Cardiovascular effects may be precipitated in patients adversely affected by fluid retention. Edema, with and without congestive heart failure, has occurred during anabolic steroid therapy.
Genitourinary effect following chronic administration and/or large dosages of anabolic steroids can result in oligospermia and decreased ejaculatory volume. Elderly male patients may experience prostatic enlargement resulting in urinary obstruction. Priapism and excessive stimulation may develop.
In female patients the use of anabolic steroids may result in virilization including deepening voice, hirsutism, acne, clitomegaly (not reversible), and menstrual abnormalities. Discontinuation of medication at signs of mild virilization may prevent irreversible virilization.
Alterations in libido may occur (increased/decreased).
Life-threatening peliosis hepatis and hepatic abnormalities including hepatic neoplasms and hepatocellular carcinomas have occurred following prolonged therapy with high doses of anabolic steroids. Tumor regression did not occur in all cases following medication withdrawal.
Cholestatic hepatitis, jaundice, and abnormal liver function tests occur at relatively low doses.
In female patients the use of anabolic steroids has resulted in virilization including deepening voice, hirsutism, acne, clitomegaly (not reversible), and menstrual abnormalities. Discontinuation of stanozolol at signs of mild virilization may prevent irreversible virilization.
Androgenic activity associated with anabolic steroids is involved in termination of linear bone growth by closure of the epiphyseal growth centers. Appropriate monitoring of bone age is recommended during stanozolol use in prepubertal patients.
Oncologic effects following prolonged therapy with large doses of anabolic steroids have included hepatic neoplasms and hepatocellular carcinomas.
Hematologic effects occurring during anabolic steroid therapy include alteration in clotting factors II, V, VII and X , prolonged prothrombin time (PT), and increased red cell production.
During exogenous administration of anabolic steroids, endogenous testosterone release is inhibited through feedback inhibition of pituitary luteinizing hormone (LH). Large doses of exogenous anabolic steroids may suppress spermatogenesis through inhibition of pituitary follicle stimulating hormone (FSH).
Decreased glucose tolerance requiring adjustments in hyperglycemic control has occurred in diabetic patients during anabolic steroid therapy.
Metabolic effects occurring during anabolic steroid therapy in immobilized patients or those with metastatic breast disease include osteolytic-induced hypercalcemia.
Anabolic steroids effect electrolyte balance, nitrogen retention, and urinary calcium excretion. Edema, with and without congestive heart failure, has occurred during anabolic steroid therapy.
The androgenic activity of anabolic steroids may decrease levels of thyroxin-binding globulin, resulting in decreased total T4 serum levels and increased resin uptake of T3 and T4. Free thyroid hormone levels remain unchanged, however, and there is no clinical evidence of thyroid dysfunction.
Significant increases in low density lipoproteins (LDL) and decreases in high density lipoproteins (HDL) have occurred.
Anabolic steroids cause retention of nitrogen, sodium, potassium, chloride, water and phosphorus, and decrease urinary excretion of calcium. Patients should be instructed to report edema