E. Iskierka-Jażdżewska, K. Giannopoulos, S. Grosicki, K. Jamroziak, T. Wróbel, J. Zaucha, M. Dudzinski, Ł. Bołkun, E. Bodzenta, J. Drozd-Sokołowska, Agnieszka Samborska, A. Wolska-Washer, I. Hus
{"title":"Polish Experts’ Position Statement on the use of granulocyte colony-stimulating factor in the treatment of chronic lymphocytic leukemia with venetoclax combined with rituximab","authors":"E. Iskierka-Jażdżewska, K. Giannopoulos, S. Grosicki, K. Jamroziak, T. Wróbel, J. Zaucha, M. Dudzinski, Ł. Bołkun, E. Bodzenta, J. Drozd-Sokołowska, Agnieszka Samborska, A. Wolska-Washer, I. Hus","doi":"10.5603/HCP.2021.0008","DOIUrl":"https://doi.org/10.5603/HCP.2021.0008","url":null,"abstract":"Chronic lymphocytic leukaemia (CLL) is the most common adult leukaemia in Western countries. Venetoclax, a BCL-2 inhibitor, in combination with rituximab is an effective therapeutic option approved for the treatment of refractory and relapsed CLL. Neutropenia diagnosed before or during the above-mentioned therapy is a significant clinical problem, which often involves the need to reduce the dose or temporarily discontinue venetoclax in the initial period of therapy. In Experts’ opinion, the use of granulocyte colony-stimulating factor (G-CSF) during venetoclaxrituximab combined therapy is reasonable in patients with baseline neutrocyte count < 1000–500/mm 3 and with high-risk neutropenia. The second important group for the use of G-CSF are patients developing grade 3 asymptomatic neutropenia during venetoclax dose escalation. Using G-CSF can prevent episodes that affect the maintenance of the venetoclax dose intensity and treatment continuity.","PeriodicalId":284891,"journal":{"name":"Hematology in Clinical Practice","volume":"1 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2021-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"122534179","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
J. Wajs, M. Lewandowska, P. Kluge, Lucyna Drążek, D. Jesionek-Kupnicka
{"title":"Blastic plasmacytoid dendritic cell neoplasm (BPDCN) — diagnostic and therapeutic challenge","authors":"J. Wajs, M. Lewandowska, P. Kluge, Lucyna Drążek, D. Jesionek-Kupnicka","doi":"10.5603/HCP.2021.0003","DOIUrl":"https://doi.org/10.5603/HCP.2021.0003","url":null,"abstract":"Blastic plasmacytoid dendritic cell neoplasm (BPDCN) is a rare and aggressive haematological malignancy. The disease usually affects the skin, bone marrow, peripheral blood and less commonly lymph nodes. The actual incidence of BPDCN is currently unknown. The data presented in the literature most often relate to one cases or small groups of patients, rarely they are multicentre studies. Diagnosis of BPDCN is based on histopathological examination and immunohistochemical stains. The diversity of the clinical manifestations and the PBDCN immunophenotype is the cause of significant difficulties in making a diagnosis and can lead to diagnostic errors. The optimal treatment for patients with this cancer has not yet been established. Responses to various chemotherapy regimens are unsatisfactory. Recent literature has reported that bone marrow allograft or targeted therapy may improve treatment outcomes in this group of patients. The paper presents the case of a 75-year-old man with BPDCN diagnosis. Attention was paid to diagnostic difficulties in patients with BPDCN and the differentiation of this rare disease with other hematological malignancies was discussed. The need for a national register of BPDCN patients has been highlighted. This could contribute to expanding knowledge about this cancer and to the development of effective, standard therapeutic treatment.","PeriodicalId":284891,"journal":{"name":"Hematology in Clinical Practice","volume":"24 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2021-09-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"126935257","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Efficacy of lenalidomide in the treatment of myelodysplastic/myeloproliferative neoplasms, unclassifiable (MDS/MPN-U) with the presence of deletion 5q– and trisomy 8+","authors":"Oliwia Bachanek-Mitura, A. Szudy-Szczyrek, M. Hus","doi":"10.5603/HCP.2021.0004","DOIUrl":"https://doi.org/10.5603/HCP.2021.0004","url":null,"abstract":"Myelodysplastic/myeloproliferative neoplasms (MDS/MPN) are very rare clonal myeloid characterized by the simultaneous presence of both of erythrocytic and/orgranulocytic dysplasia with myeloproliferative features. The etiology of the disease remains unknown. The MDS/MPN group is made up of five disorders: chronic myelomonocytic leukemia, atypical chronic myeloid leukemia, juvenile myelomonocytic leukemia, MDS/MPN ring sideroblasts with thrombocytosis and MDS/MPN, un classifiable (MDS/MPN-U). MDS/MPN-U remains the leastcharacterized entity. It accounts less than 5% of all myeloid disorder. The reare currently no well-established diagnostic criteria. The disease is heterogeneous with outclear management strategies. The aim of thispaperis to present a case of a 59-year-old female patient diagnosed with MDS/MPN-U with deletion 5q– and trisomy 8+, whom lenalidomide 10 mg daily has been used as monotherapy. The disease has initially manifested as severe cytopenias, multiple transfusions of blood preparations were required. Currently patientis in the 9th month of treatment. Hemoglobin, platelets and white blood cells returned to normal. The patient completely became independent of transfusion of red blood cell concentrates. No adverse events were observed.","PeriodicalId":284891,"journal":{"name":"Hematology in Clinical Practice","volume":"218 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2021-09-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"122396718","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Ponatinib in treatment of chronic myeloid leukemia with T315I mutation","authors":"Klaudia Cieśluk, J. Piszcz","doi":"10.5603/HCP.2021.0006","DOIUrl":"https://doi.org/10.5603/HCP.2021.0006","url":null,"abstract":"Chronic myeloid leukemia (CML) is a type of myeloproliferative neoplasm associated with a characteristic chromosomal translocation t(9;22)(q34;q11) which causes the formation of the Philadelphia chromosome (Ph). Therapeutic progress made in the last two decades and new-generation tyrosine kinase inhibitors (TKIs) introduction, signifi cantly increased patients’ prognosis. We present a case study of a Ph-positive CML patient with a point BCR/ABL1 mutation T315I treated with ponatinib.","PeriodicalId":284891,"journal":{"name":"Hematology in Clinical Practice","volume":"55 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2021-09-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"121780243","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}