Background: Patients developing cancer treatment-related left ventricular dysfunction (CTrLVD) require a prompt therapy. Hypotension, dizziness, and fatigue often limit the use of angiotensin-converting enzyme inhibitors (ACEi), angiotensin receptor blockers (ARB), and β-blockers (BB) in cancer patients who may already be afflicted by these symptoms. Ivabradine is a heart rate-lowering drug that does not cause hypotension and may be used in heart failure with reduced left ventricular ejection fraction (LVEF). Objective: The aim of this paper was to investigate the role of ivabradine to treat CTrLVD. Methods: A retrospective analysis in a cohort of 30 patients with CTrLVD (LVEF < 50%) receiving ivabradine on top of the maximal tolerated dose of ACEi/ARB and BB was performed. We evaluated cardiovascular treatment, oncologic treatment, LVEF, functional class (New York Heart Association [NYHA]), and fatigue during the study period. Results: Ivabradine was initially started at the dose of 2.5 mg/b.i.d. in most patients and then carefully titrated. Hypotension (70%) and fatigue (77%) were the main causes limiting the treatment with ACEi/ARB and BB. After a mean follow-up of 6.5 months, LVEF increased from 45.1% (SD = 6.4) to 53.2% (SD = 3.9; p < 0.001). When patients were analyzed according to the type of cancer therapy, no difference in LVEF changes across the groups was found. NYHA class ameliorated in 11 patients, while fatigue improved in 8 patients. No serious cardiovascular side effects were reported. Conclusions: The ability to improve symptoms and LVEF in unfit cancer patients makes ivabradine a reasonable pharmacological tool for treating CTrLVD.

Rituximab is a murine/human chimeric monoclonal antibody directed against the CD20 antigen. It is widely used in combination with polychemotherapy regimens for the treatment of hematological disorders. There is no evidence of direct cardiotoxicity of the drug but a few cases of cardiovascular adverse events have been reported in the literature. We report on two patients affected by stage IV non-Hodgkin lymphoma with bone marrow infiltration and peripheral blood involvement who experienced cardiovascular accidents temporally related to rituximab infusion. In both cases the monoclonal antibody was administered in association with a polychemotherapy regimen but administration was postponed several days later in order to avoid severe cytokine release syndrome because of the high tumor burden. The first case concerns an episode of atrial fibrillation in a patient with a diagnosis of small B-cell lymphoma. The episode happened immediately after rituximab infusion. In the second case there was an episode of chest pain associated with fever and chills during rituximab infusion in a patient with a diagnosis of mantle cell lymphoma. In both cases we noticed an unusual correlation between symptom recurrence and the speed of rituximab infusion. Both patients presented several cardiovascular risk factors but preliminary cardiac function assessment excluded signs of heart dysfunction. The pathogenesis of cardiovascular events during rituximab infusion remains unclear. A key role might be played by cytokine release from B cells as a consequence of rituximab activity. Moreover, pre-existing silent cardiac damage could be co-responsible for the clinical manifestations we reported. We consider our clinical experience relevant because it raises an issue of good clinical practice: despite rituximab's good tolerability profile, patients with cardiovascular risk factors should undergo accurate cardiac assessment so that silent heart disease can be detected. If the suspicion of cardiac damage is high, more extensive cardiac assessment is recommended.

No abstract

<p class="MsoNormal"> <span lang="EN-US">Human toxocariasis is a widespread parasitic disease caused by ingestion of <i>Toxocara canis</i> or <i>catis</i> larvae or eggs. Parasitic diseases are uncommon in industrialized countries, yet this problem has not disappeared. Parasitic diseases can cause different syndrome (visceral larva migrans, ocular larva migrans) and the clinical features can be confusing. Severe organ involvement affecting the liver, lungs, nervous central system and eyes can lead to serious damage. We present a case of toxocariasis presenting with fever,</span><span lang="EN-US"> </span><span lang="EN-US">desaturation and cholestatic hepatitis. Only the subsequent appearance of eosinophilia helped us to arrive at the correct diagnosis. Prompt diagnosis allowed specific therapy avoiding permanent complications.</span><span lang="EN-US"><o:p></o:p></span> </p>

Background The majority of myelodysplastic syndrome (MDS), primary myelofibrosis (MPN) and aplastic anemia (AA) patients during the course of the disease develops a symptomatic anemia requiring transfusions of packed red blood cells (PRBC), each of them containing approximately 200 mg of elementary iron. Because of the fact that human beings are unable to actively eliminate iron from the body, secondary emosiderosis yet becomes evident when body iron content is above 7-14 grams, an amount easily reached after receiving as few as 15-30 PRCB units.From a pathophysiologic point of view, long-term transfusion therapy is certainly the most important cause of iron overload (IOL) in these patients; nevertheless, others mechanism account for this phenomenon, and in particular the role of the ineffective erythropoiesis.Deferasirox (DSX) is the principal option currently available for iron chelation therapy in the management of IOL due to transfusion dependent anemia. DSX is also a potent NF-kB inhibitor, and this effect may explain in part the phenomenon of hematological improvements reported in different clinical trials and in case reports. Materials and Methods We analyzed 21 patients,16 male and 5 female, with transfusion dependent anemia and with a transfusional history of almost 10 packed PRBC, treated with DSX from 1 February 2013 to 1 February 2014. Median age was 80 years (65-88). 20 patients (95%) have almost a comorbidity, 7 of them (30%) have more than 3 comorbidities. Heart disease was the most common comorbidity. At baseline median creatinine clearance was 76 ml/min; in 12 patients was < 60ml/min but >40 ml/min, according to NCCN Guidelines. All patients (16 MDS, 3 MPN, 1 AA, 1 hemolytic anemia) were evaluated for IOL by serum ferritin (SF), while only 7 with RM T2*.Median SF at baseline was 1750 μg/L and median PRBC was 32.The starting dose of DSX was 10 mg/kg/day; the dosage should be adjusted up to 20–30 mg/kg/daily according to the transfusional regimen, SF and IOL, if tolerated. Objectives To observe safety, tolerability, and efficacy of iron chelation therapy with DSX in older patients with transfusion dependent anemia. Results The SF decreased of 50% and 66% after 3 and 6 months respectively. The SF was normalized (SF<500 μg/L) in 5 patients (24%) after six months. The IOL occurred also in patients with a short transfusional history, inferior to 10 packed red blood cells, and SF <1000 μg/L. That was more evident in MDS patients especially in RARS. The median dose tolerated of DSX was 20 mg/kg/daily.The drug related adverse events (AE) was evaluated by the Common Terminology Criteria for Adverse Events (CTCAE versione 4.02). The severe adverse events (SAE) occurred in 10%.The most Common AE were diarrhea, nausea, upper abdominal pain, serum creatinine increase and rash. Hematologic response according to IWG criteria 2006 with DSX were observed in 17% of patients and was more frequent in MPN than MDS, independently from IOL. Conclusion DSX has shown high efficacy in a variety of iron overloaded patients with different anemias. Appropriate patient selection and regular clinical multidisciplinary evaluation of comorbidity and concomitant therapy remains a critical components of successful ther­apy, combined with carefull monitoring for both adverse effects and clinical efficacy, in order to derive the most benefit from a carefully imple­mented chelation strategy.In our cohort improvement of erythropoiesis was marginal. This might be due to the very small patient group analyzed. Disclosures No relevant conflicts of interest to declare.