methenolone and testosterone-enanthate

Anabolic androgenic steroids (AAS) are used illicitly at high doses by bodybuilders. The misuse of these drugs is associated with serious adverse effects to the liver, including cellular adenomas and adenocarcinomas. We report two very different cases of adult male bodybuilders who developed hepatocellular adenomas following AAS abuse. The first patient was asymptomatic but had two large liver lesions which were detected by ultrasound studies after routine medical examination. The second patient was admitted to our hospital with acute renal failure and ultrasound (US) studies showed mild hepatomegaly with several very close hyperecogenic nodules in liver, concordant with adenomas at first diagnosis. In both cases the patients have evolved favourably and the tumours have shown a tendency to regress after the withdrawal of AAS. The cases presented here are rare but may well be suggestive of the natural course of AAS induced hepatocellular adenomas. In conclusion, sportsmen taking AAS should be considered as a group at risk of developing hepatic sex hormone related tumours. Consequently, they should be carefully and periodically monitored with US studies. In any case, despite the size of the tumours detected in these two cases, the possibility of spontaneous tumour regression must also be taken in account.

Topics: Adenoma, Liver Cell; Administration, Oral; Adult; Anabolic Agents; Biopsy, Fine-Needle; Humans; Liver Neoplasms; Magnetic Resonance Imaging; Male; Methenolone; Nandrolone; Nandrolone Decanoate; Oxymetholone; Stanozolol; Substance Abuse, Intravenous; Substance-Related Disorders; Testosterone; Testosterone Propionate; Ultrasonography; Weight Lifting

We report a case of myelodysplastic syndrome (MDS) treated effectively with testosterone enanthate. A 70-year-old man was diagnosed with low-risk MDS in 1998, and he was first given methenolone acetate orally because of gradual progression of anemia and thrombocytopenia. However, this treatment was not effective, so we changed the treatment to testosterone enanthate because of his symptoms with late-onset hypogonadism. Three months after testosterone replacement therapy (TRT), anemia and thrombocytopenia had improved, and mean platelet count and hemoglobin had significant increases from 2.36 ± 0.45 × 10(4) to 3.83 ± 0.78 × 10(4) /µL, and from 11.7 ± 0.81 to 15.2 ± 1.00 g/dL, respectively, which contributed to a decrease in platelet transfusion requirement. Since then, the patient has been on a good clinical course. The present case suggests that testosterone enanthate administration could be an alternative treatment for men with MDS, even in the case where treatment with anabolic-androgenic steroids is not successful, and suggests another interesting effect of TRT on platelets.

Topics: Aged; Androgens; Humans; Male; Methenolone; Myelodysplastic Syndromes; Testosterone; Treatment Failure

Lateral radiographs of the thoracic and lumbar spine were taken periodically in 49 patients with osteoporosis. Thirty patients were postmenopausal, and 19 nonmenopausal with osteoporosis due to steroids, male hypogonadism, alcoholism, thyrotoxicosis or unknown cause. Patients were studied before, during and after treatment with high calcium alone, or with combined calcium and sex steroids. Calcium was given as effervescent calcium lactate gluconate, and sex hormones as oestradiol valerate, testosterone oenanthate, or methenolone oenanthate. A total of 964 films covering 409 patient-years were available for measurement. On each vertebra, deformity due to loss of anterior height was measured and assigned to one of four grades. For the time interval between each consecutive pair of films, a patient's vertebral fracture rate score was calculated and expressed per thousand patient-years. In comparison with the corresponding pretreatment fracture rate score, both the postmenopausal and the nonmenopausal groups who had not received sex hormones previously, failed to show significant changes (p = 0.144; p = 0.017) on high calcium alone during mean periods of 4.3 and 2.8 years respectively. If the first 2 years on high calcium were excluded for the postmenopausal group, they still failed to show a reduction in fracture rate score (observed for a mean period of 5.0 years; p = 0.04). When treated with combined calcium and sex hormones, both postmenopausal and nonmenopausal groups showed a lower fracture rate score of 20 and 207 respectively when compared with the pretreatment levels of 1500 and 1697 (in mean treatment periods of 3.2 and 4.4 years; p less than 0.001 in each case). When given high-dose calcium alone, but after treatment with sex hormones as well, the postmenopausal group showed no change in fracture rate score from pretreatment (in a mean of 3.1 years; p = 0.069); however the nonmenopausal group still showed a significant reduction in fracture rate score from 1697 to 42 over a mean period of 2.3 years (p = 0.001). The postmenopausal group, after stopping all treatment, showed a higher fracture rate score of 1286 (in a mean of 2.6 years) than did those on combined calcium and sex hormones, in whom the fracture rate score was 20 (in a mean of 3.2 years; p = 0.008). A subgroup of 11 patients with osteoporosis of both the menopausal and nonmenopausal types, had data both before (in a mean of 5.5 years) and during (for a mean of 2.5 years) treatment with c

Topics: Adult; Calcium; Drug Therapy, Combination; Estradiol; Estrogens, Conjugated (USP); Female; Gonadal Steroid Hormones; Humans; Male; Methenolone; Middle Aged; Osteoporosis; Osteoporosis, Postmenopausal; Spinal Fractures; Testosterone; Time Factors