Transitions Among the Myeloproliferative Disorders

Glasser, Robert M.

doi:10.7326/0003-4819-71-2-285

Cited by 53 publications

(11 citation statements)

References 48 publications

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“…It has been shown using chromosome and enzyme markers that fibroblasts do not arise from the abnormal hematopoietic stem cell, and that the increased bone marrow collagen seen in myeloproliferative disease is a secondary abnormality [20-231. Most studies of bone marrow fibrosis have been carried out in patients with idiopathic myelofibrosis, but the close relationship between polycythemia Vera, chronic myelogenous leukemia and the other diseases grouped together as myeloproliferative disorders justified inclusion of patients with polycythemia Vera in our study. In fact, the finding of elevated levels of PC III peptide in patients with polycythemia Vera who did not yet show clinical evidence of marrow fibrosis supports the concept of a spectrum of diseases with possible transitions among them [ 1,24,25].…”

Section: Discussionmentioning

confidence: 72%

Increased serum procollagen III aminoterminal peptide in myelofibrosis

et al. 1983

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Myelofibrosis has been shown to involve an increase in type III collagen in the marrow. The aminoterminal procollagen III (PC III) peptide fragment is released during the production of PC III by fibroblasts and its serum level is therefore a marker for type III collagen synthesis. Using a recently developed sensitive radioimmunoassay, serum levels of PC III peptide were measured in 30 patients with myeloproliferative disease and 23 normal volunteers. Levels were found to be elevated above normal values in patients with polycythemia vera, even more elevated in patients with polycythemia and evidence of secondary myelofibrosis with myeloid metaplasia, and most strikingly elevated in patients with agnogenic myeloid metaplasia and severe marrow fibrosis. There was a significant association between serum levels of PC III peptide and the extent of reticulin fibrosis in bone marrow biopsies. Serum PC III level appears to be a quantitative marker for myelofibrosis.

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Section: Discussionmentioning

confidence: 72%

Increased serum procollagen III aminoterminal peptide in myelofibrosis

et al. 1983

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“…These findings suggest that serum lysozyme estimation can be useful in indicating transition from PRV to myelosclerosis. It might also help to define a transitional myeloproliferative group with features akin to both PRV and myelosclerosis (Glasser & Walker, 1969; Duhamel et al, It has been shown previously that the TBlzBC is increased in the myeloproliferative disorders (Beard et al, 1954;Mollin & Ross, 1955) due to an increase in transcobalamin I (Herbert, 1968;Gilbert et af, 1969). This protein occurs in many tissues including granulocytes and it has been suggested that granulocytes may secrete this protein (Simons & Weber, 1966;Hall, 1969;Corcino et a!, 1970).…”

Section: Discussionmentioning

confidence: 99%

Serum Lysozyme and Vitamin B₁₂ Binding Capacity in Myeloproliferative Disorders

et al. 1971

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Summary Estimations of serum lysozyme (muramidase), total B12 binding capacity (TB12BC) and folate were performed in 122 patients: 69 with myeloproliferative disorders (39, polycythaemia rubra vera (PRV); 10, chronic granulocytic leukaemia, Ph1‐chromosome positive (CGL); 20, myelosclerosis) and 53 with other disease which affect leucocyte production or turnover (17, monocytic leukaemias; 20, megaloblastic anaemia; 15, neutropenia; and a single case of red cell aplasia progressing to a myeloproliferative disorder). The highest serum lysozyme levels were found in monocytic leukaemia. Serum lysozyme concentrations were also elevated in myelosclerosis and to a lesser extent in CGL and in PRV. High levels in PRV occurred in patients developing myelosclerosis or with active disease, resistant to treatment. Significantly higher concentrations of lysozyme were present in patients with myelosclerosis following PRV than in patients with the primary form of the disease. Patients with myeloproliferative diseases and high lysozyme concentrations tended to have low serum folate levels. Slightly raised levels were found in about 50% of patients with megaloblastic anaemia. Moderately high serum lysozyme concentrations also occurred in patients with neutropenia and hypercellular bone marrows but not in those with hypocellular marrows. TB12BC concentrationswere increased in the myeloproliferative disorders, especially in CGL and to a lesser extent in myelosclerosis and least of all in PRV. The results suggest that serum lysozyme reflects granulocyte turnover (except in monocytic leukaemia) while TB12BC (providing liver function is normal) correlates closely with the total blood (and possibly marrow and splenic) granulocyte pool. The ratio between serum lysozyme and TB12BC proved to be a useful index of the balance between granulocyte turnover and total granulocyte pool in individual patients.

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“…151 Finally, adding to the confusion has been the uncritical acceptance or misuse of terms such as "spent phase" and "postpolycythemic myeloid metaplasia" together with the assumption that the various chronic myeloproliferative disorders are interrelated 152 when in fact proof is lacking that they are. 153 The spent phase of polycythemia vera While it has been clearly established that polycythemia vera can be complicated by anemia, myelofibrosis, and myeloid metaplasia, the frequency with which these complications occur and their clinical significance in the absence of cytotoxic therapy has rarely been ascertained prospectively. For example, the development of anemia due to bone marrow exhaustion has been considered an inevitable event in the natural history of polycythemia vera and possibly a forerunner of leukemia.…”

Section: The Natural History Hypothesismentioning

confidence: 99%