{"title":"Danazol causes significant changes in the cardiometabolic profile of patients with acquired aplastic anaemia","authors":"Hitesh Gurjar , Ankur Jain , Sujata Wangkheimayum , Subhash Varma , Rajesh Vijayvergiya , Pankaj Malhotra","doi":"10.1016/j.bcmd.2025.102921","DOIUrl":null,"url":null,"abstract":"<div><h3>Background</h3><div>Danazol is frequently used in treating patients with acquired aplastic anaemia (AA) in resource-constraint settings. We aimed to evaluate the cardiometabolic side effects of Danazol in patients with AA.</div></div><div><h3>Methods</h3><div>This prospective study included newly-diagnosed AA patients ≥13 years of age who were eligible for Danazol monotherapy (10 mg/kg/day, capped at 600 mg/day). Lipid profile and two-dimensional echocardiogram were obtained at the baseline and after 6 months of Danazol treatment. Transfusion of blood products and liver function test-based dose adjustments were done as indicated. Pre- and post-treatment parameters were compared using SPSS software version 25.</div></div><div><h3>Results</h3><div>36 patients (median age, 28.5 years) were enrolled. HDL cholesterol decreased by 30 % (p ≤0.001), and LDL cholesterol increased by 11 % (p = 0.002) at the end of 6 months. At the end of 6 months, there was a significant increase in the left ventricular (LV) ejection fraction (p = 0.001), LV mass (p ≤0.001), peak A-velocity (p = 0.01), isovolumetric relaxation time (p = 0.032), and a significant decrease in peak E-velocity (p ≤0.00) and Tei index (p = 0.031). Right ventricular E/A ratio also decreased significantly (p < 0.001).</div></div><div><h3>Conclusions</h3><div>Danazol treatment causes profound dyslipidaemia and potential cardiac dysfunction in patients with AA.</div></div>","PeriodicalId":8972,"journal":{"name":"Blood Cells Molecules and Diseases","volume":"112 ","pages":"Article 102921"},"PeriodicalIF":2.1000,"publicationDate":"2025-03-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Blood Cells Molecules and Diseases","FirstCategoryId":"3","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S1079979625000130","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"HEMATOLOGY","Score":null,"Total":0}
引用次数: 0
Abstract
Background
Danazol is frequently used in treating patients with acquired aplastic anaemia (AA) in resource-constraint settings. We aimed to evaluate the cardiometabolic side effects of Danazol in patients with AA.
Methods
This prospective study included newly-diagnosed AA patients ≥13 years of age who were eligible for Danazol monotherapy (10 mg/kg/day, capped at 600 mg/day). Lipid profile and two-dimensional echocardiogram were obtained at the baseline and after 6 months of Danazol treatment. Transfusion of blood products and liver function test-based dose adjustments were done as indicated. Pre- and post-treatment parameters were compared using SPSS software version 25.
Results
36 patients (median age, 28.5 years) were enrolled. HDL cholesterol decreased by 30 % (p ≤0.001), and LDL cholesterol increased by 11 % (p = 0.002) at the end of 6 months. At the end of 6 months, there was a significant increase in the left ventricular (LV) ejection fraction (p = 0.001), LV mass (p ≤0.001), peak A-velocity (p = 0.01), isovolumetric relaxation time (p = 0.032), and a significant decrease in peak E-velocity (p ≤0.00) and Tei index (p = 0.031). Right ventricular E/A ratio also decreased significantly (p < 0.001).
Conclusions
Danazol treatment causes profound dyslipidaemia and potential cardiac dysfunction in patients with AA.
期刊介绍:
Blood Cells, Molecules & Diseases emphasizes not only blood cells, but also covers the molecular basis of hematologic disease and studies of the diseases themselves. This is an invaluable resource to all those interested in the study of hematology, cell biology, immunology, and human genetics.