Colestasis canalicular inducida por anabolizantes esteroideos / Canalicular cholestasis induced by anabolic steroids

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Ventricular androgenic-anabolic steroid-related remodeling: an immunohistochemical study.

BACKGROUND: Several fatal cases of bodybuilders, following a myocardial infarction after long exposure to androgenic-anabolic steroids (AAS), are reported. In recent years, evidence has emerged of cases of heart failure related to AAS consumption, with no signs of coronary or aorta atherosclerosis. This study aims to further investigate the pathogenesis of the ventricular AAS-related remodeling performing immunohistochemistry (IHC). METHOD: In order to examine innate immunity activity and myocytes and endothelial cell apoptosis, IHC analyses were performed on heart tissue of two cases of bodybuilders who died after years of supratherapeutic use of metelonone and nandrolone and where no atherosclerosis or thrombosis were found, using the following antibodies: anti-CD68, anti-iNOS, anti-CD163, anti-CD 15, anti-CD8, anti-CD4, anti-HIF1 α, and in situ TUNEL staining. RESULTS: Results confirm the experimental findings of recent research that, in the absence of other pathological factors, if intensive training is combined with AAS abuse, myocytes and endothelial cells undergo apoptotic alterations. The absence of inflammatory reactions and the presence of an increased number of M2 macrophages in the areas of fibrotic remodeling confirm that the fibrotic changes in the heart are apoptosis-related and not necrosis-related. CONCLUSIONS: In conclusion, the study indicates that, in very young subjects with chronic hypoxia-related alterations of the heart, signs of a heart failure in the other organs and a history of AAS abuse, death can be ascribed to progressive heart failure due to the direct apoptotic cardiac and endothelial changes produced by AAS.

Acute myocardial infarction and renal infarction in a bodybuilder using anabolic steroids.

A 41-year-old male bodybuilder was admitted with acute inferior myocardial infarction. The patient had been using oxymetholone and methenolone to increase his performance for 15 years and quitted smoking three years before. He underwent successful primary percutaneous coronary intervention (PCI) and bare metal stenting for total occlusion of the proximal right coronary artery. Angiography also showed a critical lesion in the left anterior descending (LAD) coronary artery. Five hours after primary PCI, the patient had severe right flank pain. Abdominal computed tomography showed a large renal infarction in the right kidney. Subcutaneous enoxaparin was added to dual antiplatelet treatment. Doppler renal ultrasound performed on the eighth day showed findings of reperfusion in the right kidney and normal-size kidneys. Transthoracic echocardiography demonstrated disappearance of previously detected thrombus remnant in the left ventricle and only mild hypokinesia around the apical and middle segments of the inferior and inferoseptal walls. The patient was discharged on the 10th day. Renal arteriography during elective LAD intervention 18 days after discharge showed complete revascularization, stent patency, and improved blood flow. This is the first case of renal infarction that developed in the early hours of primary PCI, despite effective anticoagulant and antiplatelet treatment. Intensive coronary artery and left ventricular thrombi may be explained by the use of anabolic steroids.

[Effect of anabolic steroids on osteoporosis].

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.

The effect of anabolic steroids on anemia in myelofibrosis with myeloid metaplasia: retrospective analysis of 39 patients in Japan.

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.

Hepatocellular adenomas associated with anabolic androgenic steroid abuse in bodybuilders: a report of two cases and a review of the literature.

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.

Masseteric hypertrophy associated with administration of anabolic steroids and unilateral mastication: a case report.

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.

[Superior sagittal sinus thrombosis presenting with subarachnoid hemorrhage in a patient with aplastic anemia].

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).

Fatal outcome of a patient with severe aplastic anemia after treatment with metenolone acetate.

A 75-year-old man suffering from severe aplastic anemia was treated first with cyclosporin A, then with steroid pulse therapy, and subsequently with metenolone acetate. Marked elevation of transaminases was detected following initiation of treatment with metenolone acetate. This was followed by hepatic failure and death. Histopathological findings in autopsy specimens were compatible with the diagnosis of drug-induced liver impairment, for which metenolone acetate was considered the most likely causative agent. Liver impairment as a side effect of the use of this drug has been thought to be mild, reversible and rather infrequent. However, as demonstrated in the case described here, it is apparent that extreme caution should be exercised when using this drug in debilitated patients.

Superior sagittal sinus thrombosis associated with androgen therapy for hypoplastic anemia.

Of 27 patients with hypoplastic anemia treated between 1971 and 1974 with male hormone and protein-assimilating hormone, 3 developed superior sagittal sinus thrombosis (SSST). The clinical symptoms and signs and angiographic findings of SST were characteristic enough to allow an early diagnosis. Signs related to SST were seizures, hemiplegia, facial palsy, stupor, and coma, with the most important prodrome and consistent subjective complaint being headache. Following discontinuation of the hormone therapy, neurological signs and symptoms related to SSST gradually subsided. In all cases, the hematological picture improved with discontinuation of the hormone therapies. It appears that administration of male hormone can be associated with the development of SSST. If neurological symptoms and signs of SSST appear, administration of the hormones should be discontinued.

[Hyperlipoproteinaemia during additional methenolone administration in the treatment of metastasizing carcinoma of the breast]. / Hyperlipoproteinämie bei additiver Behandlung des metastasierenden Mammakarzinoms mit Metenolonönanthat.

The effect of additive administration of methenolone oenanthate (Primobolan) on lipid metabolism was studied in 28 menopausal women with metastasizing carcinoma of the breast. In ten women hyperlipoproteinaemia type IIa was demonstrated in the course of treatment, while in two there was hyperlipoproteinaemia type IIb. One of the latter patients had a myocardial infarction in the course of treatment. There was no relationship between the level of hypercholesterolaemia and the methenolone dosage. Nor was it possible to classify the type of cholesterolaemia as a bile stasis syndrome. The hyperlipoproteinaemia regressed in every case once methenolone treatment was discontinued.

Treatment of refractory anemias with methenolone.

A therapeutic trial with methenolone (Primobolan) in 19 consecutive patients with different types of refractory anemia is reported. The remission frequencies were: pancytopenia 3/6, bicytopenia 2/4, refractory anemia with hyperplastic marrow 1/5, myelofibrosis 1/4. There was no obvious prolongation of survival in the patients responding. Side-effects were negligible.

Treatment of disseminated carcinoma of the breast by metenolone enanthate.

Forty-three patients with disseminated or inoperable carcinoma of the breast were treated with Metenolone Enanthate (Primobolan Depot) with doses of 400 to 1 200 mg/week for at least 3 months. Objective remissions lasting longer than 3 months occurred in 8 out of 41 evaluable patients. Soft tissue metastases responsed best. Liver and brain metastases were unaffected. The therapeutic efficiency of Primobolan Depot is comparable to that of testosterone propionate but the agent is less virilising.