نتایج جستجو برای: pompe

تعداد نتایج: 1229  

Journal: :Pediatrics 2009
Yin-Hsiu Chien Ni-Chung Lee Beth L Thurberg Shu-Chuan Chiang Xiaokui Kate Zhang Joan Keutzer Ai-Chu Huang Mei-Hwan Wu Pei-Hsin Huang Fuu-Jen Tsai Yuan-Tsong Chen Wuh-Liang Hwu

OBJECTIVE Pompe disease causes progressive, debilitating, and often life-threatening musculoskeletal, respiratory, and cardiac symptoms. Favorable outcomes with early intravenous enzyme-replacement therapy and alglucosidase alfa have been reported, but early clinical diagnosis before the development of severe symptoms has rarely been possible in infants. METHODS We recently conducted a newbor...

2017
Katherine Johnson Ana Töpf Marta Bertoli Lauren Phillips Kristl G. Claeys Vidosava Rakocevic Stojanovic Stojan Perić Andreas Hahn Paul Maddison Ela Akay Alexandra E. Bastian Anna Łusakowska Anna Kostera-Pruszczyk Monkol Lek Liwen Xu Daniel G. MacArthur Volker Straub

BACKGROUND Late-onset Pompe disease is a rare genetic neuromuscular disorder caused by a primary deficiency of α-glucosidase and the associated accumulation of glycogen in lysosomal vacuoles. The deficiency of α-glucosidase can often be detected using an inexpensive and readily accessible dried blood spot test when Pompe disease is suspected. Like several neuromuscular disorders, Pompe disease ...

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...

2016
Phillip A Doerfler Sushrusha Nayak Manuela Corti Laurence Morel Roland W Herzog Barry J Byrne

Enzyme and gene replacement strategies have developed into viable therapeutic approaches for the treatment of Pompe disease (acid α-glucosidase (GAA) deficiency). Unfortunately, the introduction of GAA and viral vectors encoding the enzyme can lead to detrimental immune responses that attenuate treatment benefits and can impact patient safety. Preclinical and clinical experience in addressing h...

2013
CARMEN ESMER ROSARIO BECERRA-BECERRA CLAUDIA PEÑA-ZEPEDA ANTONIO BRAVO-ORO

Glycogen-storage disease type II, also named Pompe disease, is caused by the deficiency of the enzyme acid alpha-glucosidase, which originates lysosomal glycogen accumulation leading to progressive neuromuscular damage. Early-onset Pompe disease shows a debilitating and frequently fulminating course. To date, more than 300 mutations have been described; the majority of them are unique to each a...

2013
Deniz Güngör Michelle E Kruijshaar Iris Plug Ralph B D’Agostino Marloes LC Hagemans Pieter A van Doorn Arnold JJ Reuser Ans T van der Ploeg

BACKGROUND Pompe disease is a rare metabolic myopathy for which disease-specific enzyme replacement therapy (ERT) has been available since 2006. ERT has shown efficacy concerning muscle strength and pulmonary function in adult patients. However, no data on the effect of ERT on the survival of adult patients are currently available. The aim of this study was to assess the effect of ERT on surviv...

Journal: :Molecular genetics and metabolism 2016
Ans van der Ploeg Pierre G Carlier Robert-Yves Carlier John T Kissel Benedikt Schoser Stephan Wenninger Alan Pestronk Richard J Barohn Mazen M Dimachkie Ozlem Goker-Alpan Tahseen Mozaffar Loren D M Pena Zachary Simmons Volker Straub Michela Guglieri Peter Young Matthias Boentert Pierre-Yves Baudin Stephan Wens Raheel Shafi Carl Bjartmar Beth L Thurberg

BACKGROUND Late-onset Pompe disease is characterized by progressive skeletal myopathy followed by respiratory muscle weakness, typically leading to loss of ambulation and respiratory failure. In this population, enzyme replacement therapy (ERT) with alglucosidase alfa has been shown to stabilize respiratory function and improve mobility and muscle strength. Muscle pathology and glycogen clearan...

2013
ANTONIO TOSCANO FEDERICA MONTAGNESE OLIMPIA MUSUMECI

Pompe disease, also known as Glycogen Storage Disease type II (GSD II), is a rare autosomal recessive disorder , due to α-glucosidase A (GAA) deficiency. This was the first disease identified as a lysosomal storage disorder in 1963 (1) and is characterized by a glycogen accumulation in multiple tissues with a predilection of skeletal muscle and heart. Depending on age of onset, two different cl...

2016
Matthias Boentert Anca Florian Bianca Dräger Peter Young Ali Yilmaz

BACKGROUND Pompe disease is an autosomal recessive disorder caused by deficiency of the lysosomal α-1,4-glucosidase leading to accumulation of glycogen in target tissues with progressive organ failure. While the early infantile-onset form is characterized by early severe hypertrophic cardiomyopathy with cardiac and respiratory failure, clinically relevant cardiomyopathy seems to be uncommon in ...

Journal: :Clinica chimica acta; international journal of clinical chemistry 2014
Tze-Kiong Er Chih-Chieh Chen Yin-Hsiu Chien Wen-Chen Liang Tzu-Min Kan Yuh-Jyh Jong

BACKGROUND Pompe disease is an inherited autosomal recessive deficiency of acid α-glucosidase (GAA) and is due to pathogenic sequence variants in the corresponding GAA gene. While the analysis of enzyme activity remains the diagnostic test of choice for individuals with Pompe disease, mutation analysis remains for establishing a definitive diagnosis. METHODS High resolution melting (HRM) anal...

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