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      Performance-Enhancing Drugs Abuse Caused Cardiomyopathy and Acute Hepatic Injury in a Young Bodybuilder

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          Abstract

          A number of performance-enhancing drugs (PEDs) are used illicitly to improve muscle strength by the bodybuilders. The misuse of these drugs is associated with serious adverse effects to different organs. A previously healthy 22-year-old male bodybuilder after taking stanozolol, clenbuterol, and triiodothyronine for 10 days presented to the hospital with symptoms of icteric sclera, progressive dyspnea, intermittent cough, and bloody sputum. He was diagnosed with dilated cardiomyopathy and acute hepatic injury. Rapidly progressive dilated cardiomyopathy and acute hepatic injury among bodybuilders in such a short period of time have not been reported. People using these drugs must monitor liver and cardiac functions regularly, and they should discontinue using PEDs after diagnosis of liver or cardiac abnormalities. Physicians should always consider the possibility of the PED abuse in the context of a young athlete suffering cardiomyopathy or hepatic injury.

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          Most cited references 27

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          Nongenomic actions of thyroid hormone.

          The nongenomic actions of thyroid hormone begin at receptors in the plasma membrane, mitochondria or cytoplasm. These receptors can share structural homologies with nuclear thyroid hormone receptors (TRs) that mediate transcriptional actions of T3, or have no homologies with TR, such as the plasma membrane receptor on integrin αvβ3. Nongenomic actions initiated at the plasma membrane by T4 via integrin αvβ3 can induce gene expression that affects angiogenesis and cell proliferation, therefore, both nongenomic and genomic effects can overlap in the nucleus. In the cytoplasm, a truncated TRα isoform mediates T4-dependent regulation of intracellular microfilament organization, contributing to cell and tissue structure. p30 TRα1 is another shortened TR isoform found at the plasma membrane that binds T3 and mediates nongenomic hormonal effects in bone cells. T3 and 3,5-diiodo-L-thyronine are important to the complex nongenomic regulation of cellular respiration in mitochondria. Thus, nongenomic actions expand the repertoire of cellular events controlled by thyroid hormone and can modulate TR-dependent nuclear events. Here, we review the experimental approaches required to define nongenomic actions of the hormone, enumerate the known nongenomic effects of the hormone and their molecular basis, and discuss the possible physiological or pathophysiological consequences of these actions.
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            Rapid nongenomic actions of thyroid hormone.

            The binding of thyroid hormone to the thyroid hormone receptor (TR) mediates important physiological effects. However, the transcriptional effects of TR mediated by the thyroid response element (TRE) cannot explain many actions of thyroid hormone. We postulate that TR can initiate rapid, non-TRE-mediated effects in the cardiovascular system through cross-coupling to the phosphatidylinositol 3-kinase (PI3-kinase)/protein kinase Akt pathway. In vascular endothelial cells, the predominant TR isoform is TRalpha1. Treatment of endothelial cells with L-3,5,3'-triiodothyronine (T3) increased the association of TRalpha1 with the p85alpha subunit of PI3-kinase, leading to the phosphorylation and activation of Akt and endothelial nitric oxide synthase (eNOS). The activation of Akt and eNOS by T3 was abolished by the PI3-kinase inhibitors, LY294002 and wortmannin, but not by the transcriptional inhibitor, actinomycin D. To determine the physiological relevance of this PI3-kinase/Akt pathway, we administered T3 to mice undergoing transient focal cerebral ischemia. Compared with vehicle, a single bolus infusion of T3 rapidly increased Akt activity in the brain, decreased mean blood pressure, reduced cerebral infarct volume, and improved neurological deficit score. These neuroprotective effects of T3 were greatly attenuated or absent in eNOS-/- and TRalpha1-/-beta-/- mice and were completely abolished in WT mice pretreated with LY294002 or a T3 antagonist, NH-3. These findings indicate that the activation of PI3-kinase/Akt pathways can mediate some of the rapid, non-TRE effects of TR and suggest that the activation of Akt and eNOS contributes to some of the acute vasodilatory and neuroprotective effects of thyroid hormone.
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              Serious cardiovascular side effects of large doses of anabolic steroids in weight lifters.

              Pathological cardiovascular manifestations are reported in four male patients, who had taken massive amounts of anabolic steroids while undergoing many years of strength training. One patient was referred because of ventricular fibrillation during exercise, one because of clinically manifest heart failure, and one because of arterial thrombus in his lower left leg. The fourth patient was persuaded to attend for a check-up because of a long history of massive use of anabolic steroids. All four patients had cardiac hypertrophy. Two of the patients had symptoms and signs of heart failure, and one of these two had a massive thrombosis in both right and left ventricles of his heart. After cessation of the use of anabolic steroids in the other patient with heart failure, left ventricular wall thickness reduced quickly from 12 to 10.5 mm, and fractional shortening increased from 14% to 27%. Endomyocardial biopsy revealed increased fibrosis in the myocardium in two of the three cases. HDL-cholesterol was 0.58 mmol.l-1 and 0.35 mmol.l-1 in the two patients still using multiple anabolic steroids at the time of investigation. The cardiovascular findings described in the present paper should warn all physicians and athletes about the possible serious acute and long-term side effects of the massive use of anabolic steroids.
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                Author and article information

                Journal
                Am J Mens Health
                Am J Mens Health
                JMH
                spjmh
                American Journal of Men's Health
                SAGE Publications (Sage CA: Los Angeles, CA )
                1557-9883
                1557-9891
                21 June 2018
                September 2018
                : 12
                : 5
                : 1700-1704
                Affiliations
                [1 ]Department of Cardiovascular Medicine, The First Hospital of Jilin University, Changchun, China
                Author notes
                Dr. Yonggang Wang, Department of Cardiovascular Medicine, The First Hospital of Jilin University, Xinmin Street 71, Changchun 130021, China. Email: xiaogang94@ 123456163.com
                Prof Jian Sun, Department of Cardiovascular Medicine, The First Hospital of Jilin University, Xinmin Street 71, Changchun 130021, China. Email: sunjianemail@ 123456126.com
                Article
                10.1177_1557988318783504
                10.1177/1557988318783504
                6142118
                29926766
                © The Author(s) 2018

                This article is distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 License ( http://www.creativecommons.org/licenses/by-nc/4.0/) which permits non-commercial use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access pages ( https://us.sagepub.com/en-us/nam/open-access-at-sage).

                Funding
                Funded by: Jilin Province Science and Technology Project, ;
                Award ID: 20170520012JH
                Funded by: National Natural Science Foundation of China, FundRef https://doi.org/10.13039/501100001809;
                Award ID: 81400279
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                Original Articles

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