Literature DB >> 18757064

Cardiac evaluation in children and adults with Pompe disease sharing the common c.-32-13T>G genotype rarely reveals abnormalities.

N A M E van der Beek1, O I I Soliman, C I van Capelle, M L Geleijnse, W B Vletter, M A Kroos, A J J Reuser, I M E Frohn-Mulder, P A van Doorn, A T van der Ploeg.   

Abstract

BACKGROUND AND
OBJECTIVE: Pompe disease is an inherited metabolic disorder caused by deficiency of acid alpha-glucosidase. All affected neonates have a severe hypertrophic cardiomyopathy, leading to cardiac failure and death within the first year of life. We investigated the presence and extent of cardiac involvement in children and adults with Pompe disease with the common c.-32-13T>G genotype to determine the usefulness of cardiac screening in these patients with relatively 'milder' phenotypes.
METHODS: Cardiac dimensions and function were evaluated through echocardiography, electrocardiography and Holter monitoring. The total group comprised 68 patients with Pompe disease, of whom 22 patients had disease onset before the age of 18.
RESULTS: Two patients (3%) had cardiac abnormalities possibly related to Pompe disease: Electrocardiography showed a Wolff-Parkinson-White pattern in an 8-year-old girl, and one severely affected adult patient had a mild hypertrophic cardiomyopathy. This hypertrophy did not change during treatment with recombinant human alpha-glucosidase. In addition, four adult patients showed minor cardiac abnormalities which did not exceed the prevalence in the general population and were attributed to advanced age, hypertension or pre-existing cardiac pathology unrelated to Pompe disease.
CONCLUSIONS: Cardiac involvement is rare in Pompe patients with the common c.-32-13T>G genotype. The younger patients were not more frequently affected than the adults. Electrocardiographic evaluation appears to be appropriate as initial screening tool. Extensive cardiac screening seems indicated only if the electrocardiogram is abnormal or the patient has a history of cardiac disease.

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Year:  2008        PMID: 18757064     DOI: 10.1016/j.jns.2008.07.013

Source DB:  PubMed          Journal:  J Neurol Sci        ISSN: 0022-510X            Impact factor:   3.181


  5 in total

1.  Cardiovascular abnormalities in late-onset Pompe disease and response to enzyme replacement therapy.

Authors:  Daniel Forsha; Jennifer S Li; P Brian Smith; Ans T van der Ploeg; Priya Kishnani; Sara K Pasquali
Journal:  Genet Med       Date:  2011-07       Impact factor: 8.822

2.  Clinical features and predictors for disease natural progression in adults with Pompe disease: a nationwide prospective observational study.

Authors:  Nadine A M E van der Beek; Juna M de Vries; Marloes L C Hagemans; Wim C J Hop; Marian A Kroos; John H J Wokke; Marianne de Visser; Baziel G M van Engelen; Jan B M Kuks; Anneke J van der Kooi; Nicolette C Notermans; Karin G Faber; Jan J G M Verschuuren; Arnold J J Reuser; Ans T van der Ploeg; Pieter A van Doorn
Journal:  Orphanet J Rare Dis       Date:  2012-11-12       Impact factor: 4.123

3.  Small-fiber neuropathy in pompe disease: first reported cases and prospective screening of a clinic cohort.

Authors:  Lisa D Hobson-Webb; Stephanie L Austin; Sneha Jain; Laura E Case; Karla Greene; Priya S Kishnani
Journal:  Am J Case Rep       Date:  2015-04-03

4.  GAA Deficiency in Pompe Disease Is Alleviated by Exon Inclusion in iPSC-Derived Skeletal Muscle Cells.

Authors:  Erik van der Wal; Atze J Bergsma; Tom J M van Gestel; Stijn L M In 't Groen; Holm Zaehres; Marcos J Araúzo-Bravo; Hans R Schöler; Ans T van der Ploeg; W W M Pim Pijnappel
Journal:  Mol Ther Nucleic Acids       Date:  2017-03-14

5.  Pattern and prognostic value of cardiac involvement in patients with late-onset pompe disease: a comprehensive cardiovascular magnetic resonance approach.

Authors:  Matthias Boentert; Anca Florian; Bianca Dräger; Peter Young; Ali Yilmaz
Journal:  J Cardiovasc Magn Reson       Date:  2016-12-07       Impact factor: 5.364

  5 in total

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