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Small M, McArdle BM, Lowe GD, Forbes CD, Prentice CR.
The effects of a single 50 mg intramuscular injection of the anabolic steroid stanozolol (Stromba) on fibrinolysis, blood coagulation and lipids was evaluated in 12 healthy male volunteers. Significantly increased plasminogen activator levels (p less than 0.05) was noted 24 hours following the injection and these remained elevated for one week. Plasminogen levels increased significantly by day two (p less than 0.01) and remained elevated for three weeks. HDL cholesterol fell (p less than 0.01) and both total and LDL cholesterol increased (p less than 0.05) when measured one month post injection. Stanozolol appears to have therapeutic potential as an activator of the fibrinolytic system when given by intramuscular injection.
PMID: 6891506 [PubMed - indexed for MEDLINE]
Belch JJ, Madhok R, McArdle B, McLaughlin K, Kluft C, Forbes CD, Sturrock RD.
Fibrin deposition in rheumatoid arthritis may be responsible for some of the clinical manifestations of the disease. It has been shown that in severe rheumatoid arthritis fibrinolysis is decreased but can be stimulated using the fibrinolytic enhancing agent stanozolol. A prolonged increase in fibrinolysis may decrease joint fibrin deposition and lead to clinical improvement and we have therefore investigated stanozolol as a therapeutic agent. Forty patients were enrolled. Twenty patients received stanozolol 5 mg twice daily for six months and 20 received a matching placebo. Assessment of disease activity was made in the conventional way. Results show that the two groups were comparable. After six months nine of the control patients had withdrawn because of drug ineffectiveness compared with two stanozolol patients, and five control patients felt they had improved compared with 15 stanozolol patients. Disease activity had significantly decreased by the end of the study in the treated group, and detailed analysis showed improvement in ESR, articular index, duration of morning stiffness and visual analogue pain scale. We suggest that stanozolol may be of value in rheumatoid arthritis although this pilot study has looked at only small numbers of patients over a short period.
PMID: 3517926 [PubMed - indexed for MEDLINE]
Blamey SL, McArdle BM, Burns P, Carter DC, Lowe GD, Forbes CD.
Fibrinolytic shutdown may be important in the development of postoperative deep vein thrombosis (DVT). We have previously shown that stanozolol 50 mg, given intramuscularly 24 hr before surgery, prevents the decrease in plasminogen activator activity (PA) seen on the first postoperative day in patients at high risk of DVT. To investigate the role of fibrinolytic shutdown in causation of DVT, sixty patients were randomized in a double-blind controlled trial to receive stanozolol or placebo intramuscularly, and DVT was detected by leg scanning and confirmed by venography. Scan positive DVT occurred in 11 of 31 placebo patients (35%) and 12 of 29 who received stanozolol (41%). A significant decrease in PA was confirmed in the placebo group, while stanozolol caused a significant increase in PA on the first postoperative day. Patients in either group who did not develop DVT showed minimal changes in PA. We conclude that prevention of fibrinolytic shutdown by this regimen of stanozolol does not prevent postoperative DVT, and that further studies are required to clarify the relationship of postoperative fibrinolysis and DVT.
PMID: 6539002 [PubMed - indexed for MEDLINE]
Habscheid W, Abele U, Dahm HH.
Medizinische Klinik, Paracelsus-Krankenhaus Ruit, Esslingen.
HISTORY AND ADMISSION FINDINGS: A 28-year-old body builder was admitted because of jaundice. For 80 days, until 3 weeks before hospitalization, he had been taking moderately high doses of anabolic steroids: metandienone (methandienone), 10-50 mg daily by mouth, and stanozolol, 50 mg intramuscularly every other day. Physical examination was unremarkable except for yellow discoloration of the skin and sclerae. INVESTIGATIONS: Bilirubin concentration was raised to 4.5 mg/dl, cholestasis enzymes were normal, while transaminase activities were raised. Liver biopsy was compatible with cholestasis induced by anabolic steroids. TREATMENT AND COURSE: Although the steroids had been discontinued, the patient's general condition deteriorated over 7 weeks. Serum bilirubin rose up to a maximum of 77.9 mg/dl. In addition renal failure developed with a creatinine concentration of 4.2 mg/dl. The patient's state improved simultaneously with the administration of ursodeoxycholic acid and the biochemical values gradually reached normal levels after several weeks. CONCLUSION: Anabolic steroids can cause severe cholestasis and acute renal failure. In this case there was a notable temporal coincidence between the administration of ursodeoxycholic acid and the marked clinical improvement.
