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Is growth hormone deficiency contributing to heart failure in patients with beta-thalassemia major?
Eva Marie Erfurth1, Helene Holmer, Per-Gunnar Nilsson
1Department of Endocrinology, Lund University Hospital, Lund, Sweden. Eva_Marie.Erfurth@med.lu.se
Insights
Growth hormone (GH) deficiency in beta-thalassemia major patients can cause heart failure. Restoring GH therapy reversed heart failure, suggesting GH
Area of Science:
- Cardiology
- Endocrinology
- Hematology
Background:
- Beta-thalassemia major (beta-TM) patients often experience complications due to iron overload.
- Growth hormone (GH) deficiency is a known endocrine complication in beta-TM.
- Heart failure is a severe manifestation in advanced beta-TM.
Observation:
- A 21-year-old woman with beta-TM and GH deficiency presented with end-stage heart failure (NYHA class IV).
- Her condition rapidly worsened after discontinuing recombinant human GH (rhGH) therapy.
- Myocardial biopsy revealed iron deposits but excluded myocarditis.
Findings:
- Intensified standard heart failure treatments and chelation were ineffective.
- Reintroducing rhGH alongside cardiac medications and low-dose desferrioxamine (DFO) led to reversal of heart failure.
- Cardiac function normalized within one year of GH reinitiation.
Implications:
- GH deficiency, potentially from iron-induced hypothalamic-pituitary damage, may significantly contribute to heart failure in adult beta-TM patients.
- This highlights the critical role of endocrine management, specifically GH replacement, in preventing and treating cardiac dysfunction in beta-TM.
- Early detection and management of GH deficiency are crucial for improving cardiovascular outcomes in beta-TM.
Abstract:
A 21-year-old woman with beta-thalassemia major (beta-TM) and GH deficiency developed end-stage heart failure, New York Heart Association (NYHA) functional class IV, within 3 months after withdrawal of recombinant human growth hormone (GH). A myocardial biopsy excluded myocarditis and showed moderate iron deposit in the heart. Before her admission, intensified treatments with digoxin, angiotensin-converting enzyme inhibitor, diuretics and extra chelation therapy (desferrioxamine (DFO)) had not improved her progressive heart failure. At admission, GH was reinstituted together with intensified treatment of cardiac drugs and low doses of DFO, and her heart failure reversed. Four months later, NYHA functional class II was reached and within 1 year her cardiac function was normalised. We suggest that GH deficiency due to iron-induced damage to the hypothalamic-pituitary axis can contribute to heart failure in adult patients with beta-TM.
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