scholarly journals What is the right dosage of dasatinib for treating chronic myeloid leukaemia?

Author(s):  
Rüdiger Hehlmann
1998 ◽  
Vol 65 (1) ◽  
pp. 120-122
Author(s):  
L.F. Martino ◽  
R. Gemelli ◽  
M. De Pasquale ◽  
V. Arcuri ◽  
O.L. Sicuro ◽  
...  

In this work the authors describe a case of priapism lasting approx. 15 hours presenting chronic myeloid leukaemia in a 15-year-old boy. Aspiration of the corpora cavernosa was carried out and the boy remained in intensive care for 2 months, after which a Doppler examination was performed. This showed a moderate flow in the left artery and a poorer situation in the right.


2019 ◽  
Vol 12 (10) ◽  
pp. e232005
Author(s):  
Paolo Fraticelli ◽  
Devis Benfaremo ◽  
Marco Cardinali ◽  
Armando Gabrielli

We report the case of an otherwise healthy 60-year-old man presenting with fever, leucocytosis and a painful swelling of the right calf. We initially performed cultural and cytological examination of the popliteal fossa mass, but the results were disappointingly inconclusive. The subsequent development of several erythematous subcutaneous nodules, rapidly evolving to broad ulcerative lesions, prompted us to reconsider the clinical setting as a whole, which included fever, marked leucocytosis and multiple subcutaneous nodules. A biopsy of the ulcerative lesions finally led to the diagnosis of neutrophilic panniculitis, which was sustained by a hybrid myelodysplastic/myeloproliferative disorder like BCR-ABL1-negative atypical chronic myeloid leukaemia. The patient was initially treated with high-dose intravenous corticosteroids, resulting in a dramatic improvement of the skin lesions and normalisation of blood tests. Azacytidine treatment was subsequently started, and the haematological disease remained stable.


2018 ◽  
Vol 2 (02) ◽  
pp. 39-41
Author(s):  
Md. Rafiquzzaman Khan ◽  
Arifur Rahman ◽  
Khaza Amirul Islam ◽  
AQM Ashraful Haque ◽  
Masuda Begum

The aim of this retrospective observational study was to observe the pattern and frequency of haematological disorders among the patients attending in the specialized Haematology outpatient Department (HOPD) in Bangabandhu Sheikh Mujib Medical University. Consecutive 201 patients over the period of one year were enrolled. Their age ranged from 01 to 72 years with a mean age of 36.76 years. Most of the patients (34.3%) were in between the ages of 31 to 45 years followed by 16 to 30 years (27.9%). Male to female ratio was 0.65. Iron deficiency anaemia is the most common (24.9%) followed by chronic myeloid leukaemia (11.9%), Hb E beta thalassaemia (9.5%), idiopathic thrombocytopenic purpura (9.5%), beta thalassaemia trait (7.0%), Hb E trait (5.5 %), aplastic anaemia (5.0%), multiple myeloma (3.5%), acute lymphoblastic leukaemia (3.0%). Acute myeloid leukaemia, autoimmune haemolytic anaemia, chronic lymphocytic leukaemia, anaemia of chronic disease, non-Hodgkin lymphoma, polycythaemia, beta thalassemia major and alpha thalassemia was 2.5%, 2.5%, 2.0%, 1.5%, 1.5%, 1.5%, 1.0% and 1.0%, respectively. In the present study, we observed that iron deficiency anaemia the most common non-malignant disease and chronic myeloid leukaemia is the common haematological malignancy.


2017 ◽  
Vol 1 (01) ◽  
pp. 16-22
Author(s):  
Mohiuddin Ahmed Khan ◽  
Mafruh Akter ◽  
Muhammad Kamruzzaman

Author(s):  
Simone Claudiani ◽  
Jane F. Apperley ◽  
Richard Szydlo ◽  
Afzal Khan ◽  
George Nesr ◽  
...  

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Yotaro Ochi ◽  
Kenichi Yoshida ◽  
Ying-Jung Huang ◽  
Ming-Chung Kuo ◽  
Yasuhito Nannya ◽  
...  

AbstractBlast crisis (BC) predicts dismal outcomes in patients with chronic myeloid leukaemia (CML). Although additional genetic alterations play a central role in BC, the landscape and prognostic impact of these alterations remain elusive. Here, we comprehensively investigate genetic abnormalities in 136 BC and 148 chronic phase (CP) samples obtained from 216 CML patients using exome and targeted sequencing. One or more genetic abnormalities are found in 126 (92.6%) out of the 136 BC patients, including the RUNX1-ETS2 fusion and NBEAL2 mutations. The number of genetic alterations increase during the transition from CP to BC, which is markedly suppressed by tyrosine kinase inhibitors (TKIs). The lineage of the BC and prior use of TKIs correlate with distinct molecular profiles. Notably, genetic alterations, rather than clinical variables, contribute to a better prediction of BC prognosis. In conclusion, genetic abnormalities can help predict clinical outcomes and can guide clinical decisions in CML.


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