Aim: To evaluate the effectiveness of L-arginine in the prevention of endothelial dysfunction, which may be a predictor of anthracycline-induced myocardial injury, in patients with acute leukemia (AL) on the background of anthracycline antibiotics low cumulative doses from 100 to 200 mg/m2. Materials and Methods: A total of 81 adult AL patients (38 males and 43 females with the age of 16–59 years) were studied. The patients were divided into two groups: group I (n = 34), AL patients treated with chemotherapy (CT) and L-arginine hydrochloride; group II (n = 47) — AL patients treated with CT only. Cardiac evaluation and endothelial function assessment were performed at baseline and after second CT. Electrocardiography (ECG) parameters, lipid peroxidation activity, antioxidant protection and NO system state were evaluated. Results: The bioelectric activity abnormalities of the myocardium were observed in studied patients with low cardiac risk after induction CT. In case of L-arginine administration, only minimal daily ECG changes were recorded. A significant difference in the lipid peroxidation and antioxidant defense system activity in patients of groups I and II was determined. We noticed deepening of endothelial dysfunction on the background of cytostatic therapy with anthracycline antibiotics compared with baseline values in patients of group II. It was found that prophylactic L-arginine increases superoxide dismutase level and reduces the total NOS activity due to its inducible isoform. Conclusion: The leading factor of anthracycline-induced cardiotoxicity is the imbalance between free radical generation and their inactivation that leads to endothelial dysfunction development. L-arginine eliminates the prooxidant-antioxidant imbalance and improves the endothelial function.

detected in two ED patients (1 HR and 1 IR patients), which was the same mutation NRAS G12C. FLT3 gene mutations (including FLT3-ITD and FLT3-TKD) were the most frequently found in HR APL patients. 88.33% of HR patients(10/12) harbored FLT3 mutations, while 20% of IR patients (5/25) and 22.22% of LR patients (2/9) were found harbored FLT3 mutations(P < 0.05). Among the 17 cases of FLT3 mutant patients, only one HR patient (5.88%, 1/17), who carried FLT3-TKD D835Y mutation, died 3 days after induction treatment. Meanwhile, the less common WT1 gene mutations were all found in IR APL patients. Summary/Conclusion: HR APL patients had the highest frequency of gene mutations, however there were no significant difference between the three risk groups regarding the median mutation numbers. ED patients did not have more gene mutations compared with non-ED patients. FLT3 gene mutations were the most frequently occurred mutations, especially in HR APL patients, though might have no relation with early mortality.

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Background: At present there is no cure for RRMM, yet pts have prolonged survival due to improved treatments, and therefore ensuring acceptable QoL throughout treatment is worthwhile. We aimed to evaluate QoL, safety and response to treatment with IRd as ! 2nd line in RRMM pts in a real world setting.Methods: Adult pts with RRMM who have been assigned IRd as !2nd line treatment were enrolled in multicenter observational prospective study. Treatment response was evaluated by IMWG 2011, adverse events (AEs) e by CTCAE v.4.0. Pts filled out SF-36 and ESAS-R at baseline and during IRd treatment. Descriptive statistics and paired t-test were employed.Results: At time of analysis 32 pts with RRMM were enrolled: median age e 65 yrs, 72% females, DurieeSalmon stage III e 56%, ECOG status 2/3 e 28%. Half of pts had 3-7 lines of prior therapy. The median number of cycles administered is 4, median follow-up e 4.5 (0.4-10.5) mos. Treatment response was not evaluated in 9 pts: 1 e death (at 3 months), 1e refusal, 7 e too early for evaluation. Out of 23 pts 6 achieved partial response, 10 e minor response, yielding a clinical benefit rate of 67%. AEs were revealed in 43% pts: grades 1-2 AEs e 9 pts; grades 3-4 AEs e 4 pts; SAEs e 3 pts (neurological toxicity, gastric bleeding, hypotension). Baseline QoL was dramatically impaired by the majority of SF-36 scales with significant QoL impairment in 50% pts. 88% pts had moderate-to severe symptoms (!4 scores on the scale from 0 to 10); moderate-to severe tiredness, pain or shortness of breath had 72%, 59% and 50% pts, respectively. At 1 month of IRd treatment QoL improved or was stable (without significant impairment) in 53% pts, at 3 months e in 45% pts. Better general and mental health were observed 1 month after treatment start (p¼0.01). At 1 month of treatment meaningful decrease of shortness of breath (in 60% pts), tiredness and pain (in 30% pts) was revealed; this proportion decreased twice at 3 months. Conclusions:The first results of our real-world study demonstrate significant clinical benefits of IRd regimen in RRMM pts. The treatment has acceptable safety profile and is accompanied with QoL maintenance and satisfactory symptom control in this heavily pretreated patients' cohort.

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