نتایج جستجو برای: pompe disease

تعداد نتایج: 1490290  

2013
Kristin M. Taylor Elizabeth Meyers Michael Phipps Priya S. Kishnani Seng H. Cheng Ronald K. Scheule Rodney J. Moreland

Pompe disease, also known as glycogen storage disease (GSD) type II, is caused by deficiency of lysosomal acid α-glucosidase (GAA). The resulting glycogen accumulation causes a spectrum of disease severity ranging from a rapidly progressive course that is typically fatal by 1 to 2 years of age to a slower progressive course that causes significant morbidity and early mortality in children and a...

2011
L. Martino

(the only available biomarker of muscle glycogenosis type II) and brain MRI if there are symptoms suggestive of CNS involvement. In conclusion, being available the ERT therapy, it is really important to diagnose Pompe disease as soon as possible to avoid respiratory and skeletal muscle degeneration. Group Observational clinical study in juvenile-adult glycogenosis type 2 patients undergoing enz...

Journal: :Molecular therapy : the journal of the American Society of Gene Therapy 2013
Darin J Falk Cathryn S Mah Meghan S Soustek Kun-Ze Lee Mai K Elmallah Denise A Cloutier David D Fuller Barry J Byrne

Pompe disease is a neuromuscular disease resulting from deficiency in acid α-glucosidase (GAA), results in cardiac, skeletal muscle, and central nervous system (CNS) pathology. Enzyme replacement therapy (ERT) has been shown to partially correct cardiac and skeletal muscle dysfunction. However, ERT does not cross the blood-brain barrier and progressive CNS pathology ensues. We tested the hypoth...

Journal: :Clinical chemistry 2002
Tina Rozaklis Steven L Ramsay Phillip D Whitfield Enzo Ranieri John J Hopwood Peter J Meikle

BACKGROUND The development of therapies for lysosomal storage disorders has created a need for biochemical markers to monitor the efficacy of therapy and methods to quantify these markers in biologic samples. In Pompe disease, the concentration of a tetrasaccharide, consisting of four glucose residues, is reputedly increased in urine and plasma, but faster and more sensitive methods are require...

Journal: :Orphanet Journal of Rare Diseases 2015

Journal: :Orphanet journal of rare diseases 2016
C I van Capelle J C van der Meijden J M P van den Hout J Jaeken M Baethmann T Voit M A Kroos T G J Derks M E Rubio-Gozalbo M A Willemsen R H Lachmann E Mengel H Michelakakis J C de Jongste A J J Reuser A T van der Ploeg

BACKGROUND As little information is available on children with non-classic presentations of Pompe disease, we wished to gain knowledge of specific clinical characteristics and genotypes. We included all patients younger than 18 years, who had been evaluated at the Pompe Center in Rotterdam, the Netherlands, between 1975 and 2012, excluding those with the classic-infantile form. None were treate...

Journal: :Journal of Internal Medicine 2009

Journal: :Molecular Genetics and Metabolism Reports 2016

Journal: :BMC Musculoskeletal Disorders 2013

Journal: :Annals of Translational Medicine 2019

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