Angiogenesis has been implicated in the pathogenesis and prognosis of myelodysplastic syndrome (MDS). In this study, we investigated the relationship between microvessel density (MVD), vascular endothelial growth factor (VEGF) expression, common morphological and clinical factors, and survival in patients with MDS. We examined the MVD of paraffin-embedded bone marrow sections from 70 MDS patients and 31 controls. VEGF expression was determined in 50 patients and 20 controls. The median MVD in MDS patients was significantly higher than that in controls (p = 0.025), whereas there was no difference in VEGF expression between MDS patients and controls. In univariate analysis, increased MVD was associated with a shorter survival time (p = 0.023). However, in multivariate analysis, MVD was not an independent predictor of survival. The VEGF expression did not influence survival in univariate analysis. Survival was independently influenced by platelet count (p = 0.0073), cytogenetic risk category (p = 0.022), and transfusion dependence (p = 0.0073). Neither MVD nor VEGF expression were predictors for progression to acute myeloid leukemia in univariate analysis. Progression to acute myeloid leukemia was independently influenced only by the cytogenetic risk category (p = 0.022). This study confirmed increased MVD in MDS. It does not support an independent prognostic role of angiogenesis in MDS.
Methods: This non-randomised prospective study included 77 patients of age ≥ 12 years with confirmed diagnosis of iron deficiency anemia between January 2018 & January 2019. Detailed history was taken & examination performed for signs & etiology of IDA. The cut-off serum ferritin level for IDA diagnosis was < 15 ng/ml. Pregnant females and patients with concurrent vitamin B12 deficiency were excluded. All patients were treated with Injection Ferric Carboxymaltose (FCM) by I.V. infusion over 30 minutes in day care. Total dose of parenteral iron was calculated according to Ganzoni Formula: Total iron deficit (mg) = 2.4 x body weight (kg) x [target haemoglobin -actual haemoglobin (g/dl)] + 500 mg (depot iron). The maximum dose of FCM administered in a single infusion was 1000 mg. Patients with total iron dose > 1000 mg received two divided doses one week apart. Patients also received oral folic acid at 5 mg/day dose for at least 3 weeks. Appropriate workup for etiology of IDA was performed in all patients. Therapeutic response was assessed after 3 weeks of first FCM dose & was defined as hemoglobin increase of ≥ 2 g/dl from baseline. Results: The median age of patients was 33 years (range 16 -75 years) and majority (78%) were females. The median baseline hemoglobin was 5 g/dl (range 2.0 -8.6 g/dl). Therapeutic response was achieved in 100% patients. Mean increase in haemoglobin at 3 weeks was 4.2 g/dl (range 2.8 -5.5 g/dl). One patient had mild headache during FCM infusion. There was no infusion-related toxicity or any other adverse event. Summary/Conclusion: In our study, intravenous ferric carboxymaltose was found to be highly effective & safe alternative to oral iron for treatment of iron deficiency anemia, with excellent patient compliance. It is ideally suited for patients who require rapid replenishment of iron stores.
Introduction. Acute myeloid leukemia is a malignant, clonal disease of a hematopoietic stem/progenitor cell, characterized by accumulation of acquired somatic genetic and epigenetic alterations. Acute myeloid leukemia is, basically, highly heterogeneous disease, so individual treatment approach is needed. With the use of high-throughput genome sequencing technologies, a full spectrum of recurrent gene mutations in acute myeloid leukemia has been discovered, which has also provided deeper insight into leukemogenesis and acute myeloid leukemia ontogeny. This review focuses on molecular markers with proven prognostic significance, which form, together with standard cytogenetics, basis for current acute myeloid leukemia risk stratification. Even in the era of molecular markers, standard prognostic factors (pre-treatment and postinduction factors) have a strong influence on the choice of postremission therapy. Conclusion. Evaluation of molecular markers and their impact on prognosis in acute myeloid leukemia should be interpreted in the context of complex gene interactions. Only comprehensive understanding of acute myeloid leukemia biology and integration of all prognostic markers enable us to timely plan risk adapted treatment.
Imatinib (Gleevec) has shown long-term efficancy and safety in published randomized clinical trials. Anzovip (Imatinib) is a new generic drug produced by Zdravlje Actavis,which was approved by the Medicines and Medical Devices Agency of Serbia in January 2012. In July 2012, National Health Insurance Fund of Serbia introduced this drug in the positive list. All the patients using Glivec were switched to Anzovip and all newly diagnosed patients started with Anzovip therapy. In this study, hematologic and cytogenetic responses were evaluated in CML patients who received generic Imatinib as the first line therapy and in patients who switched from branded Imatinib to an Imatinib copy drug. Materials and methods. During August and September 2012, all the patients were switched from Glivec to Anzovip and all new CML patients were treated with Imatinib copy. 55 patients treated with branded Imatinib were switched to generic Imatinib. Out of 17 newly diagnosed patients with CML-CP, who started with generic Imatinib, 7 patients could be followed up for 18 months. All patients underwent hematologic, cytogenetic monitoring based of the recommendations of the ELN. Results. These are the results of using Anzovip after 18 months. Of the 55 patients who were switched from branded Imatinib to Imatinib copy, 11 patients (20 %) have lost complete cytogenetic response they already had, but without signs of biological illness transformation. They were switched to 2nd line therapy nilotinib.Of the 7 newly diagnosed patients who started with genereic Imatinib, all 7 patients (100%) have achieved complete hematologic response (CHR) in the period of 6 months. 3 (42,8%) patients have achieved CCgR and 2 patients (28,6%) have achieved MMR in the period of 12 months. 57% of patients have switched to second generation of TKI because of failure or intolerance according to ELN and national recommendation. The drug has been well tolerated, wild mild adverse event, more frequently, fluid retention and gastrointestinal symptoms. Only one patient have had skin changes grade ¾ and he has been switched to second generation of TKI. Conclusions. It is unknown whether patients, who responded to branded Imatinib and than switched to its copy versions, will tolerate the copy drug and maintain the previous response. Because of that, it is important to careful follow up of a selected patients several months after the switch to generic imatinib. Despite of the small number of patients who started with Imatinib copy, our results in term of hematologic and cytogenetic response were close to the international series. Disclosures Urosevic: Novartis: Consultancy, Honoraria. Savic:Roche: Honoraria; NovoNordisc: Honoraria. Rajic:NovoNordisc: Honoraria.
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