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Objective: The aim of this study was to clarify the effect of administration of an anabolic steroid (AS) without the addition of specific training in stroke patients by measuring the cross-sectional area (CSA) of the thigh., Design: Twenty-six hemiplegic stroke patients during subacute rehabilitation were randomly assigned to a metenolone enanthate (ME) administration group or a control group (CT group). In the ME group, ME (100 mg) was injected intramuscularly weekly for 6 wks in the ME group. The CSA of the bilateral thigh muscles was measured using computed tomography. Motor subscore of the Functional Independence Measure (FIM-M) was assessed before the experimental period., Results: At the end of 6 wks, the CSA increase in the ME group (13.4%, affected side; 14.5%, unaffected side) was significantly larger than that in the CT group (3.3%, affected side; 5.2%, unaffected side). Correlation coefficients between the initial FIM-M score and the CSA increase at 6 wks were -0.754 for the affected side and -0.567 for the unaffected side in the ME group and 0.199 for the affected side and 0.431 for the unaffected side in the CT group., Conclusions: ME administration is effective for improving muscle CSA and, thus, muscle strengthening in stroke rehabilitation. The CSA increase in the ME group was most prominent in patients with a low initial FIM-M score.

Androgen inhibits osteoclastic bone resorption with increase of bone formation through androgen receptor in bone tissue. Anabolic steroids are synthetic derivates of testoterone. Anobolic steroids have favorable anabolic actions, lessening virilizing effects. Several anabolic steroids have been synthesized and some of them have been approved as a drug for anti osteoporosis. Anabolic steroids have revealed the increased bone mineral content or bone mineral density at the radius, and the lumbar spine in osteoporosis patients. Anabolic steroids have also decreased fat mass with increase of lean body mass and muscle mass, and lessened bone pain in osteoporosis patients having bone fracture, which seem to be favorable effects for especially elder osteoporosis patients. But in recent years the number of osteoporosis patients treated with anabolic steroids has been decreasing. Furthermore recently few clinical trials about the effect of anabolic steroids on osteoporosis have been reported, and prospective study for bone fracture using anabolic steroids has not reported yet. We would like to expect additional effects except on bone formation will enhance the frequency in use of anabolic steroids, and the prospective clinical study about the prevention against bone fracture will be reported in the future.

Between 1999 and 2005, 285 patients received new diagnoses of myelofibrosis with myeloid metaplasia (MMM) in Japan. Anemic symptoms were present in 162 patients, and hemoglobin (Hb) concentrations were <10 g/dL in 197 patients. Fifty-five MMM patients were treated with anabolic steroids, and their effect on anemia during MMM was evaluated in 39 patients. A "good" response was defined as an Hb increase of >or=1.5 g/dL, cessation of transfusion dependence, and an Hb concentration of >10 g/dL maintained for at least 8 weeks. A "minimum" response was defined as an Hb increase of >or=1.5 g/dL and transfusion independence for at least 8 weeks. Both good and minimum responses were considered "favorable." Favorable responses were achieved in 17 patients (44%, 8 good and 9 minimum responses). None of the pretreatment variables, such as the lack of transfusion dependence, a higher Hb concentration at the start of treatment, or the absence of cytogenetic abnormalities, were associated with a response to anabolic steroid therapy. Adverse events associated with anabolic steroid therapy were moderate and transient. Two patients required definitive withdrawal of treatment. Thus, anabolic steroids are well tolerated and effective for the treatment of anemia in a subset of MMM patients.

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.

A successful case of pericardiectomy without median sternotomy for an immunosuppressive 59-year-old man with constrictive pericarditis (CP) was reported. He had a history of invasive thymoma, myasthenia gravis and pure red cell aplasia, and he was on oral steroid and immunosuppressant. Pericardiectomy was performed by the approach of bilateral anterolateral thoracotomy to avoid troubles due to median sternotomy under immunosuppression, and there was no postoperative infection such as mediastinitis. Bilateral anterolateral thoracotomy was considered to be useful for immunosuppressive cases.

In this report we present a patient with unilateral masseteric hypertrophy who used anabolic steroids and was chewing entirely unilaterally for 1 month. Computed tomography and histologic examination were used to confirm the diagnosis. The combined action of unilateral mastication and anabolic steroid use is probably responsible for the rapid development of unilateral masseteric hypertrophy.

A 54-year-old female, who had been treated for aplastic anemia by metenolone acetate since 1981, developed a sudden unconsciousness in September 1995. On admission, she was drowny, CT showed a subarachnoid hemorrhage (SAH) in the right Sylvian fissure. Angiography demonstrated a complete occlusion of the superior sagittal sinus. The SAH was assumed to be originated from rupture of the right Sylvian vein, which was irregularly dilated on angiography. The dural sinus thrombosis was thought to be caused by a long term use of metenolone acetate, and it was discontinued. But her platelet count dropped due to the aggravation of aplastic anemia, and she developed repeated hemorrhagic infarction. An active anticoagulant therapy for the dural sinus thrombosis was thought to be inappropriate because she had the aplastic anemia and the hemorrhagic infarction recurred. We have successfully treated this case by mild anticoagulant therapy with nafamostat mesilate (Futhan).

