ABSTRACT
Anthracycline-induced cardiomyopathy has been noted as a non-neglectable issue in the field of clinical oncology. Remarkable progress has been achieved in searching for inherited susceptible genetic deficits underlying anthracycline cardiotoxicity in the past several years. In this case report, we present the preliminary results of a genetic study in a young male patient who was treated with standard dose anthracycline-based chemotherapy for his acute myeloid leukemia and attacked by acute congestive heart failure after just two courses of therapy. After a survey of 76 target genes, an in-frame deletion of the titin gene was recognized as the most possible genetic defect responsible for his cardiomyopathy caused by anthracycline. This defect proved to pass down from the patient's mother and did not exist in seven unrelated chemotherapy-treated cancer patients without chemotherapy-induced cardiomyopathy and four other healthy volunteer DNA donors.
Subject(s)
Anthracyclines , Cardiomyopathies , Anthracyclines/adverse effects , Antibiotics, Antineoplastic/adverse effects , Cardiomyopathies/chemically induced , Cardiomyopathies/complications , Cardiomyopathies/genetics , Cardiotoxicity/etiology , Causality , Connectin/genetics , Humans , MaleABSTRACT
A 66-year-old man with a previous history of advanced prostate cancer failing complete androgen blockade, docetaxel chemotherapy, denosumab, and abiraterone acetate as judged by persistent high serum levels of prostate specific antigen presented with exertional dyspnea, normocytic anemia, and thrombocytopenia. Leukoery - throblastosis was noted in his peripheral blood. Bone marrow examination disclosed diffuse bone marrow carcinomatosis from prostate cancer. Prolonged activated partial thromboplastin time, prothrombin time, and an extremely elevated serum level of Ddimer led to a diagnosis of disseminated intravascular coagulation. Magnetic resonance imaging of spine revealed extensive bone marrow involvement but bone scan showed only scanty bony metastasis. We like to call attention to the importance of prompt bone marrow examination once recognizing leukoerythroblastosis in patients with advanced prostate cancer. Survey of a possible coexistent disseminated intravascular coagulation is as well strongly recommended in this condition.
