Myeloid & Lymphoid disorders in practice - 2010


Comment: Molecular diagnostics – the need for rationalisation?
John Reilly
pp 2-2
Pathology costs £2.5 billion a year in the UK, a figure that represents 4% of the total NHS expenditure. To improve efficiency, it has been proposed that large-scale consolidation of services could result in greater purchasing power, better utilisation of equipment and, ultimately, reduced costs.
The current status of JAK2 inhibitors for treating MPNs
Ruben A Mesa
pp 3-7
The myeloproliferative neoplasms (MPNs) currently include myelofibrosis (MF), essential thrombocythaemia (ET) and polycythaemia vera (PV). Patients with MF include those with primary myelofibrosis (PMF) and those in whom MF evolved from an antecedent, ET or PV. These disorders share several key features.
Skin-related side-effects of treatment for ET – a review
Yasmine Robson and Andrew Morris
pp 8-9
Essential thrombocythaemia (ET) is a chronic myeloproliferative neoplasm (MPN) defined by the WHO as a platelet count >600 x 109/l and a bone marrow biopsy showing proliferation of the megakaryocyte lineage. Symptoms of ET include headache and visual disturbances, and splenomegaly is a common finding. ET can transform, with up to 5% of patients eventually developing myelofibrosis or acute myeloid leukaemia.
Classification and treatment of congenital erythocytoses
Mary Frances McMullin
pp 10-12
An erythrocytosis is present when the red cell mass is >=125% of that predicted for the individual’s sex and body mass. The increased red cell mass is reflected in the fact that haemoglobin (Hb) and haematocrit (Hct) levels are also higher. An Hct of 0.60 in a man and 0.56 in a woman always indicates a true increase in red cell mass and, therefore, an erythrocytosis. At lower Hct levels, it may be necessary to formally measure the red cell mass to establish the presence of a true erythrocytosis.
FLT3 mutations in acute myeloid leukaemia
S Osman Ahmed and Panagiotis D Kottaridis
pp 13-15
The last two decades have seen significant progress in understanding many of the underlying genetic and molecular abnormalities in acute myeloid leukaemia (AML). In parallel, there has been an evolution of therapeutic regimes with modest gains in survival. An array of mutations and deregulated gene expression have been identified, which, even if not causative, contribute to the leukaemic phenotype. Here, we review mutations of Fms-like tyrosine kinase-3 (FLT3) and the associated diagnostic and therapeutic implications.

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