A 63-year-old woman was found to have thrombocythemia and was referred to our hospital for further evaluation in September 1990. Peripheral blood showed platelet 170.0 x 10(4)/microliter, WBC 14,900/microliter and Hb 9.8 g/dl. Bone marrow was hypercellular with increased megakaryocytes and normal karyotype. She was diagnosed as essential thrombocythemia (ET), and treated with 2 mg of busulfan daily for 3 months until her platelet count decreased to 33.1 x 10(4)/microliter. Busulfan was given again for 40 days (a total of 80 mg) in another hospital when the platelet count increased to 71.1 x 10(4)/microliter in September 1991. In December 1991, she was admitted to our hospital because of pancytopenia. Examination of blood revealed platelet 0.4 x 10(4)/microliter, WBC 1,800/microliter and Hb 7.0 g/dl with hypocellular marrow. A diagnosis of busulfan-induced severe bone marrow aplasia was made. We administered metenolone acetate 15 mg and G-CSF 300 micrograms daily. Blood transfusions were given frequently. However, no effect was observed during her hospitalization. After discharge, G-CSF 600 micrograms and erythropoietin 24,000 units were continued twice a week in combination with metanolone acetate. Pancytopenia gradually began to improve as of June 1992, and then trilineage recovery was achieved in March 1994 with platelet 13.3 x 10(4)/microliter, WBC 5,500/microliter and Hb 12.1 g/dl. The platelet count has been within the normal range for more than 2 years after recovery.

Anabolic-androgenic steroids are widely misused in human sports and are also used as growth promoters in livestock. Athletes who consume meat containing such hormone residues may risk failing a sports drug test. Prompted by an athlete's defense case, we questioned whether the consumption of small livestock given doses of anabolic steroid, orally or intramuscularly, could generate positive results in samples tested by our analytical procedures. We analyzed urine from eight men who consumed chickens that had been either fed with methenolone acetate (1 mg/day) from day 0 to 21 or injected with methenolone heptanoate depot (1 mg/intramuscular injection) on days 0, 7, and 14 and slaughtered on day 22. No methenolone or characteristic major metabolite was detected in samples from subjects who ate meat from the orally dosed chickens. However, 50% of the samples collected 24 h after consumption of the intramuscularly dosed chickens were confirmed positive. Hence, eating meat containing small amounts of injected hormone may constitute a serious liability to the athlete.

Forty-eight patients with refractory anemia (RA) were retrospectively analyzed for their prognosis and subclassified into three groups: 12 patients with hematological improvement (A), 23 patients with no changes (B), and 13 patients with progression to RAEB or acute leukemia (C). For all patients, the median survival were 49.2 months, and the rate of leukemic transformation was 16%. The median survivals were 60.6, 32.1, and 17.9 months, respectively, for groups A, B and C. The factors indicating poor prognosis were low reticulocyte counts, low neutrophil alkaline phosphatase activity, low% red cell utilization, high M/E ratio, high blast percentage in the bone marrow and cytological abnormalities in the granulocyte and megakaryocyte series. By using multiple discriminant analysis, we obtained a formula for the prognostic estimation with a discrimination probability of 62.5%. This formula could predict either the patients with good (Y greater than 0.85) or poor (Y less than 0.59) prognosis, and might be useful to select the treatment for this intractable anemia at the time of diagnosis.

The anabolic effect of steroid hormones was investigated in rabbits by measuring the skeletal accumulation rate of 85Sr following the continuous administration of estrogens, androgens and corticosteroids over a period of eight weeks. Androgenic hormones did not influence the accumulation rate of 85Sr, whereas following castration and prolonged administration of estrogens an increase of 85Sr accumulation was found. There was no correlation of the changes observed with serum calcium levels, since the latter remained stable throughout the observation period during long-term administration of various hormones.

A 7-year-old boy was admitted to our department complaining pale face and subcutaneous bleeding in August, 1987. Peripheral blood analysis showed pancytopenia of WBC 2,600/microliter, RBC 148 x 10(4)/microliter and platelets 5,000/microliter. Bone marrow biopsy revealed hypocellularity. Granulocytes 104/microliter, reticulocytes 4,290/microliter and platelets 5,000/microliter were compatible with the diagnosis of severe aplastic anemia based on the criteria of the Ministry of Public Welfare in Japan. Prednisolone (PDN) was initially indicated and bolus methylprednisolone, metenolone and ALG therapy followed with no hematological improvement. Fifteen months after admission, in addition to 0.5-1 mg/kg/day of metenolone, Cyclosporin A (CyA) was started at a dose of 12 mg/kg/day for a week and 6 mg/kg/day thereafter. After a week from administration of CyA, 1 mg/kg/day of PDN was given because his bleeding tendency became worse. But this combination was complicated with liver damage and hyperglycemia to discontinue both drugs. These adverse effects were subsided within 7 days by cessation of the drugs. CyA was started again at a dose of 6 mg/kg/day without any response for 4 weeks. Then PDN was added together at a reduced dose of 0.5-1 mg/kg/day. Hematological response was obtained promptly. Granulocytes reached 1,500/microliter, hemoglobin 10.2 g/dl and platelets 26,000/microliter after 3 months of therapy. Afterward the patient became transfusion independent. The most effective method of CyA administration for aplastic anemia is still controversial. Alternative use of CyA, considering combination of steroids or anabolic steroids, in patients who failed to respond to conventional immunosuppressive treatments should be further investigated.

15 patients with a histologically and/or peritoneoscopically proven cirrhosis of the liver were treated for four weeks with 200 mg metenolonenanthate (Depot-Primobolan) per week. Before and after the treatment the intravascular and extravascular pool and daily turnover of albumin were measured with 125J-albumin. All patients had a well "compensated" cirrhosis. The only significant difference between the values of the cirrhotic patients and those of a control group of patients was a reduction of the albumin turn-over. The anabolic steroid enlarged the turn-over, the effect was the more pronounced the more pronounced the more the turn over was diminished before the treatment.