PMID: 10506840 [PubMed - indexed for MEDLINE]
Division of Gastroenterology, Department of Internal Medicine, Clinical Hospital Center Rijeka, Rijeka, Croatia. [email protected]
Athletes and bodybuilders often misuse androgenic/anabolic steroids. When used in therapeutic doses, these drugs produce clinical jaundice in just a small number of recipients. We present a 26-year-old male bodybuilder who self-administered high doses of androgenic/anabolic steroids that induced liver damage. One month before admission to the hospital, he used testosterone enanthate (500 mg intramuscularly, twice weekly), stanozolol (40 mg/d), and methylandrostenediol (30 mg/d by mouth, for 5 weeks). On admission, his bilirubin level was 470 micromol/L (direct, 360 micromol/L), his aspartate aminotransferase (AST) level was 5,870 IU/L, his alanine aminotransferase (ALT) level was 10,580 IU/L, his alkaline phosphatase (ALP) level was 152 IU/L, his gamma-glutamyl-transpeptidase level was 140 IU/L, his albumin level was 27.6 g/L, and his prothrombin time was 29%. During the patient's prolonged hospitalization, multiple tests and liver biopsy were performed, showing only toxic hepatic lesions. The patient was provided with supportive medical treatment. Clinical signs and laboratory findings improved substantially 12 weeks after the patient discontinued androgenic/anabolic steroids. The reasons for presenting this case were the much higher values of AST and ALT levels than reported in other studies, although the values of bilirubin and ALP were similar to those found in the literature. To our knowledge, it is the first case of toxic hepatitis induced by androgenic/anabolic steroids with predominantly hepatocellular necrosis instead of intrahepatic cholestasis.
The effects of a single 50 mg intramuscular injection of the anabolic steroid stanozolol (Stromba) on fibrinolysis, blood coagulation and lipids was evaluated in 12 healthy male volunteers. Significantly increased plasminogen activator levels (p less than 0.05) was noted 24 hours following the injection and these remained elevated for one week. Plasminogen levels increased significantly by day two (p less than 0.01) and remained elevated for three weeks. HDL cholesterol fell (p less than 0.01) and both total and LDL cholesterol increased (p less than 0.05) when measured one month post injection. Stanozolol appears to have therapeutic potential as an activator of the fibrinolytic system when given by intramuscular injection.
PMID: 6891506 [PubMed - indexed for MEDLINE]
Belch JJ, Madhok R, McArdle B, McLaughlin K, Kluft C, Forbes CD, Sturrock RD.
Fibrin deposition in rheumatoid arthritis may be responsible for some of the clinical manifestations of the disease. It has been shown that in severe rheumatoid arthritis fibrinolysis is decreased but can be stimulated using the fibrinolytic enhancing agent stanozolol. A prolonged increase in fibrinolysis may decrease joint fibrin deposition and lead to clinical improvement and we have therefore investigated stanozolol as a therapeutic agent. Forty patients were enrolled. Twenty patients received stanozolol 5 mg twice daily for six months and 20 received a matching placebo. Assessment of disease activity was made in the conventional way. Results show that the two groups were comparable. After six months nine of the control patients had withdrawn because of drug ineffectiveness compared with two stanozolol patients, and five control patients felt they had improved compared with 15 stanozolol patients. Disease activity had significantly decreased by the end of the study in the treated group, and detailed analysis showed improvement in ESR, articular index, duration of morning stiffness and visual analogue pain scale. We suggest that stanozolol may be of value in rheumatoid arthritis although this pilot study has looked at only small numbers of patients over a short period.
PMID: 3517926 [PubMed - indexed for MEDLINE]
Blamey SL, McArdle BM, Burns P, Carter DC, Lowe GD, Forbes CD.
