HackTwat
MuscleChemistry Registered Member
[h=2]Adverse Effects[/h]Most of the adverse effects of anabolic-androgenic steroid (AAS) use are dose dependent and are reversible with cessation of the offending agent or agents. This overview of side effects and interactions is just that, an overview, and is not meant to represent the full spectrum of potential side effects that may be seen with this class of agents. Vital signs, including heart rate and blood pressure, and basic chemistries, such as sodium, potassium, hemoglobin, hematocrit, BUN (blood urea nitrogen), creatinine, hepatic, and lipid profiles, must be monitored carefully. Monitoring these parameters will help the clinician to determine drug choice, treatment dose, and duration, and will help to alert the prescriber to potentially serious adverse effects that necessitate the discontinuation of therapy.
[h=3]Cardiovascular effects[/h]The most common deleterious effects of AAS use on the cardiovascular system include increased heart rate, increased blood pressure, and changes in lipid metabolism, including lowered high-density lipoprotein (HDL) and increased low-density lipoprotein (LDL). The increase in heart rate is thought to be more profound with the androgens, especially those resistant to aromatase, and is believed to be due to the inhibition of monoamine oxidase (MAO). This effect, when combined with the increased renal recovery of ions, such as sodium, causing subsequent fluid retention, can lead to dramatic increases in blood pressure. Combine this with a tendency to lower HDL and raise LDL, and the stage is set for untoward atherogenic and cardiac effects. Anabolic steroid users can have a lower left ventricle ejection fraction. Ananbolic steroid abuse has been associated with ventricular arrhythmias.[SUP][11, 15, 16, 17, 18] [/SUP]
[h=3]Hepatic effects[/h]The changes made to C-17 to inhibit hepatic degradation make nearly all oral preparations hepatotoxic. The alanine aminotransferase/aspartate aminotransferase (ALT/AST) can be seen to rise, usually in a dose-dependent fashion. Levels approaching 2-3 times baseline are often set as upper limits of reference ranges when administering oral AASs, but the risk-to-benefit ratio must be constantly evaluated.
AAS use also results in suppression of clotting factors II, V, VII, and X, as well as an increase in prothrombin time. Another life-threatening, albeit rare, adverse effect that is seen in the liver and sometimes in the spleen is peliosis hepatitis, which is characterized by the appearance of blood-filled, cystic structures. These cysts, which may rupture and bleed profusely, have been found in patients with near-normal liver function test (LFT) values, as well as in individuals who are in liver failure. Fortunately, drug cessation usually results in complete recovery.
Primary liver tumors have been reported, most of which are benign, androgen-dependent growths that regress with the discontinuation of AAS therapy. Several case reports exist of young, healthy athletes who have died from primary malignant liver carcinoma, with the only identifiable risk factor being oral AAS use.
Anabolic steroid abuse has been considered a risk factor for nonalcoholic fatty liver disease.[SUP][19] [/SUP]
[h=3]Endocrine effects[/h]The endocrine system has a remarkable array of checks and balances that ensure the human body is at or near homeostasis at any point in time. Interruption of one feedback system has been shown to produce changes in other hormone feedback systems via direct receptor changes, as well as through competition for common enzymes and metabolic pathways. Studies have shown that AASs bind to glucocorticoid, progesterone, and estrogen receptors and exert multiple effects. Discussions exist as to how the endogenous testosterone and spermatogenic functions of the testes are inhibited by the use of testosterone and AASs. By suppressing FSH, spermatogenic function should be reduced.
AASs have also been shown to alter fasting blood sugar levels and decrease glucose tolerance, presumably due to either a hepatic effect or changes in the insulin receptor. Thyroxine-binding globulin (TBG) may also be lowered by AASs and result in lowered total T4 levels, with free T4 levels remaining normal. An up-regulation of sex-hormone binding globulin, with a concomitant decrease in TBG, is thought to cause the changes in total T4 levels.
The aromatization of testosterone/AASs to estradiol and related compounds can render many adverse estrogenic effects. The most apparent and common adverse effect is the growth of tender, estrogen-sensitive tissue under the male nipple. This unsightly growth is termed gynecomastia and can be treated medically or surgically.[SUP][20] [/SUP]
[h=3]Urologic effects[/h]The male prostate is very sensitive to androgens, especially those that are reduced in prostatic tissue to dihydrotestosterone (DHT) or DHT analogs. In response to this stimulation, the prostate grows in size, potentially causing or exacerbating benign prostatic hyperplasia (BPH). Worsening BPH may indeed cause severe bladder and secondary renal damage. In addition, the use of AASs in patients with underlying carcinoma of the prostate is absolutely contraindicated due to the potential for hormone-sensitive tumor growth. However, a 3-year study of hypogonadal men on testosterone replacement therapy failed to show significant differences between the group and the controls in urinary symptoms, urine flow rate, or urine postvoid residual.[SUP][21] [/SUP]
[h=3]Hematologic effects[/h]Direct clotting factors may be reduced with an increase in prothrombin time. In patients on concomitant anticoagulant therapy, this increase could cause bleeding. AASs cause increases in hemoglobin and hematocrit and are used in many cases of anemia, although the clinician must be aware of the potential for polycythemia.
