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(Circulation Research. 2003;93:e75.)
© 2003 American Heart Association, Inc.

Letter to the Editor

Cardiac Failure Associated With G6PD Deficiency

Marjolein Drent

Department of Respiratory Medicine, Sarcoidosis Management Center, University Hospital Maastricht, Maastricht, The Netherlands, m.drent@lung.azm.nl

Anton P. Gorgels

Department of Cardiology, University Hospital Maastricht, Maastricht, The Netherlands

Aalt Bast

Department of Pharmacology and Toxicology, University Hospital Maastricht, Maastricht, The Netherlands

An extract of the first 250 words of the full text is provided, because this article has no abstract.

To the Editor:

Jain et al¹ made the very interesting suggestion that glucose-6-phosphate dehydrogenase (G6PD) deficiency contributes to cardiac dysfunction through increased susceptibility to oxidative injury and impairment of intracellular calcium transport in cardiomyocytes from rats. Additionally, they demonstrated the development of in vivo adverse structural remodeling and contractile dysfunction over time in a murine model of G6PD deficiency. A clinical finding in our hospital appears to corroborate and extend to humans the concepts enunciated by Jain et al.¹

In 2000, a 64-year-old black woman, originating from Curacao, was referred to the Sarcoidosis Management Center, a tertiary referral center for sarcoidosis in the Netherlands. The diagnosis of sarcoidosis, which she had carried for 6 years, was histologically confirmed by a liver biopsy in another hospital. In 1999, she consulted for the first time a pulmonary physician because of dyspnea and severe fatigue. Her complaints of dyspnea were progressive, especially during exercise. She never smoked and had no prior history of respiratory illness or relevant comorbidity. No environmental or occupational pulmonary risk factors were apparent. She had never been treated for her sarcoidosis. Physical examination revealed biventricular enlargement of the heart, an apical systolic murmur consistent with mitral regurgitation, and signs of right- and left-sided congestion with basal lung crepitations, increased central venous pressure, hepatomegaly, and ankle edema. Lung function tests revealed a mild restrictive defect with a moderate reduction of the CO diffusion test (69% of predicted.) A chest radiograph showed cardiomegaly and minimal pleural effusions on both sides without . . . [Full Text of this Article]