<i>In vitro</i> culture growth of erythroid progenitors and serum erythropoietin assay in the differential diagnosis of polycythaemia

Ly, S.; Ct, Lee; See, Lai‐Chu; Yu-xiang, OU; Dunn, Po; Pn, Wang; Mc, Kuo; Jh, Wu

doi:10.1046/j.1365-2362.1998.00331.x

Cited by 19 publications

(29 citation statements)

References 26 publications

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“…[10][11][12] In patients with erythrocytosis, EECs are specific for PV and can be used to distinguish PV from SE. [13][14][15][16] However, the EEC assay is technically demanding and not available in most hematologic laboratories. It has therefore been included in the revised criteria only as a facultative major ("A") criterion or as a minor ("B") criterion.…”

Section: Introductionmentioning

confidence: 99%

Quantification of PRV-1 mRNA distinguishes polycythemia vera from secondary erythrocytosis

Klippel

Strunck

Temerinac

et al. 2003

Blood

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To date, the diagnosis of polycythemia vera (PV) relies on clinical criteria. We have recently described the overexpression of a hematopoietic receptor, polycythemia rubra vera-1 (PRV-1), in patients with PV. Here, we report a quantitative reverse transcriptase-polymerase chain reaction (RT-PCR) assay for the measurement of PRV-1 mRNA levels. We have determined PRV-1 expression in 71 patients with PV, 11 patients with secondary erythrocytosis (SE), as well as in 80 healthy controls. PV patients express significantly higher amounts of PRV-1 than healthy controls or patients with SE (P < .0001). Because there is no overlap between the PRV-1 expression in PV patients versus healthy controls or SE patients, the assay has a very high sensitivity and specificity for the diagnosis of PV in our population. In patients with erythrocytosis, the quantitative RT-PCR assay described here therefore provides a rapid, highly specific and sensitive tool for the diagnosis of PV.

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Section: Introductionmentioning

confidence: 99%

Quantification of PRV-1 mRNA distinguishes polycythemia vera from secondary erythrocytosis

Klippel

Strunck

Temerinac

et al. 2003

Blood

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“…Amongst the EEC assays available there is data to suggest that serum free assays which utilize collagen (as opposed to a methycellulose base) may be more sensitive, and easier to interpret [23]. EEC formation is clearly a feature of PV (and helpful for distinguishing PV from secondary erythrocytosis), but may be present in a subset of patients with ET (some of which end up developing PV) [24]. The presence of EEC in CMPD led to the evaluation of spontaneous megakaryocyte colony formation in ET [25].…”

Section: Growth Factor/cytokine Hypersensitivitymentioning

confidence: 99%

“…PRV-I and EEC assays were positive in all the PV patients, and ET patients who displayed PRV-I also would form EEC. It has been suggested that ET patients who form EEC ofien end up developing the PV phenotype and may be diagnosed in a phase of their disease that precedes the erythrocytosis [24]. Overall, PRV-1 may not play a causal role in PV, it may really be CD177, but appears to be of potential discriminatory benefit between PV and secondary erythrocytosis.…”

Section: Prv-1mentioning

confidence: 99%

Clinical and scientific advances in the philadelphia-chromosome negative chronic myeloproliferative disorders

Mesa

2002

Int J Hematol

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The chronic myeloproliferative disorders are clonal hematopoietic stem cell disorders and include chronic myeloid leukemia (CML), polycythemia vera (PV), essential thrombocythemia (ET), and agnogenic myeloid metaplasia (AMM). These diseases are characterized by clonal expansion of the myeloid compartment, increased marrow angiogenesis, and varying risks for blastic transformation. A clear molecular abnormality exists (t(9;22) leading to the fusion of BCR-Abl) only for CML, which led to effective targeted therapy (STI-571). Since no similar pathogenetic mechanism has been discovered for the t(9;22) negative chronic myeloproliferative disorders, their respective diagnosis is currently based on a variety of rather cumbersome diagnostic criteria. Polycythemia vera is distinguished from reactive erythrocytosis through erythropoietin independent growth of erythroid progenitors in vitro, suppressed levels of endogenous erythropoietin, possible overexpression of PRV-1 (polycythemia rubra vera-1), decreased c-Mpl expression on megakaryocytes, as well as overexpression of bcl-xL, and potentially aberrant activity of the Jak-Stat pathway. ET is defined by thrombocytosis and is distinguished from reactive states by decreased megakaryocyte c-Mpl expression, and a propensity for thrombosis. AMM has been associated with a variety of observations including increased concentrations of pro-fibrotic cytokines, increased angiogenesis, and myeloid expansion. AMM is often indistinguishable clinically and prognostically from the advanced phases of other CMPD (specifically post-polycythemic and post-thrombocythemia myeloid metaplasia), all of which are subentities of a diagnosis of myelofibrosis with myeloid metaplasia (MMM). The management of CMPD patients is quite varied given the broad range of disease severity and survival observed. The role of stem cell transplantation is limited by the age and comorbidities encountered in CMPD patients. Since no broadly applicable therapy effects the mortality of the CMPD, management currently focuses on the prevention/palliation of disease morbidity (i.e. vascular complications, pruritus, organomegaly, constitutional symptoms). Palliative strategies which currently focus on non-specific myelosuppresion, will hopefully be soon replaced by targeted therapies as insight into pathogenetic mechanisms of these diseases evolves.

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“…This may occur through an increased proliferation of the abnormal BFU-E compared to the healthy cells. Alternatively, under conditions of low serum EPO, which have been demonstrated in PV patients [14], the normal precursors may not be able to divide or differentiate.…”

Section: Endogenous Erythroid Coloniesmentioning

confidence: 99%

“…Since then, many researchers have supported this recommendation [14, 20, 21]. The usefulness and validity of EECs as an aid in the diagnosis of PV have been reviewed in two excellent articles [22, 23]and shall therefore not be repeated here in detail.…”

Section: Pathophysiological and Diagnostic Markersin Pvmentioning

confidence: 99%

Polycythaemia vera: Will New Markers Help Us Answer Old Questions?

Pahl

2002

Acta Haematol

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The publication of the first molecular markers for polycythaemia vera (PV) has led to a renewed interest in finding the mutations leading to the development of this myeloproliferative disorder. A substantial amount of cell biological data on the PV stem cell, however, have been available for over two decades. This review will summarise, combine and integrate both fields of investigation. Based on this analysis, two alternative models for the development of myeloproliferative disorders are proposed.

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In vitro culture growth of erythroid progenitors and serum erythropoietin assay in the differential diagnosis of polycythaemia

Abstract: The present study showed that apart from EEC assay, the post-phlebotomy serum EPO level was a sensitive and specific parameter in the differential diagnosis of polycythaemia, in particular for the identification of PV among patients with unclassifiable polycythaemia.

Cited by 19 publications

References 26 publications

Quantification of PRV-1 mRNA distinguishes polycythemia vera from secondary erythrocytosis

Quantification of PRV-1 mRNA distinguishes polycythemia vera from secondary erythrocytosis

Clinical and scientific advances in the philadelphia-chromosome negative chronic myeloproliferative disorders

Polycythaemia vera: Will New Markers Help Us Answer Old Questions?

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