[h=3]Dermatologic effects[/h]Skin, especially the face and scalp, has a high degree of androgen receptors and 5AR. DHT is known to cause increases in sebum production, leading to clinical acne. Also, male pattern baldness is related to scalp DHT production and binding, along with genetic factors influencing hair growth. Male pattern baldness is greatly exacerbated by most AASs in susceptible individuals.
[h=3]Cardiovascular effects[/h]The most common deleterious effects of AAS use on the cardiovascular system include increased heart rate, increased blood pressure, and changes in lipid metabolism, including lowered high-density lipoprotein (HDL) and increased low-density lipoprotein (LDL). The increase in heart rate is thought to be more profound with the androgens, especially those resistant to aromatase, and is believed to be due to the inhibition of monoamine oxidase (MAO). This effect, when combined with the increased renal recovery of ions, such as sodium, causing subsequent fluid retention, can lead to dramatic increases in blood pressure. Combine this with a tendency to lower HDL and raise LDL, and the stage is set for untoward atherogenic and cardiac effects. Anabolic steroid users can have a lower left ventricle ejection fraction. Ananbolic steroid abuse has been associated with ventricular arrhythmias.[SUP][11, 15, 16, 17, 18] [/SUP]
[h=3]Hepatic effects[/h]The changes made to C-17 to inhibit hepatic degradation make nearly all oral preparations hepatotoxic. The alanine aminotransferase/aspartate aminotransferase (ALT/AST) can be seen to rise, usually in a dose-dependent fashion. Levels approaching 2-3 times baseline are often set as upper limits of reference ranges when administering oral AASs, but the risk-to-benefit ratio must be constantly evaluated.
AAS use also results in suppression of clotting factors II, V, VII, and X, as well as an increase in prothrombin time. Another life-threatening, albeit rare, adverse effect that is seen in the liver and sometimes in the spleen is peliosis hepatitis, which is characterized by the appearance of blood-filled, cystic structures. These cysts, which may rupture and bleed profusely, have been found in patients with near-normal liver function test (LFT) values, as well as in individuals who are in liver failure. Fortunately, drug cessation usually results in complete recovery.
Primary liver tumors have been reported, most of which are benign, androgen-dependent growths that regress with the discontinuation of AAS therapy. Several case reports exist of young, healthy athletes who have died from primary malignant liver carcinoma, with the only identifiable risk factor being oral AAS use.
Anabolic steroid abuse has been considered a risk factor for nonalcoholic fatty liver disease.[SUP][19] [/SUP]
[h=3]Endocrine effects[/h]The endocrine system has a remarkable array of checks and balances that ensure the human body is at or near homeostasis at any point in time. Interruption of one feedback system has been shown to produce changes in other hormone feedback systems via direct receptor changes, as well as through competition for common enzymes and metabolic pathways. Studies have shown that AASs bind to glucocorticoid, progesterone, and estrogen receptors and exert multiple effects. Discussions exist as to how the endogenous testosterone and spermatogenic functions of the testes are inhibited by the use of testosterone and AASs. By suppressing FSH, spermatogenic function should be reduced.
AASs have also been shown to alter fasting blood sugar levels and decrease glucose tolerance, presumably due to either a hepatic effect or changes in the insulin receptor. Thyroxine-binding globulin (TBG) may also be lowered by AASs and result in lowered total T4 levels, with free T4 levels remaining normal. An up-regulation of sex-hormone binding globulin, with a concomitant decrease in TBG, is thought to cause the changes in total T4 levels.
The aromatization of testosterone/AASs to estradiol and related compounds can render many adverse estrogenic effects. The most apparent and common adverse effect is the growth of tender, estrogen-sensitive tissue under the male nipple. This unsightly growth is termed gynecomastia and can be treated medically or surgically.[SUP][20] [/SUP]
[h=3]Urologic effects[/h]The male prostate is very sensitive to androgens, especially those that are reduced in prostatic tissue to dihydrotestosterone (DHT) or DHT analogs. In response to this stimulation, the prostate grows in size, potentially causing or exacerbating benign prostatic hyperplasia (BPH). Worsening BPH may indeed cause severe bladder and secondary renal damage. In addition, the use of AASs in patients with underlying carcinoma of the prostate is absolutely contraindicated due to the potential for hormone-sensitive tumor growth. However, a 3-year study of hypogonadal men on testosterone replacement therapy failed to show significant differences between the group and the controls in urinary symptoms, urine flow rate, or urine postvoid residual.[SUP][21] [/SUP]
[h=3]Hematologic effects[/h]Direct clotting factors may be reduced with an increase in prothrombin time. In patients on concomitant anticoagulant therapy, this increase could cause bleeding. AASs cause increases in hemoglobin and hematocrit and are used in many cases of anemia, although the clinician must be aware of the potential for polycythemia.
[h=3]Dermatologic effects[/h]Skin, especially the face and scalp, has a high degree of androgen receptors and 5AR. DHT is known to cause increases in sebum production, leading to clinical acne. Also, male pattern baldness is related to scalp DHT production and binding, along with genetic factors influencing hair growth. Male pattern baldness is greatly exacerbated by most AASs in susceptible individuals.
