نتایج جستجو برای: pompe

تعداد نتایج: 1229  

Journal: :Human molecular genetics 2011
Barry J Byrne Darin J Falk Christina A Pacak Sushrusha Nayak Roland W Herzog Melissa E Elder Shelley W Collins Thomas J Conlon Nathalie Clement Brian D Cleaver Denise A Cloutier Stacy L Porvasnik Saleem Islam Mai K Elmallah Anatole Martin Barbara K Smith David D Fuller Lee Ann Lawson Cathryn S Mah

Pompe disease is an autosomal recessive metabolic myopathy caused by the deficiency of the lysosomal enzyme acid alpha-glucosidase and results in cellular lysosomal and cytoplasmic glycogen accumulation. A wide spectrum of disease exists from hypotonia and severe cardiac hypertrophy in the first few months of life due to severe mutations to a milder form with the onset of symptoms in adulthood....

2012
George Papadimas Gerassimos Terzis Constantinos Papadopoulos Anna Areovimata Konstantinos Spengos Stavros Kavouras Panagiota Manta

BACKGROUND Pompe disease is an inherited metabolic disorder characterized by α-glycosidase deficiency, which leads to lysosomal glycogen accumulation in many different tissues. The infantile form is the most severe with a rapidly fatal outcome, while the late onset form has a greater phenotypic variability, characterized by skeletal muscle dysfunction and early respiratory involvement. Bone min...

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...

2014
Istvan Katona Joachim Weis Frank Hanisch

BACKGROUND Glycogenosis type II or Pompe disease is an autosomal-recessive lysosomal storage disease due to mutations in the gene encoding acid alpha-glucosidase (GAA), an enzyme required for lysosomal glycogen degradation. The disease predominantly affects the skeletal and respiratory muscles but there is growing evidence of the involvement of smooth muscle cells in blood vessel walls, suggest...

Journal: :Revista Colombiana de Cardiología 2021

2013
Stephan C A Wens Carin M van Gelder Michelle E Kruijshaar Juna M de Vries Nadine A M E van der Beek Arnold J J Reuser Pieter A van Doorn Ans T van der Ploeg Esther Brusse

BACKGROUND Pompe disease has a broad clinical spectrum, in which the phenotype is partially explained by the genotype. The aim of this study was to describe phenotypical variation among siblings with non-classic Pompe disease. We hypothesized that siblings and families with the same genotype share more similar phenotypes than the total population of non-classic Pompe patients, and that this mig...

2005

Trois principaux stimulants rCgulent les secretions de l’estomac: l’acetylcholine, relarguee 2 partir des nerfs parasympathiques du vagus, la gastrine, relarguCe partir des cellules G de I’antrum du pylore de l’estomac, et l’histamine relarguke B partir de cellules contenues dans la muqueuse du fond. Pour tous ces trois s6crCtagogues des rCcepteurs ont CtC identifies sur la membrane basolatkral...

2014
I. Schneider M. Deschauer F. Hanisch

http://dx.doi.org/10.1016/j.ymgmr.2014.01.001 2214-4269/© 2014 The Authors. Published by Elsevier Inc. This is an open access article under the CC BY-NC-ND licen (http://creativecommons.org/licenses/by-nc-nd/3.0/). Patients with late-onset Pompe disease receiving enzyme replacement therapy (ERT) usually develop IgG antibodies against algucosidase alpha (anti-rhGAA) within the first 3 months. Th...

Journal: :Neuromuscular Disorders 2015
Laura E. Case Carl Bjartmar Claire Morgan Robin Casey Joel Charrow John P. Clancy Majed Dasouki Stephanie DeArmey Khan Nedd Mary Nevins Heidi Peters Dawn Phillips Zachary Spigelman Cynthia Tifft Priya S. Kishnani

Emerging phenotypes in long-term survivors with Pompe disease on standard enzyme replacement therapy (ERT) (alglucosidase alfa 20 mg/kg/2 weeks) can include patients with worsening motor function. Whether higher doses of ERT improve skeletal function in these patients has not been systematically studied. This exploratory, randomized, open-label, 52-week study examined the safety and efficacy of...

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