The international prognostic index (IPI) and the revised IPI (R-IPI) are used to determine the prognosis in diffuse large B-cell lymphoma (DLBCL). However, these scoring systems are insufficient to identify very high-risk patients. Recently, the prognostic nutritional index (PNI) -calculated with lymphocyte count and albumin- has been used to determine the prognosis in DLBCL. This study aimed to evaluate the effect of PNI score on prognosis and survival in patients with high-risk DLBCL. Patients diagnosed with DLBCL and treated with rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisolone were included. Pre-treatment IPI, R-IPI, and PNI scores and progression-free survival (PFS) and overall survival (OS) times were calculated. The cutoff value for PNI according to OS was determined by using the X-Tile program. One hundred and ten patients were included, the median age was 63 years and the median follow-up period was 25 months. According to R-IPI, the median OS could not be reached for the very good risk group, and the median OS values were 83 and 17 months in the good and poor-risk groups, respectively (p=0.001). The cohort was divided into three groups according to the cut-off value for the PNI: patients with PNI <33 were classified as high-risk, 33-42 intermediate-risk, and ≥42 as low-risk. According to PNI, the median durations of PFS and OS were 2 months and 3 months in the high-risk group, 9 months and 19 months in the intermediate-risk group respectively, and in the low-risk group the median duration for PFS and OS could not be reached (p=0.001). The R-IPI is widely used to estimate the prognosis in DLBCL. But in our cohort, in the poor-risk patient group, the OS was 17 months according to R-IPI, while this period was 3 months according to PNI. This finding demonstrated that PNI might predict early mortality in DLBCL.

Chronic lymphocytic leukemia (CLL) is a progressive disease with an indolent course, and tumor lysis syndrome (TLS) is rarely seen in CLL. Ibrutinib is a novel bruton kinase (BTK) inhibitor increasingly used in CLL treatment. Ibrutinib has significant side effects such as atrial fibrillation, bleeding, diarrhea, and infections. However, TLS is reported rarely with ibrutinib treatment. This report focuses on a 69-year-old female patient diagnosed with relapsed CLL who developed grade 4 TLS after ibrutinib monotherapy. The patient developed TLS on the third day of ibrutinib treatment necessitating discontinuation of the treatment and initiation of hemodialysis and supportive care. Ibrutinib treatment was re-initiated at a daily dose of 140 mg therapy after an interval of seven days, and then any additional side effect was not seen. Tumor lysis syndrome secondary to ibrutinib has been reported in an increasing number of cases. There is currently no information on managing adverse effects of TLS attributed to ibrutinib. Consequently, ibrutinib treatment of this patient was not terminated, and restarted after a short interval. It must not be forgotten that TLS secondary to ibrutinib treatment may be rarely seen, and can be life-threatening. Treatment with ibrutinib should be initiated in consideration of this side effect, and the development of complication of TLS may not necessitate discontinuation of ibrutinib treatment.

Background: The most frequent cytogenetic aberration is 13q14.3 deletion in Chronic Lymphocytic Leukemia (CLL). HsamiR-15a/hsa-miR-16-1 are tumor suppressor miRNAs encoded from 13q14.3 region. Objectives: The aim of this study was to investigate the 13q14.3 deletion using molecular and cytogenetic techniques and association with miRNA-15a/miRNA-16-1. Materials And Methods: We used peripheral blood samples of 30 CLL patients who were either induced and or non-induced with DSP30+IL-2 to determine 13q14.3 deletion by karyotyping and iFISH. Expression levels of hsa-miR-15a/miR-16-1 were measured using qRT PCR and compared with deletions. Results: 13q14.3 deletion was detected in 8.6% of cases by karyotyping and in 65% by iFISH. Mosaic forms (monoallelic+biallelic) were observed in 50% of cases. Besides determining common chromosome abnormalities such as add(2)(q37), t(2;7) (p11.2;q22), del(6)(q13q21), del(6)(q25), add(9)(q21), del(11)(q23), t(11;14)(q13;q32), del(13)(q11q12), del(13)(q12q14), add(14)(q23), del(14)(q23), t(14;19)(q32;q13.1), del(15)(q23), del(17)(p12), t(18;22)(q21;q11.2), add(21)(p13) and t(17;21)(q11.2;122), we also determined t(1;13)(q32;q34), inv(2)(p25q21), del(13)(q22q32), t(14;19) (q24;q13), dup(17)(q21q23), der(21;21)(p13;p13) which have not been reported previously. Mitotic index data was found statistically significant and DSP30+IL-2 increased mitotic index by 2.5 folds. Association between decreased miR-16-1 expression and deletions was statistically significant. Conclusion: We suggest that cytogenetic and iFISH analyses are complementary and use of DSP30+IL-2 is effective .in CLL. Decreased expression of hsa-miR-16-1 is remarkable. Keywords: CLL; miR-15a/miR-16-1; 13q14.3 deletion.