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Hi,
Could you tell me if you notice any improvement on Losartan?
Thank you very much
Tina said:
Dr. Chris Spurney, cardiologist at CNMC in Washington, DC is suppose to run the losartan trial at CNMC. He may be coordinating all efforts with the Hopkins team. Atleast this is my understanding from a recent meeting I attended. I have no idea when this trial will launch off the ground. My son is taking 50mg at bedtime and tolertaing the drug without experiencing any adverse side effects thus far. He was started on the drug in July 2009. I handed Dr. Leshner, our son's neurologist at CNMC, several articles re: the losartan's effects in muscle in mdx models and then dog models. He finally consented to writing the prescription for the drug. At first, our son was prescribed 12.5mg daily then the dosage was slowly increased to where he is now, at 50mg daily. Feel free to inbox me if you are interested in receiving the articles. I can email them to you.
Paul - UC Davis in Sacramento is starting (finally!) the trial to compare Losartan vs. Linosopril (the ACE Inhibitor Sharon mentions below). They are recruiting participants now.
Christopher F. Spurney, Arpana Sali, Alfredo D. Guerron, Micaela Iantorno, Qing Yu, Heather Gordish-Dressman, Sree Rayavarapu, Jack van der Meulen, Eric P. Hoffman, and Kanneboyina Nagaraju - USA
Recent studies showed that chronic administration of losartan, an angiotensin II type I receptor antagonist, improved skeletal muscle function in dystrophin-deficient mdx mice. In this study, C57BL/10ScSn-Dmdmdx/J female mice were either untreated or treated with losartan (n = 15) in the drinking water at a dose of 600 mg/L over a 6-month period. Cardiac function was assessed via in vivo high frequency echocardiography and skeletal muscle function was assessed using grip strength testing, Digiscan monitoring, Rotarod timing, and in vitro force testing. Fibrosis was assessed using picrosirius red staining and Image J analysis. Gene expression was evaluated using real-time polymerized chain reaction (RT-PCR). Percentage shortening fraction was significantly decreased in untreated (26.9% ± 3.5%) mice compared to losartan-treated (32.2% ± 4.2%; P < .01) mice. Systolic blood pressure was significantly reduced in losartan-treated mice (56 ± 6 vs 69 ± 7 mm Hg; P < .0005). Percentage cardiac fibrosis was significantly reduced in losartan-treated hearts (P < .05) along with diaphragm (P < .01), extensor digitorum longus (P < .05), and gastrocnemius (P < .05) muscles compared to untreated mdx mice. There were no significant differences in skeletal muscle function between treated and untreated groups. Chronic treatment with losartan decreases cardiac and skeletal muscle fibrosis and improves cardiac systolic function in dystrophin-deficient mdx mice.
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