obstruction, which distorts the ureterovesicular junction. The obstructions may be anatomical or functional. Secondary VUR can be further divided into anatomical and functional groups. Anatomical
Posterior urethral valves; urethral or meatal stenosis. These causes are treated surgically when possible. Functional
Bladder instability, neurogenic bladder and non-neurogenic bladder. Bladder infections may cause reflux due to the elevated pressures associated with inflammation.Resolution of functional VUR will usually occur if the precipitating cause is treated and resolved. Medical and/or surgical treatment may be indicated.