Fibrinolytic shutdown may be important in the development of postoperative deep vein thrombosis (DVT). We have previously shown that stanozolol 50 mg, given intramuscularly 24 hr before surgery, prevents the decrease in plasminogen activator activity (PA) seen on the first postoperative day in patients at high risk of DVT. To investigate the role of fibrinolytic shutdown in causation of DVT, sixty patients were randomized in a double-blind controlled trial to receive stanozolol or placebo intramuscularly, and DVT was detected by leg scanning and confirmed by venography. Scan positive DVT occurred in 11 of 31 placebo patients (35%) and 12 of 29 who received stanozolol (41%). A significant decrease in PA was confirmed in the placebo group, while stanozolol caused a significant increase in PA on the first postoperative day. Patients in either group who did not develop DVT showed minimal changes in PA. We conclude that prevention of fibrinolytic shutdown by this regimen of stanozolol does not prevent postoperative DVT, and that further studies are required to clarify the relationship of postoperative fibrinolysis and DVT.
PMID: 6539002 [PubMed - indexed for MEDLINE]
Habscheid W, Abele U, Dahm HH.
Medizinische Klinik, Paracelsus-Krankenhaus Ruit, Esslingen.
HISTORY AND ADMISSION FINDINGS: A 28-year-old body builder was admitted because of jaundice. For 80 days, until 3 weeks before hospitalization, he had been taking moderately high doses of anabolic steroids: metandienone (methandienone), 10-50 mg daily by mouth, and stanozolol, 50 mg intramuscularly every other day. Physical examination was unremarkable except for yellow discoloration of the skin and sclerae. INVESTIGATIONS: Bilirubin concentration was raised to 4.5 mg/dl, cholestasis enzymes were normal, while transaminase activities were raised. Liver biopsy was compatible with cholestasis induced by anabolic steroids. TREATMENT AND COURSE: Although the steroids had been discontinued, the patient's general condition deteriorated over 7 weeks. Serum bilirubin rose up to a maximum of 77.9 mg/dl. In addition renal failure developed with a creatinine concentration of 4.2 mg/dl. The patient's state improved simultaneously with the administration of ursodeoxycholic acid and the biochemical values gradually reached normal levels after several weeks. CONCLUSION: Anabolic steroids can cause severe cholestasis and acute renal failure. In this case there was a notable temporal coincidence between the administration of ursodeoxycholic acid and the marked clinical improvement.
PMID: 10506840 [PubMed - indexed for MEDLINE]
Division of Gastroenterology, Department of Internal Medicine, Clinical Hospital Center Rijeka, Rijeka, Croatia. [email protected]
Athletes and bodybuilders often misuse androgenic/anabolic steroids. When used in therapeutic doses, these drugs produce clinical jaundice in just a small number of recipients. We present a 26-year-old male bodybuilder who self-administered high doses of androgenic/anabolic steroids that induced liver damage. One month before admission to the hospital, he used testosterone enanthate (500 mg intramuscularly, twice weekly), stanozolol (40 mg/d), and methylandrostenediol (30 mg/d by mouth, for 5 weeks). On admission, his bilirubin level was 470 micromol/L (direct, 360 micromol/L), his aspartate aminotransferase (AST) level was 5,870 IU/L, his alanine aminotransferase (ALT) level was 10,580 IU/L, his alkaline phosphatase (ALP) level was 152 IU/L, his gamma-glutamyl-transpeptidase level was 140 IU/L, his albumin level was 27.6 g/L, and his prothrombin time was 29%. During the patient's prolonged hospitalization, multiple tests and liver biopsy were performed, showing only toxic hepatic lesions. The patient was provided with supportive medical treatment. Clinical signs and laboratory findings improved substantially 12 weeks after the patient discontinued androgenic/anabolic steroids. The reasons for presenting this case were the much higher values of AST and ALT levels than reported in other studies, although the values of bilirubin and ALP were similar to those found in the literature. To our knowledge, it is the first case of toxic hepatitis induced by androgenic/anabolic steroids with predominantly hepatocellular necrosis instead of intrahepatic cholestasis.
