IntroductionCardiac toxicity is one of the life-threatening complications of cancer therapy. Systemic anticancer treatments may exert their own toxic effects or can aggravate adverse effects of other drugs. We report a case of cyclophosphamide-induced cardiotoxicity in a patient with normal cardiac functions before chemotherapy.Case presentationA 66-year-old Caucasian woman with a mediastinal mass diagnosed with Burkitt lymphoma underwent chemotherapy with rituximab-hyperfractionated-cyclophosphamide-vincristine-doxorubicin-dexamethasone. On the seventh day of chemotherapy, she developed dyspnea. An electrocardiogram demonstrated low voltage in the limb and precordial leads. It also showed diffusely increased myocardial echogenicity, mild pericardial and pleural effusion, generally impaired biventricular systolic functions with a left ventricular ejection fraction of 31%, and right ventricular mid-apical akinesia, even though she had normal biventricular functions before chemotherapy. Cyclophosphamide-induced cardiotoxicity was suspected and she was given treatment for congestive heart failure. Her dyspnea decreased and she was discharged on the tenth day with a left ventricular ejection fraction of 37% and normal right ventricular function. After 1 month, echocardiography showed normal biventricular functions with a left ventricular ejection fraction of 60%.ConclusionsDrug-induced cardiotoxicity, therefore, should be taken into consideration when using cyclophosphamide therapy, especially when anthracyclines are co-administered. Close communication between hematologists and cardiologists is required.
The novel drug protocols significantly increased the quality of the responses of elderly patients with MM to therapy, but they did not increase the patients' tolerability.
Congenital dysfibrinogenemia is a rare autosomal recessive bleeding disorder, which is characterized by the absence of functional fibrinogen. Patients may have bleeding and paradoxical arterial and venous thrombotic problems from early childhood. The optimal antithrombotic therapy in these patients hasn't been determined yet. In this report we present a dysfibrogenemic patient, who has suffered recurrent arterial thrombosis under aspirin treatment. Intravenous fibrinogen concentrates (fc) along with reduced doses of rivaroxaban (10 mg daily), cilostazol (50 mg bid) and aspirin (100 mg daily) were given as antithrombotic treatment. The pain and the cyanosis clinically recovered within 6 weeks. This is, to our knowledge, the first time in which a new oral anticoagulant, rivaroxaban and cilostazol combination was used in a dysfibrinogenemic patient with thrombotic episodes. We determined the type, the dosage and the duration of antithrombotic treatment according to the clinical progress of the symptoms. Rivaroxaban, cilostazol and fibrinogen concentrate replacement; combination may represent a useful alternative for the antithrombotic treatment in dysfibrinogenemic patients.
Molecular balance between Angiopoietin-1 (Ang-1) and Angiopoietin-2 (Ang-2) has important effects in tumor angiogenesis. Ang-2 was shown to be elevated and proved to be a prognostic factor in acute myeloid leukemia (AML). To date studies revealed increased angiogenesis in bone marrows (BMs) of both myeloproliferative neoplasm (MPN) and AML patients. We conducted this study to demonstrate circulating levels of Ang-1 and Ang-2 in MPN patients since no data exists in literature. Thirty-three newly diagnosed MPN, 27 newly diagnosed AML patients and 25 controls (HC) were enrolled and Angiopoietin levels were determined with ELISA. We found that Ang-1 levels were higher whereas Ang-2 levels were lower in MPN and HC when compared to AML. Our results suggest that though angiogenesis is increased in both AML and MPN, angiopoietin serum level profile of the two diseases are different, and MPN patients have similar Ang-1 and Ang-2 levels as HC. We conclude that, according to our results Ang-1 and Ang-2 do not only regulate tumor angiogenesis and the difference between angiopoietin levels of acute and chronic myeloid neoplasms could be a reflection of other effects of these growth factors on tumor malignancy.
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